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141 results on '"Garlaschelli, K."'

7. Translating the microRNA signature of microvesicles derived from human coronary artery smooth muscle cells in patients with familial hypercholesterolemia and coronary artery disease

Author

de Gonzalo-Calvo, D, Cenario, A, Garlaschelli, K, Pellegatta, F, Vilades, D, Nasarre, L, Camino-Lopez, S, Crespo, J, Carreras, F, Leta, R, Catapano, AL, Norata, GD, Civeira, F, and Llorente-Cortes, V

Subjects
MicroRNAs, Coronary artery smooth muscle cells, Familial hypercholesterolemia, Biomarker, Coronary artery disease, Microvesicles
Abstract

Aims: To analyze the impact of atherogenic lipoproteins on the miRNA signature of microvesicles derived from human coronary artery smooth muscle cells (CASMC) and to translate these results to familial hypercholesterolemia (FH) and coronary artery disease (CAD) patients. Methods: Conditioned media was collected after exposure of CASMC to atherogenic lipoproteins. Plasma samples were collected from two independent populations of diagnosed FH patients and matched normocholesterolemic controls (Study population 1, N = 50; Study population 2, N = 24) and a population of patients with suspected CAD (Study population 3, N = 50). Extracellular vesicles were isolated and characterized using standard techniques. A panel of 30 miRNAs related to vascular smooth muscle cell (VSMC) (patho-)physiology was analyzed using RT-qPCIt Results: Atherogenic lipoproteins significantly reduced levels of miR-15b-5p, 24-3p, 29b-3p, 130a-3p, 143-3p, 146a-3p,-222-3p,-663a levels (P< 0.050) in microvesicles (0.1 mu m-1 pm in diameter) released by CASMC. Two of these miRNAs, miR-24-3p and miR-130a-3p, were reduced in circulating microvesicles from FH patients compared with normocholesterolemic controls in a pilot study (Study population 1) and in different validation studies (Study populations 1 and 2) (P < 0.050). Supporting these results, plasma levels of miR-24-3p and miR-130a-3p were also downregulated in FH patients compared to controls (P < 0.050). In addition, plasma levels of miR-130a-3p were inversely associated with coronary atherosclerosis in a cohort of suspected CAD patients (Study population 3) (P < 0.050). Conclusions: Exposure to atherogenic lipoproteins modifies the miRNA profile of CASMC-derived microvesicles and these alterations are reflected in patients with FH. Circulating miR-130a-3p emerges as a potential biomarker for coronary atherosclerosis. (C) 2017 Elsevier Ltd. All rights reserved.

Published
2017

8. PCSK9 deficiency results in altered glucose control and increased ectopic fat accumulation in experimental models and in humans

Author

Baragetti, A., primary, Grejtakova, D., additional, Zampoleri, V., additional, Uboldi, P., additional, Garlaschelli, K., additional, Balzarotti, G., additional, Grigore, L., additional, Pellegatta, F., additional, Guerrini, U., additional, Pisano, G., additional, Fracanzani, A.L., additional, Fargion, S., additional, Norata, G.D., additional, and Catapano, A.L., additional

Published
2018
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9. The long pentraxin 3 (PTX3) plays a key role in the immunomodulation of diet induced-obesity in mice

Author

Bonacina, F., primary, Moregola, A., additional, Baragetti, A., additional, Bonavita, E., additional, Garlaschelli, K., additional, Salatin, A., additional, Grigore, L., additional, Pellegatta, F., additional, Garlanda, C., additional, Bottazzi, B., additional, Mantovani, A., additional, Catapano, A.L., additional, and Norata, G.D., additional

Published
2018
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10. Disease trends over time and CD4 + CCR5 + T-cells expansion predict carotid atherosclerosis development in patients with systemic lupus erythematosus

Author

Baragetti, A., primary, Ramirez, G.A., additional, Magnoni, M., additional, Garlaschelli, K., additional, Grigore, L., additional, Berteotti, M., additional, Scotti, I., additional, Bozzolo, E., additional, Berti, A., additional, Camici, P.G., additional, Catapano, A.L., additional, Manfredi, A.A., additional, Ammirati, E., additional, and Norata, G.D., additional

Published
2018
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11. Disease trends over time and effector memory T-cells predict atherosclerosis development in Systemic Lupus Erythematosus

Author

Baragetti, A., primary, Ramirez, G.A., additional, Magnoni, M., additional, Garlaschelli, K., additional, Grigore, L., additional, Berteotti, M., additional, Scotti, I., additional, Bozzolo, E., additional, Berti, A., additional, Manfredi, A.A., additional, Ammirati, E., additional, Catapano, A.L., additional, and Norata, G.D., additional

