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3. Large-scale assessment of polyglutamine repeat expansions in Parkinson disease

Author

Wang, L, Aasly, J, Annesi, G, Bardien, S, Bozi, M, Brice, A, Carr, J, Chung, S, Clarke, C, Crosiers, D, Deutschländer, A, Eckstein, G, Farrer, M, Goldwurm, S, Garraux, G, Hadjigeorgiou, G, Hicks, A, Hattori, N, Klein, C, Jeon, B, Kim, Y, Lesage, S, Lin, J, Lynch, T, Lichtner, P, Lang, A, Mok, V, Jasinska-Myga, B, Mellick, G, Morrison, K, Opala, G, Pihlstrøm, L, Pramstaller, P, Park, S, Quattrone, A, Rogaeva, E, Ross, O, Stefanis, L, Stockton, J, Silburn, P, Theuns, J, Tan, E, Tomiyama, H, Toft, M, Van Broeckhoven, C, Uitti, R, Wirdefeldt, K, Wszolek, Z, Xiromerisiou, G, Yueh, K, Zhao, Y, Gasser, T, Maraganore, D, Krüger, R, Sharma, M, Boyle, RS, Sellbach, A, O'Sullivan, JD, Sutherland, GT, Siebert, GA, Dissanayaka, NN, Pickut, B, Engelborghs, S, Meeus, B, De Deyn, PP, Cras, P, Lang, AE, Tzourio, C, Amouyel, P, Loriot, MA, Mutez, E, Duflot, A, Legendre, JP, Waucquier, N, Riess, O, Berg, D, Schulte, C, Djarmati, A, Hagenah, J, Lohman, K, Auburger, G, Hilker, R, van de Loo, S, Dardiotis, E, Tsimourtou, V, Ralli, S, Kountra, P, Patramani, G, Vogiatzi, C, Funayama, M, Yoshino, H, Li, Y, Imamichi, Y, Toda, T, Satake, W, Valente, EM, Ferraris, A, Dallapiccola, B, Ialongo, T, Brighina, L, Corradi, B, Ferrarese, C, Piolti, MR, Tarantino, P, Annesi, F, Gagliardi, M, Jeon, BS, Klodowska-Duda, G, Boczarska-Jedynak, M, Tan, EK, Belin, AC, Olson, L, Galter, D, Westerlund, M, Sydow, O, Nilsson, C, Puschmann, A, Lin, JJ, Maraganore, DM, Ahlskog, J, de Andrade, M, Lesnick, TG, Rocca, WA, Checkowa, H, Ross, OA, Wszolek, ZK, Uitti, RJ, Pathologic Biochemistry and Physiology, GEO-PD Consortium, Wang, L, Aasly, J, Annesi, G, Bardien, S, Bozi, M, Brice, A, Carr, J, Chung, S, Clarke, C, Crosiers, D, Deutschländer, A, Eckstein, G, Farrer, M, Goldwurm, S, Garraux, G, Hadjigeorgiou, G, Hicks, A, Hattori, N, Klein, C, Jeon, B, Kim, Y, Lesage, S, Lin, J, Lynch, T, Lichtner, P, Lang, A, Mok, V, Jasinska-Myga, B, Mellick, G, Morrison, K, Opala, G, Pihlstrøm, L, Pramstaller, P, Park, S, Quattrone, A, Rogaeva, E, Ross, O, Stefanis, L, Stockton, J, Silburn, P, Theuns, J, Tan, E, Tomiyama, H, Toft, M, Van Broeckhoven, C, Uitti, R, Wirdefeldt, K, Wszolek, Z, Xiromerisiou, G, Yueh, K, Zhao, Y, Gasser, T, Maraganore, D, Krüger, R, Sharma, M, Boyle, R, Sellbach, A, O'Sullivan, J, Sutherland, G, Siebert, G, Dissanayaka, N, Pickut, B, Engelborghs, S, Meeus, B, De Deyn, P, Cras, P, Tzourio, C, Amouyel, P, Loriot, M, Mutez, E, Duflot, A, Legendre, J, Waucquier, N, Riess, O, Berg, D, Schulte, C, Djarmati, A, Hagenah, J, Lohman, K, Auburger, G, Hilker, R, van de Loo, S, Dardiotis, E, Tsimourtou, V, Ralli, S, Kountra, P, Patramani, G, Vogiatzi, C, Funayama, M, Yoshino, H, Li, Y, Imamichi, Y, Toda, T, Satake, W, Valente, E, Ferraris, A, Dallapiccola, B, Ialongo, T, Brighina, L, Corradi, B, Ferrarese, C, Piolti, M, Tarantino, P, Annesi, F, Gagliardi, M, Klodowska-Duda, G, Boczarska-Jedynak, M, Belin, A, Olson, L, Galter, D, Westerlund, M, Sydow, O, Nilsson, C, Puschmann, A, Ahlskog, J, de Andrade, M, Lesnick, T, Rocca, W, and Checkowa, H

Subjects
Male, Age at onset, confidence interval, Genetic Epidemiology of Parkinson's Disease, Parkinson disease, spinocerebellar ataxia, Nerve Tissue Proteins, Disease, Biology, Parkinson Disease/epidemiology, Trinucleotide Repeat Expansion/genetics, Gene Frequency, Ataxins/genetics, Humans, Nerve Tissue Proteins/genetics, Genetic Predisposition to Disease, Risk factor, Allele frequency, Nuclear Protein, Aged, risk, Genetics, Medicine(all), Nuclear Proteins, Parkinson Disease, Ataxin, Odds ratio, Middle Aged, Phenotype, Nuclear Proteins/genetics, Genetic epidemiology, Ataxins, Gene Frequency/genetics, Nerve Tissue Protein, Peptide, Cohort, Female, Neurology (clinical), Human medicine, Trinucleotide repeat expansion, Peptides, Trinucleotide Repeat Expansion, Peptides/genetics, Human
Abstract

Objectives: We aim to clarify the pathogenic role of intermediate size repeat expansions of SCA2, SCA3, SCA6, and SCA17 as risk factors for idiopathic Parkinson disease (PD). Methods: We invited researchers from the Genetic Epidemiology of Parkinson9s Disease Consortium to participate in the study. There were 12,346 cases and 8,164 controls genotyped, for a total of 4 repeats within the SCA2, SCA3, SCA6, and SCA17 genes. Fixed- and random-effects models were used to estimate the summary risk estimates for the genes. We investigated between-study heterogeneity and heterogeneity between different ethnic populations. Results: We did not observe any definite pathogenic repeat expansions for SCA2, SCA3, SCA6, and SCA17 genes in patients with idiopathic PD from Caucasian and Asian populations. Furthermore, overall analysis did not reveal any significant association between intermediate repeats and PD. The effect estimates (odds ratio) ranged from 0.93 to 1.01 in the overall cohort for the SCA2, SCA3, SCA6, and SCA17 loci. Conclusions: Our study did not support a major role for definite pathogenic repeat expansions in SCA2, SCA3, SCA6, and SCA17 genes for idiopathic PD. Thus, results of this large study do not support diagnostic screening of SCA2, SCA3, SCA6, and SCA17 gene repeats in the common idiopathic form of PD. Likewise, this largest multicentered study performed to date excludes the role of intermediate repeats of these genes as a risk factor for PD.

Published
2015

16. Ruolo di N-Acetyl-Seryl-Aspartyl-Lysyl-Proline (Ac-SDKP) nella progressione della Nefropatia Diabetica

Author

DEL PUPPO, MARINA, Corradi, B, CASTOLDI, GIOVANNA, CORRADI, BARBARA, DEL PUPPO, MARINA, Corradi, B, CASTOLDI, GIOVANNA, and CORRADI, BARBARA

Abstract

La nefropatia diabetica è la principale causa di insufficienza renale terminale. N-Acetyl-Seryl-Aspartyl-Lysyl-Proline (Ac-SDKP), tetrapeptide fisiologicamente presente nel plasma e nei tessuti, viene idrolizzato dall’ enzima di conversione dell’angiotensina. Il tetrapeptide ha un effetto antifibrotico sul sistema cardiovascolare e nel rene in modelli sperimentali di ipertensione, infarto del miocardio e nefropatie. Lo scopo del nostro lavoro è stato studiare gli effetti antifibrotici di Ac-SDKP in un modello sperimentale di nefropatia diabetica, e il potenziale effetto additivo del tetrapeptide, in aggiunta al singolo trattamento con ACE-inibitore, sulla progressione della fibrosi renale. A 28 ratti Sprague Dawley e’ stato indotto diabete con un’iniezione di streptozotocina, mentre a 10 ratti controllo e’ stata somministrata solo soluzione tampone. Dopo l’ insorgenza di diabete a 11 ratti è stato somministrato un inibitore dell’enzima di conversione dell’angiotensina (ACE-inibitore, ramipril 3 mg/Kg/die). Dopo 2 mesi di trattamento con ACE-inibitore a 7 ratti diabetici e a 6 ratti diabetici trattati con ramipril è stato somministrato per 8 settimane Ac-SDKP, alla dose di 1 mg/Kg/die, attraverso minipompe osmotiche impiantate nella regione infrascapolare. A 10 ratti controllo, a 10 ratti diabetici e a 5 ratti diabetici trattati con ramipril la minipompa osmotica rilasciava, per lo stesso periodo, solo soluzione fisiologica. Al termine del trattamento i ratti diabetici rispetto ai ratti del gruppo di controllo mostravano un significativo aumento del livello di glucosio, dell’ escrezione urinaria di albumina, della fibrosi renale e una significativa riduzione dell’espressione di nefrina a livello dei glomeruli. La somministrazione di Ac-SDKP riduceva significativamente la fibrosi renale nei ratti diabetici, ma non modificava significativamente l’escrezione urinaria di albumina. Il trattamento farmacologico con ACE-inibitore causava una significativa diminuzione de

Published
2013

17. Renal antifibrotic effect of N-acetyl-seryl-aspartyl-lysyl-proline in diabetic rats

Author

Castoldi, G, di Gioia, C, BOMBARDI ROSA, C, Preziuso, C, Leopizzi, M, Maestroni, S, Corradi, B, Zerbini, G, Stella, A, CASTOLDI, GIOVANNA, BOMBARDI ROSA, CAMILA, STELLA, ANDREA, di Gioia, CR, Castoldi, G, di Gioia, C, BOMBARDI ROSA, C, Preziuso, C, Leopizzi, M, Maestroni, S, Corradi, B, Zerbini, G, Stella, A, CASTOLDI, GIOVANNA, BOMBARDI ROSA, CAMILA, STELLA, ANDREA, and di Gioia, CR

Abstract

Background and Aim: Diabetic nephropathy is the main cause of end-stage renal disease. N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP), a physiological tetrapeptide hydrolyzed by the angiotensin-converting enzyme (ACE), has antifibrotic effects in the cardiovascular system and in the kidney in experimental models of hypertension, heart failure and renal disease. The aim of the study was to evaluate the effect of Ac-SDKP in diabetic nephropathy and the potential additive effect of Ac-SDKP, when compared to ACE inhibitors alone, on the development of renal fibrosis. Method: Diabetes was induced in 28 Sprague-Dawley rats by a single intraperitoneal injection of streptozotocin. Control rats (n = 10) received only buffer solution. An ACE inhibitor (ramipril, 3 mg/kg/day) was administered to 11 diabetic rats. After 2 months, Ac-SDKP (1 mg/kg/day) was administered by osmotic minipumps for 8 weeks to 7 diabetic rats and to 6 diabetic rats treated with ramipril. Osmotic minipumps delivered saline solution in the corresponding sham-treated rats (diabetic rats, n = 10, and ramipril-treated diabetic rats, n = 5). Results: Diabetic rats showed a significant increase in blood glucose level, urinary albumin excretion and renal fibrosis, and a reduction of glomerular nephrin expression with respect to control rats. Ac-SDKP administration significantly reduced renal fibrosis in diabetic rats, without significantly reducing urinary albumin excretion. Ramipril treatment caused a significant decrease in albuminuria and renal fibrosis and restored glomerular nephrin expression. Administration of Ac-SDKP, in addition to ramipril, further reduced renal fibrosis with respect to ramipril alone, while it did not improve the antiproteinuric effect of ramipril. Conclusion: Ac-SDKP administration reduces renal fibrosis in diabetic nephropathy. Addition of Ac-SDKP to ACE inhibition therapy improves the reduction of renal fibrosis with respect to ACE inhibition alone, suggesting a beneficial effe