Published
2017
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15. Characterization of metabolic syndrome in PLIC cohort

Author

Chiodo, L., primary, Casula, M., additional, Catapano, A.L., additional, Baragetti, A., additional, Garlaschelli, K., additional, Grigore, L., additional, Loggia, E., additional, Norata, G.D., additional, Pellegatta, F., additional, Redaelli, L., additional, Tidone, C., additional, Tincani, A., additional, and Tragni, E., additional

Published
2017
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16. Plasma resistin levels correlate with determinants of the metabolic syndrome

Author

Norata, G.D., Ongari, M., Garlachelli, K., Raselli, S., Grigore, L., Catapano, A.L., and Garlaschelli, K.

Subjects
Adult, Male, medicine.medical_specialty, Adolescent, Endocrinology, Diabetes and Metabolism, Adipokine, Type 2 diabetes, Intra-Abdominal Fat, Severity of Illness Index, chemistry.chemical_compound, Endocrinology, High-density lipoprotein, Insulin resistance, Risk Factors, Internal medicine, Blood plasma, medicine, Humans, Resistin, intima-media thickness, coronary-heart-disease, insulin-resistance, adipose-tissue, serum resistin, inflammatory markers, nondiabetic patients, diabetic subjects, expression, obesity, Obesity, Aged, Aged, 80 and over, Metabolic Syndrome, business.industry, General Medicine, Middle Aged, Atherosclerosis, medicine.disease, chemistry, Settore BIO/14 - Farmacologia, Regression Analysis, Female, Insulin Resistance, Metabolic syndrome, business
Abstract

Objective: The role of resistin in insulin sensitivity and obesity is controversial. Some authors suggest that increased serum resistin levels are associated with obesity, visceral fat, insulin resistance, type 2 diabetes and inflammation, while others failed to observe such correlations. The aim of the present study was to investigate the relationship of plasma resistin levels with markers of the metabolic syndrome and atherosclerosis in a large population-based study. Design and patients: Plasma resistin levels were determined in 1090 subjects free of any medication selected from the PLIC study (designed to verify the presence of atherosclerotic lesions and progression intima-media thickness (IMT) in the common carotid artery in the general population) and related to the presence of obesity, metabolic syndrome, metabolic abnormalities, cardiovascular risk, and progression of IMT. Results: Plasma resistin levels were highly positively correlated with triglycerides, waist circumference, waist/hip ratio, systolic blood pressure, and ApoAI/ApoB ratio, while they were inversely correlated with high density lipoprotein and ApoAI levels. This finding was gender specific (mainly in women). Plasma resistin levels were significantly higher in women with the metabolic syndrome compared with controls (4.90 (0.24) ng/ml vs 3.90 (0.11) ng/ml; PP Conclusion: Plasma resistin levels are increased in presence of the metabolic syndrome and are associated with increased cardiovascular risk.

Published
2007

17. Clinical, molecular and functional characterization of two novel mutations associated to compound heterozygous FHBL

Author

VALENTI, Vincenza, CEFALU', Angelo Baldassare, SPINA, Rossella, NOTO, Davide, AVERNA, Maurizio, Garlaschelli K, Grigore L, Uboldi P, Norata GD, Ghiglioni D, Fiocchi L, Terracciano L, Zoja A, Catapano AL, Valenti V, Garlaschelli K, Cefalù AB, Grigore L, Spina R, Uboldi P, Noto D, Norata GD, Ghiglioni D, Fiocchi L, Terracciano L, Zoja A, Catapano AL, and Averna M

Subjects
Compound heterozygou, Settore MED/09 - Medicina Interna, FHBL, splicing mutations
Abstract