Published
2013

18. MiR-133a regulates collagen 1A1: Potential role of miR-133a in myocardial fibrosis in angiotensin II-dependent hypertension

Author

Castoldi, G, Di Gioia, C, Bombardi, C, Catalucci, D, Corradi, B, Gualazzi, M, Leopizzi, M, Mancini, M, Zerbini, G, Condorelli, G, Stella, A, CASTOLDI, GIOVANNA, Di Gioia, CR, Gualazzi, MG, STELLA, ANDREA, Castoldi, G, Di Gioia, C, Bombardi, C, Catalucci, D, Corradi, B, Gualazzi, M, Leopizzi, M, Mancini, M, Zerbini, G, Condorelli, G, Stella, A, CASTOLDI, GIOVANNA, Di Gioia, CR, Gualazzi, MG, and STELLA, ANDREA

Abstract

MicroRNAs play an important role in myocardial diseases. MiR-133a regulates cardiac hypertrophy, while miR-29b is involved in cardiac fibrosis. The aim of this study was to evaluate whether miR-133a and miR-29b play a role in myocardial fibrosis caused by Angiotensin II (Ang II)-dependent hypertension. Sprague-Dawley rats were treated for 4 weeks with Ang II (200ng/kg/min) or Ang II+irbesartan (50mg/kg/day in drinking water), or saline by osmotic minipumps. At the end of the experimental period, cardiac miR-133a and miR-29b expression was measured by real-time PCR, and myocardial fibrosis was evaluated by morphometric analysis. A computer-based prediction algorithm led to the identification of collagen 1a1 (Col1A1) as a putative target of miR-133a. A reporter plasmid bearing the 3'-untranslated regions (UTRs) of Col1A1 mRNA was constructed and luciferase assay was performed. MiR-133a suppressed the activity of luciferase when the reporter gene was linked to a 3'-UTR segment of Col1A1 (P<0.01). Mutation of miR-133a binding sites in the 3'-UTR of Col1A1 mRNA abolished miR-133a-mediated repression of reporter gene activity, showing that Col1A1 is a real target of miR-133a. In vivo, Ang II caused an increase in systolic blood pressure (P<0.0001, tail cuff) and myocardial fibrosis in presence of a decrease in miR-133a (P<0.01) and miR-29b (P<0.01), and an increase in Col1A1 expression (P<0.01). These effects were abolished by Ang II administration+irbesartan. These data demonstrate a relationship between miR-133a and Col1A1, suggesting that myocardial fibrosis occurring in Ang II-dependent hypertension is regulated by the down-regulation of miR-133a and miR-29b through the modulation of Col1A1 expression

Published
2012

19. TIMP1 plasma levels are correlated with arterial stiffening process.

Author

Cesana, F, Alloni, M, Sormani, P, Colombo, G, Maloberti, A, Nava, S, Galbiati, M, Stucchi, M, Cairo, M, Corradi, B, Castoldi, G, Giannattasio, C, Mancia., G, F. Cesana, M. Alloni, P. Sormani, G. Colombo, A. Maloberti, S. Nava, M. Galbiati, M. Stucchi, M. Cairo, B. Corradi, G. Castoldi, C. Giannattasio, G. Mancia., Cesana, F, Alloni, M, Sormani, P, Colombo, G, Maloberti, A, Nava, S, Galbiati, M, Stucchi, M, Cairo, M, Corradi, B, Castoldi, G, Giannattasio, C, Mancia., G, F. Cesana, M. Alloni, P. Sormani, G. Colombo, A. Maloberti, S. Nava, M. Galbiati, M. Stucchi, M. Cairo, B. Corradi, G. Castoldi, C. Giannattasio, and G. Mancia.

Published
2011

20. Vascular access

Author

van der Veer, S. N., primary, Labriola, L., additional, Fluck, R., additional, Jager, K. J., additional, Coentrao, L., additional, Kleophas, W., additional, Ravani, P., additional, van Biesen, W., additional, Mandolfo, S., additional, Acconcia, P., additional, Bucci, R., additional, Corradi, B., additional, Farina, M., additional, Corbett, R., additional, Ashby, D., additional, Edwards, C., additional, Prout, V., additional, Singh, S., additional, Bedi, R., additional, Duncan, N., additional, Roca-Tey, R., additional, Ramirez de Arellano, M., additional, Gonzalez-Oliva, J. C., additional, Samon, R., additional, Ibrik, O., additional, Roda, A., additional, Viladoms, J., additional, Jankovic, A., additional, Damjanovic, T., additional, Djuric, Z., additional, Popovic, J., additional, Dimkovic, N., additional, Kirkpantur, A., additional, Turkvatan, A., additional, Balci, M., additional, Kirbas, I., additional, Mandiroglu, S., additional, Afsar, B., additional, and Mandiroglu, F., additional

Published
2013
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22. SNP MINING BY NANOGEN DEVICE: A SENSITIVE TOOL FOR THE IDENTIFICATION OF BCR/ABL MUTATIONS IN PH+ PATIENTS

Author

Corradi, B, Piazza, R, Monn, K, Masera, G, GAMBACORTI PASSERINI, C, Biondi, A, Cazzaniga, G, CORRADI, BARBARA, PIAZZA, ROCCO GIOVANNI, GAMBACORTI PASSERINI, CARLO, BIONDI, ANDREA, CAZZANIGA, GIOVANNI ITALO, Monn K, Masera G, Corradi, B, Piazza, R, Monn, K, Masera, G, GAMBACORTI PASSERINI, C, Biondi, A, Cazzaniga, G, CORRADI, BARBARA, PIAZZA, ROCCO GIOVANNI, GAMBACORTI PASSERINI, CARLO, BIONDI, ANDREA, CAZZANIGA, GIOVANNI ITALO, Monn K, and Masera G

Published
2004

26. ANTIHYPERTENSIVE DRUG TREATMENT DOES NOT ALLOW TO ACHIEVE A FULL NORMALIZATION OF THE ARTERIAL STIFFNESS AND METALLOPROTEINASES ALTERATIONS SEEN IN HYPERTENSION

Author

Cesana, F., primary, Castoldi, G., additional, Corradi, B., additional, Alloni, M., additional, Galbiati, M., additional, Stucchi, M., additional, Corciulo, M., additional, Sormani, P., additional, Menni, C., additional, Bagnardi, V., additional, Stella, A., additional, Grassi, G., additional, Giannattasio, C., additional, and Mancia, G., additional

Published
2011
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27. HEART FAILURE WITH PRESERVED EJECTION FRACTION (HFPEF): AORTIC STIFFNESS, BIOHUMORAL MARKERS AND ECHOCARDIOGRAPHIC EVALUATION

Author

Alloni, M., primary, Castoldi, G., additional, Corradi, B., additional, Cesana, F., additional, Cirò, A., additional, Vincenzi, A., additional, Trocino, G., additional, Montemerlo, E., additional, Campadello, P., additional, Facchetti, R., additional, Stella, A., additional, Grassi, G., additional, Giannattasio, C., additional, and Mancia, G., additional

Published
2011
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28. Chronic renal failure due to atheromatous renovascular disease in the elderly

Author

Corradi B, Malberti F, Farina M, Cosci P, Imbasciati E, Raieli G, and FABRIZIO CALLIADA

Subjects
Aged, 80 and over, Male, Arteriosclerosis, Incidence, Comorbidity, Middle Aged, Renal Artery Obstruction, Sensitivity and Specificity, Renal Circulation, Subtraction Technique, Hypertension, Humans, Kidney Failure, Chronic, Diabetic Nephropathies, Female, Prospective Studies, Radionuclide Imaging, Blood Flow Velocity, Aged, Ultrasonography
Published
1993

36. Calcium balance and serum ionized calcium fluctuations in on-line haemodiafiltration in relation to ultrafiltration rate and dialysate calcium concentration.

Author

Malberti, F., Corradi, B., Tetta, C., and Imbasciati, E.

Abstract

The use of high ultrafiltration rates in haemodiafiltration (HDF) has been suggested for improving the clearance of small and large molecules. This strategy has become economically applicable with the development of safe techniques for on-line production of sterile infusate from dialysate, which enables us to infuse large substitution fluid volumes without further increasing the cost of the sessions. The effect of increasing the ultrafiltration rate in HDF on electrolyte balance has not yet been evaluated. The aim of this study was to evaluate the effects of variations of the ultrafiltration rate on calcium kinetics in HDF using three different dialysate calcium concentrations. Since the increase in ultrafiltration rate augments the convective calcium loss, variations of intrasession calcium balance could result from modifications of the ultrafiltration rate. In the present study we found no significant variations in calcium balance and serum ionized calcium (iCa) levels during on-line HDF treatment when increasing the mean ultrafiltration rate from 60 to 100 ml/min in the presence of an adequate and corresponding increase in the infusion rate (from 2.5 to 5 l/h). During the balance studies, pretreatment serum iCa was on the average 1.32 mmol/l and weight loss 3.2 kg. Mean calcium loss during treatment was 2.8 and 3.3 mmol at infusion rates of 2.5 and 5 l/h with 1.63 mmol/l of calcium in both the dialysate and infusate; calcium loss rose to 5.9 and 11.2mmol at infusion rates of 2.5 l/h and to 5.7 and 14.2 mmol at infusion rates of 5 l/h when the dialysate and infusate calcium was reduced respectively to 1.5 and 1.25 mmol/l. Serum iCa significantly increased at the end of the session with the higher dialysate concentration, while it decreased to 1.28 mmol/l and 1.20 mmol/l with the lower two concentrations. Linear regression ana lysis showed no variation in serum iCa during treatment when the iCa concentration in the dialysate was equal to pretreatment serum iCa. A neutral calcium balance would be expected using 1.75 mmol/l of calcium in the dialysate. In conclusion, increasing the ultrafiltration rate from 60 to 100 ml/min did not significantly affect calcium kinetics in on-line HDF. The main factors affecting calcium mass transfer and serum iCa fluctuation during treatment were the dialysate calcium concentration and the iCa gradient between dialysate and pretreatment serum levels. [ABSTRACT FROM PUBLISHER]

Published
1994

37. Adequacy of Haemodiafiltration.

Author

Surian, M., Malberti, F., Corradi, B., Orlandini, G., Varini, E., Colussi, G., and Minetti, L.

Abstract

In this study we have evaluated the influence of blood and ultrafiltration flow rate on the performance of five different high-flux membrane dialysers during haemodiafiltration. On the basis of clearance data we optimised the haemodiafiltration schedule of six uraemic patients to maintain an adequate midweek blood urea nitrogen concentration, while reducing the treatment time from 285±23min to 210 min. After a follow-up of 6 months, we observed no difference in the clinical tolerance or in the biochemical parameters, compared to those found during the preceding haemodialysis period. Our data confirm the suggestions of other authors that haemodiafiltration is an effective alternative to conventional haemodialysis. [ABSTRACT FROM PUBLISHER]

Published
1989

40. High-dose oral calcitriol and zero calcium peritoneal solutions in CAPD patients with refractory secondary hyperparathyroidism.

Author

Malberti, F., Scanziani, R., Corradi, B., Dozio, B., Bonforte, G., Imbasciati, E., and Surian, M.

Abstract

Abstract. We evaluated the effect of pulse oral calcitriol (4 μg three times weekly for 6 months) on parathyroid function in nine CAPD patients with hyperparathyroidism refractory to conventional lowdose oral calcitriol. Zero calcium peritoneal solutions were used to prevent the development of hypercalcaemia. The peritoneal loss of calcium increased from 168á40 to 417á48 mg/day using zero calcium solutions. Pulse oral calcitriol resulted in a significant decrease in PTH (from 617á272 to 382á299 pg/ml) by the 15th day of therapy, while serum iCa did not change from baseline. During the first month of therapy the mean PTH levels remained significantly reduced compared to baseline, thereafter PTH increased in four of nine patients. Hyperphosphataemia was not satisfactorily controlled in four patients, despite large amounts of binders used; seven of nine patients developed hypercalcaemia and required either the substitution of calcium acetate for calcium carbonate or reduction of calcitriol dose. Three patients showed a progressive increase in PTH. In conclusion our data suggest that in most CAPD patients with severe hyperparathyroidism oral calcitriol pulse therapy is not effective in maintaining a permanent suppression in PTH levels. [ABSTRACT FROM PUBLISHER]

Published
1994

45. Ruolo di N-Acetyl-Seryl-Aspartyl-Lysyl-Proline (Ac-SDKP) nella progressione della Nefropatia Diabetica

Author

CORRADI, BARBARA, Corradi, B, and CASTOLDI, GIOVANNA

Subjects
nefropatia diabetica, N-Acetyl-Seryl-Aspartyl-Lysyl-Proline (Ac-SDKP),fibrosi renale, MED/14 - NEFROLOGIA
Abstract

La nefropatia diabetica è la principale causa di insufficienza renale terminale. N-Acetyl-Seryl-Aspartyl-Lysyl-Proline (Ac-SDKP), tetrapeptide fisiologicamente presente nel plasma e nei tessuti, viene idrolizzato dall’ enzima di conversione dell’angiotensina. Il tetrapeptide ha un effetto antifibrotico sul sistema cardiovascolare e nel rene in modelli sperimentali di ipertensione, infarto del miocardio e nefropatie. Lo scopo del nostro lavoro è stato studiare gli effetti antifibrotici di Ac-SDKP in un modello sperimentale di nefropatia diabetica, e il potenziale effetto additivo del tetrapeptide, in aggiunta al singolo trattamento con ACE-inibitore, sulla progressione della fibrosi renale. A 28 ratti Sprague Dawley e’ stato indotto diabete con un’iniezione di streptozotocina, mentre a 10 ratti controllo e’ stata somministrata solo soluzione tampone. Dopo l’ insorgenza di diabete a 11 ratti è stato somministrato un inibitore dell’enzima di conversione dell’angiotensina (ACE-inibitore, ramipril 3 mg/Kg/die). Dopo 2 mesi di trattamento con ACE-inibitore a 7 ratti diabetici e a 6 ratti diabetici trattati con ramipril è stato somministrato per 8 settimane Ac-SDKP, alla dose di 1 mg/Kg/die, attraverso minipompe osmotiche impiantate nella regione infrascapolare. A 10 ratti controllo, a 10 ratti diabetici e a 5 ratti diabetici trattati con ramipril la minipompa osmotica rilasciava, per lo stesso periodo, solo soluzione fisiologica. Al termine del trattamento i ratti diabetici rispetto ai ratti del gruppo di controllo mostravano un significativo aumento del livello di glucosio, dell’ escrezione urinaria di albumina, della fibrosi renale e una significativa riduzione dell’espressione di nefrina a livello dei glomeruli. La somministrazione di Ac-SDKP riduceva significativamente la fibrosi renale nei ratti diabetici, ma non modificava significativamente l’escrezione urinaria di albumina. Il trattamento farmacologico con ACE-inibitore causava una significativa diminuzione dell’albuminuria e della fibrosi renale, ripristinando l’espressione della nefrina glomerulare. La somministrazione di Ac-SDKP, in aggiunta al trattamento con ACE-inibitore, riduceva ulteriormente la fibrosi renale rispetto al solo trattamento con ramipril, mentre non incrementava l’effetto antiproteinurico dell’ACE-inibitore. In conclusione questo studio ha dimostrato che la somministrazione di Ac-SDKP in un modello di nefropatia diabetica riduce la fibrosi renale. Il trattamento combinato (Ac-SDKP + ACE-inibitore) aumenta l’effetto antifibrotico dell’ACE-inibitore nel tessuto renale, suggerendo il benefico effetto di questa associazione farmacologica nel trattamento della nefropatia diabetica.

Published
2013

46. Renal antifibrotic effect of n-acetyl-seryl-aspartyl-lysyl-proline in diabetic rats

Author

Gianpaolo Zerbini, C. Di Gioia, Martina Leopizzi, Giovanna Castoldi, C. Bombardi, Silvia Maestroni, Carmela Preziuso, Andrea Stella, B. Corradi, Castoldi, G, di Gioia, C, BOMBARDI ROSA, C, Preziuso, C, Leopizzi, M, Maestroni, S, Corradi, B, Zerbini, G, and Stella, A

Subjects
Ramipril, Male, medicine.medical_specialty, Kidney Glomerulus, Drug Evaluation, Preclinical, experimental models, diabetic nephropathy, angiotensin-converting enzyme inhibitors, n-acetyl-seryl- aspartyl-lysyl-proline, fibrosis, rats, urologic and male genital diseases, Diabetic nephropathy, Nephrin, Rats, Sprague-Dawley, Fibrosis, Diabetes mellitus, Internal medicine, medicine, Renal fibrosis, Albuminuria, Animals, Diabetic Nephropathies, Kidney, Nephrosclerosis, biology, business.industry, Membrane Proteins, medicine.disease, Kidney, fibrosis, experimental models, Ac-SDKP, Growth Inhibitors, medicine.anatomical_structure, Endocrinology, Nephrology, ACE inhibitor, biology.protein, business, Oligopeptides, medicine.drug, Glomerular Filtration Rate
Abstract

Background and Aim: Diabetic nephropathy is the main cause of end-stage renal disease. N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP), a physiological tetrapeptide hydrolyzed by the angiotensin-converting enzyme (ACE), has antifibrotic effects in the cardiovascular system and in the kidney in experimental models of hypertension, heart failure and renal disease. The aim of the study was to evaluate the effect of Ac-SDKP in diabetic nephropathy and the potential additive effect of Ac-SDKP, when compared to ACE inhibitors alone, on the development of renal fibrosis. Method: Diabetes was induced in 28 Sprague-Dawley rats by a single intraperitoneal injection of streptozotocin. Control rats (n = 10) received only buffer solution. An ACE inhibitor (ramipril, 3 mg/kg/day) was administered to 11 diabetic rats. After 2 months, Ac-SDKP (1 mg/kg/day) was administered by osmotic minipumps for 8 weeks to 7 diabetic rats and to 6 diabetic rats treated with ramipril. Osmotic minipumps delivered saline solution in the corresponding sham-treated rats (diabetic rats, n = 10, and ramipril-treated diabetic rats, n = 5). Results: Diabetic rats showed a significant increase in blood glucose level, urinary albumin excretion and renal fibrosis, and a reduction of glomerular nephrin expression with respect to control rats. Ac-SDKP administration significantly reduced renal fibrosis in diabetic rats, without significantly reducing urinary albumin excretion. Ramipril treatment caused a significant decrease in albuminuria and renal fibrosis and restored glomerular nephrin expression. Administration of Ac-SDKP, in addition to ramipril, further reduced renal fibrosis with respect to ramipril alone, while it did not improve the antiproteinuric effect of ramipril. Conclusion: Ac-SDKP administration reduces renal fibrosis in diabetic nephropathy. Addition of Ac-SDKP to ACE inhibition therapy improves the reduction of renal fibrosis with respect to ACE inhibition alone, suggesting a beneficial effect of this pharmacological association in diabetic nephropathy.

Published
2013

47. MiR-133a regulates collagen 1A1: Potential role of miR-133a in myocardial fibrosis in angiotensin II-dependent hypertension

Author

Daniele Catalucci, Andrea Stella, Giovanna Castoldi, Martina Leopizzi, C. Bombardi, B. Corradi, Gianpaolo Zerbini, Maria Giovanna Gualazzi, Gianluigi Condorelli, Massimiliano Mancini, Cira Di Gioia, Castoldi, G, Di Gioia, C, Bombardi, C, Catalucci, D, Corradi, B, Gualazzi, M, Leopizzi, M, Mancini, M, Zerbini, G, Condorelli, G, and Stella, A

Subjects
Male, medicine.medical_specialty, Heart Diseases, Physiology, Cardiac fibrosis, Clinical Biochemistry, Collagen Type I, Rats, Sprague-Dawley, In vivo, Internal medicine, microRNA, medicine, Animals, Luciferase, Reporter gene, business.industry, Angiotensin II, angiotensin, myocardial fibrosis, mir-133a, Cell Biology, medicine.disease, Fibrosis, Rats, Collagen Type I, alpha 1 Chain, MicroRNAs, Blood pressure, Endocrinology, Gene Expression Regulation, Hypertension, Myocardial fibrosis, business, angiotensin II, myocardial fibrosis, mir-133a, animal models, collagen 1a1
Abstract

MicroRNAs play an important role in myocardial diseases. MiR-133a regulates cardiac hypertrophy, while miR-29b is involved in cardiac fibrosis. The aim of this study was to evaluate whether miR-133a and miR-29b play a role in myocardial fibrosis caused by Angiotensin II (Ang II)-dependent hypertension. Sprague–Dawley rats were treated for 4 weeks with Ang II (200 ng/kg/min) or Ang II + irbesartan (50 mg/kg/day in drinking water), or saline by osmotic minipumps. At the end of the experimental period, cardiac miR-133a and miR-29b expression was measured by real-time PCR, and myocardial fibrosis was evaluated by morphometric analysis. A computer-based prediction algorithm led to the identification of collagen 1a1 (Col1A1) as a putative target of miR-133a. A reporter plasmid bearing the 3′-untranslated regions (UTRs) of Col1A1 mRNA was constructed and luciferase assay was performed. MiR-133a suppressed the activity of luciferase when the reporter gene was linked to a 3′-UTR segment of Col1A1 (P

Published
2012

48. TIMP1 plasma levels are correlated with arterial stiffening process

Author

F. Cesana, M. Alloni, P. Sormani, G. Colombo, A. Maloberti, S. Nava, M. Galbiati, M. Stucchi, M. Cairo, B. Corradi, G. Castoldi, C. Giannattasio, G. Mancia., Cesana, F, Alloni, M, Sormani, P, Colombo, G, Maloberti, A, Nava, S, Galbiati, M, Stucchi, M, Cairo, M, Corradi, B, Castoldi, G, Giannattasio, C, and Mancia., G

Subjects
TIMP1, arterial stiffening
Published
2011

49. Non-Replication of Association for Six Polymorphisms From Meta-Analysis of Genome-Wide Association Studies of Parkinson's Disease: Large-Scale Collaborative Study

Author

Peter A. Silburn, Grazia Annesi, Aldo Quattrone, Christine Van Broeckhoven, Evangelos Evangelou, Nancy L. Pedersen, George D. Mellick, Alexis Brice, Demetrius M. Maraganore, Eng-King Tan, Jean-Charles Lambert, Karin Wirdefeldt, Carlo Ferrarese, Rejko Krueger, Alexis Elbaz, Katerina Markopoulou, Laura Brighina, Georgios M. Hadjigeorgiou, John P. A. Ioannidis, Suzanne Lesage, Bram Meeus, Manu Sharma, Clinical and Molecular Epidemiology Unit, Department of Hygiene and Epidemiology, University of Ioannina, Institute of Microbiology, Université de Lausanne = University of Lausanne (UNIL), Department of Neurology, Mayo Clinic College of Medicine, Institute of Neurological Sciences, National Research Council [Italy] (CNR), Section of Neurology, Università degli Studi di Milano-Bicocca = University of Milano-Bicocca (UNIMIB)-San Gerardo Hospital of Monza, Neurologie et thérapeutique expérimentale, Université Pierre et Marie Curie - Paris 6 (UPMC)-IFR70-Institut National de la Santé et de la Recherche Médicale (INSERM), Neuroépidémiologie, Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratory of Neurogenetics, Deparment of Neurology, University of Thessaly [Volos] (UTH), Institute of Biomedical Research & Technology, CERETETH, University Hospital Tuebingen-Hertie Institute for Clinical Brain Research, Epidémiologie des maladies chroniques : impact des interactions gène environnement sur la santé des populations, Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille, Droit et Santé, Eskitis Institute for Cell and Molecular Therapies, Griffith University [Brisbane], Neurodegenerative Brain Diseases Group, VIB, Laboratory of Neurogenetics, Born-Bunge Institute [Anvers], University of Antwerp (UA), Department of Medical Epidemiology and Biostatistics (MEB), Karolinska Institutet [Stockholm], Institute of Neurology, Università degli Studi 'Magna Graecia' di Catanzaro = University of Catanzaro (UMG), Duke-NUS Medical School [Singapore], Singapore General Hospital-National Neuroscience Institute, Biomedical Research Institute, Foundation for Research and Technology - Hellas (FORTH), Institute for Clinical Research and Health Policy Studies, Tufts Universiy, Inserm, MSA, Agence Nationale de la Recherche, Agence Francaise de Securite Sanitaire de l'Environnement et du Travail, France Parkinson, FIRB 2003 GENOPOLIS Project, National Institutes of Health (NIH) 2R01 ES10751 ES10758 AG 08724, Michael J. Fox Grants, Swedish Medical Research Council, Swedish Society of Medicine, Parkinson Foundation in Sweden, VIB Genetic Service Facility, The Biobank of the Institute Born-Bunge, Fund for Scientific Research Flanders Institute for Science and Technology - Flanders (IWT-V), Foundation for Alzheimer Research (SAO/FRMA), Interuniversity Attraction Poles Program P6/43 of the Belgian Science Policy Office, Belgium, Genetic Epidemiology of Parkinson's Disease (GEOPD) Consortium, Evangelou, E, Maraganore, D, Annesi, G, Brighina, L, Brice, A, Elbaz, A, Ferrarese, C, Hadjigeorgiou, G, Krueger, R, Lambert, J, Lesage, S, Markopoulou, K, Mellick, G, Meeus, B, Pedersen, N, Quattrone, A, Van Broeckhoven, C, Sharma, M, Silburn, P, Tan, E, Wirdefeldt, K, Ioannidis, J, Genetic Epidemiology of Parkinson's Disease, C, University of Ioannina Medical School, Université de Lausanne (UNIL), Università degli Studi di Milano-Bicocca [Milano] (UNIMIB)-San Gerardo Hospital, Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR70-Université Pierre et Marie Curie - Paris 6 (UPMC), Università degli Studi 'Magna Graecia' di Catanzaro [Catanzaro, Italie] (UMG), Theuns, Jessie, Crosiers, David, Pals, Philippe, Engelborghs, Sebastiaan, De Deyn, Peter Paul, Cras, Patrick, et al., Genetic Epidemiology of Parkinson's Disease Consortium, Sutherland, G.T., Siebert, G.A., Theuns, J., Crosiers, D., Pickut, B., Pals, P., Engelborghs, S., Nuytemans, K., De Deyn, P.P., Cras, P., Agid, Y., Bonnet, A.M., Borg, M., Brice, A., Broussolle, E., Damier, P., Destée, A., Dürr, A., Durif, F., Lesage, S., Lohmann, E., Pollak, P., Rascol, O., Tison, F., Tranchant, C., Viallet, F., Vidailhet, M., Tzourio, C., Amouyel, P., Loriot, M.A., Gasser, T., Riess, O., Berg, D., Schulte, C., Klein, C., Djarmati, A., Lohmann, K., Xiromerisiou, G., Dardiotis, E., Kountra, P., Hattori, N., Tomiyama, H., Funayama, M., Yoshino, H., Li, Y., Valente, E.M., Ferraris, A., Bentivoglio, A.R., Ialongo, T., Riva, C., Corradi, B., Opala, G., Jasinska-Myga, B., Klodowska-Duda, G., Boczarska-Jedyna, M., Belin, A., Olson, L., Galter, D., Westerlund, M., Sydow, O., Nilsson, C., Puschmann, A., Maraganore, D.M., Ahlskog, J.E., de Andrade, M., Lesnick, T.G., Rocca, W.A., Checkoway, H., Savasta, Marc, and Pathologic Biochemistry and Physiology

Subjects
medicine.medical_specialty, Parkinson Disease/*genetics, Parkinson's disease, Single-nucleotide polymorphism, Genome-wide association study, challenges, Polymorphism, Genetic, Biology, Article, 03 medical and health sciences, Cellular and Molecular Neuroscience, 0302 clinical medicine, Replication (statistics), MESH: Polymorphism, Genetic, medicine, Humans, Meta-analysi, [SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Genome-Wide Association Study, Parkinson Disease/genetics, uncertainty, Genetics (clinical), 030304 developmental biology, Medicine(all), Genetics, 0303 health sciences, Genome-wide association, MESH: Humans, axon guidance, pathway, Parkinson Disease, Odds ratio, Random effects model, meta-analysis, Psychiatry and Mental health, Genetic epidemiology, Meta-analysis, MESH: Genome-Wide Association Study, parkinson's disease, genome-wide association, Medical genetics, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Human medicine, heterogeneity, 030217 neurology & neurosurgery, MESH: Parkinson Disease
Abstract

Early genome-wide association (GWA) studies on Parkinson's disease (PD) have not been able to yield conclusive, replicable signals of association, perhaps due to limited sample size. We aimed to investigate whether association signals derived from the meta-analysis of the first two GWA investigations might be replicable in different populations. We examined six single-nucleotide polymorphisms (SNPs) (rs1000291, rs1865997, rs2241743, rs2282048, rs2313982, and rs3018626) that had reached nominal significance with at least two of three different strategies proposed in a previous analysis of the original GWA studies. Investigators from the "Genetic Epidemiology of Parkinson's Disease" (GEOPD) consortium were invited to join in this study. Ten teams contributed replication data from 3,458 PD cases and 3,719 controls. The data from the two previously published GWAs (599 PD cases, 592 controls and 443 sibling pairs) were considered as well. All data were synthesized using both fixed and random effects models. The summary allelic odds ratios were ranging from 0.97 to 1.09 by random effects, when all data were included. The summary estimates of the replication data sets (excluding the original GWA data) were very close to 1.00 (range 0.98-1.09) and none of the effects were nominally statistically significant. The replication data sets had significantly different results than the GWA data. Our data do not support evidence that any of these six SNPs reflect susceptibility markers for PD. Much stronger signals of statistical significance in GWA platforms are needed to have substantial chances of replication. Specifically in PD genetics, this would require much larger GWA studies and perhaps novel analytical techniques. (C) 2009 Wiley-Liss, Inc. American Journal of Medical Genetics Part B-Neuropsychiatric Genetics

Published
2010

50. Prevention of myocardial fibrosis by N-acetyl-seryl-aspartyl-lysyl-proline in diabetic rats

Author

Carla Perego, Cira R. T. Di Gioia, Lucia Perego, Gianpaolo Zerbini, Martina Leopizzi, A. Stella, Stefano Perlini, Massimiliano Mancini, Giovanna Castoldi, C. Bombardi, B. Corradi, Università degli Studi di Milano-Bicocca [Milano] (UNIMIB), Castoldi, G, Di Gioia, C, Bombardi, C, Perego, C, Perego, L, Mancini, M, Leopizzi, M, Corradi, B, Perlini, S, Zerbini, G, and Stella, A

Subjects
Male, Fibrosi, medicine.medical_treatment, Angiotensin-Converting Enzyme Inhibitors, Smad Proteins, 030204 cardiovascular system & hematology, Rats, Sprague-Dawley, 0302 clinical medicine, Ramipril, Fibrosis, Diabetic cardiomyopathy, diabetic cardiomyopathy, Insulin, echocardiography, transforming growth factor-β1 (tgf-β1), 0303 health sciences, General Medicine, 3. Good health, Medicine, Cardiomyopathies, Oligopeptides, angiotensin-converting enzyme inhibitor (acei), medicine.drug, smad, medicine.medical_specialty, Heart Ventricles, n-acetyl-seryl-aspartyl-lysyl-proline (ac-sdkp), fibrosis, transforming growth factor-beta 1 (tgf-beta 1), Diabetes Mellitus, Experimental, Diabetes Complications, Transforming Growth Factor beta1, 03 medical and health sciences, Internal medicine, Diabetes mellitus, medicine, Animals, Hypoglycemic Agents, 030304 developmental biology, business.industry, Myocardium, medicine.disease, Streptozotocin, Rats, Endocrinology, ACE inhibitor, Myocardial fibrosis, business
Abstract

Ac-SDKP (N-acetyl-seryl-aspartyl-lysyl-proline) is a physiological tetrapeptide hydrolysed by ACE (angiotensin-converting enzyme). In experimental models of hypertension, Ac-SDKP has antifibrotic effects in the heart; however, the role of Ac-SDKP in diabetic cardiomyopathy is currently unknown. The aim of the present study was to evaluate the effect of Ac-SDKP on cardiac systolic and diastolic function, and interstitial and perivascular fibrosis in the heart of diabetic rats. Diabetes was induced in 55 Sprague - Dawley rats by streptozotocin injection. Control rats (n=18) underwent only buffer injection. Out of the 55 diabetic rats, 19 were chronically treated with insulin and 13 with the ACEI (ACE inhibitor) ramipril (3 mg · kg-1 of body weight · day-1). At 2 months after the onset of diabetes, Ac-SDKP (1 mg · kg-1 of body weight · day-1) was administered by osmotic minipumps for 8 weeks to eight control rats, 13 diabetic rats, seven diabetic rats treated with ramipril and nine insulin-treated diabetic rats. Diabetic rats had a significant increase in blood glucose levels. Left ventricular interstitial and perivascular fibrosis, and TGF-β1 (transforming growth factor-β1) protein levels were increased in diabetic rats, but not in insulin-treated diabetic rats and ramipril-treated diabetic rats, compared with control rats. Ac-SDKP administration significantly reduced left ventricular interstitial and perivascular fibrosis in diabetic rats and in diabetic rats treated with ramipril. This was accompanied by a significant reduction in active TGF-β1 and phospho-Smad2/3 protein levels in myocardial tissue of diabetic rats. Echocardiography showed that diabetes was associated with increased end-systolic diameters, and depressed global systolic function and diastolic dysfunction, as assessed by transmitral Doppler velocity profile. These changes were completely reversed by insulin or ramipril treatment. Ac-SDKP treatment partially restored diastolic function in diabetic rats. In conclusion, Ac-SDKP administration in diabetic rats reduces left ventricular interstitial and perivascular fibrosis, active TGF-β1 and phospho-Smad2/3 levels, and improves diastolic function. Taken together, these findings suggest that, by inhibiting the TGF-β/Smad pathway, Ac-SDKP protects against the development of diabetic cardiomyopathy. © The Authors Journal compilation © 2010 Biochemical Society.

Published
2009

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