Introduction. Primary hypobetalipoproteinemia (pHBL) is a monogenic heterogeneous condition characterized by total cholesterol (TC) and/or LDL cholesterol (LDL-C) levels below the 5th percentile of the reference population. Heterozygous APOB gene mutations are responsible for the majority of the dominant pHBL causing the familial hypobetalipoproteinemia (FHBL). The clinical phenotype of heterozygous FHBL is usually mild. The homozygous or compound heterozygous APOB mutations are in some cases responsible for a more severe biochemical and clinical phenotype, similar to the abetalipoproteinemia (ABL) due to homozygous mutations in the MTP gene, characterized by intestinal malabsorption, pigmentary retinal degeneration, ataxic neuropathy, and almost undetectable levels of LDL-C and APOB. methods and Results. In this report we describe the clinical and molecular characterization of a child with severe hypolipidemia and a clinical phenotype suggesting the clinical diagnosis of ABL. Parents serum total cholesterol (TC) and LDL cholesterol (LDLC) levels however were below the 5th percentile thus suggesting that the proband could have been homozygous or compound heterozygous FHBL. Western blot analysis showed the presence of two truncated forms of apoB protein of different molecular weight in the serum of the proband; a single truncated form was then observed in the mother on in the father. The direct sequence the apoB gene in the proband allowed to identify two novel mutations: a) a mutation of the donor splice site of intron 23 of the APOB gene (c.3824+1G>C) and b) a mutation of the acceptor site of intron 23 of of the ApoB gene (c.3825-1G>A). The parents were heterozygous carriers. Splicing mechanisms of both mutations were further characterized by minigene assay in vitro. Conclusion. In this report we have characterized at the clinical and molecular level a rare case of compound heterozygous FHBL which carries two novel splicing mutations of the APOB gene affecting the splicing machinery.

Published
2012

25. Disease trends over time and CD4+CCR5+ T-cells expansion predict carotid atherosclerosis development in patients with systemic lupus erythematosus.

Author

Baragetti, A., Ramirez, G.A., Magnoni, M., Garlaschelli, K., Grigore, L., Berteotti, M., Scotti, I., Bozzolo, E., Berti, A., Camici, P.G., Catapano, A.L., Manfredi, A.A., Ammirati, E., and Norata, G.D.

Abstract

Background and Aim: Patients with Systemic Lupus Erythematosus (SLE) present increased cardiovascular mortality compared to the general population. Few studies have assessed the long-term development and progression of carotid atherosclerotic plaque in SLE patients. Our aim was to investigate the association of clinical and laboratory markers of disease activity and classical cardiovascular risk factors (CVRF) with carotid atherosclerosis development in SLE patients in a prospective 5-year study.Methods and Results: Clinical history and information on principal CVRFs were collected at baseline and after 5 years in 40 SLE patients (36 women, mean age 42 ± 9 years; 14.4 ± 7 years of mean disease duration) and 50 age-matched controls. Carotid Doppler ultrasonography was employed to quantify the atherosclerotic burden at baseline and at follow up. Clinimetrics were applied to assess SLE activity over time (SLEDAI). The association between basal circulating T cell subsets (including CD4+CCR5+; CD4+CXCR3+; CD4+HLADR+; CD4+CD45RA+RO-, CD4+CD45RO+RA- and their subsets) and atherosclerosis development was evaluated. During the 5-year follow up, 32% of SLE patients, developed carotid atherosclerosis compared to 4% of controls. Furthermore, considering SLEDAI changes over time, patients within the highest tertile were those with increased incidence of carotid atherosclerosis independently of CVRF. In addition, increased levels of CD4+CCR5+ T cells were independently associated with the development of carotid atherosclerosis in SLE patients.Conclusion: Serial clinical evaluations over time, rather than a single point estimation of disease activity or CVRF burden, are required to define the risk of carotid atherosclerosis development in SLE patients. Specific T cell subsets are associated with long-term atherosclerotic progression and may further be of help in predicting vascular disease progression. [ABSTRACT FROM AUTHOR]

Published
2018
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34. Cardiometabolic and immune factors associated with increased common carotid artery intima-media thickness and cardiovascular disease in patients with systemic lupus erythematosus

Author

Ammirati, E., primary, Bozzolo, E.P., additional, Contri, R., additional, Baragetti, A., additional, Palini, A.G., additional, Cianflone, D., additional, Banfi, M., additional, Uboldi, P., additional, Bottoni, G., additional, Scotti, I., additional, Pirillo, A., additional, Grigore, L., additional, Garlaschelli, K., additional, Monaco, C., additional, Catapano, A.L., additional, Sabbadini, M.G., additional, Manfredi, A.A., additional, and Norata, G.D., additional

Published
2014
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36. Effector Memory T cells Are Associated With Atherosclerosis in Humans and Animal Models

Author

Ammirati, E., primary, Cianflone, D., additional, Vecchio, V., additional, Banfi, M., additional, Vermi, A. C., additional, De Metrio, M., additional, Grigore, L., additional, Pellegatta, F., additional, Pirillo, A., additional, Garlaschelli, K., additional, Manfredi, A. A., additional, Catapano, A. L., additional, Maseri, A., additional, Palini, A. G., additional, and Norata, G. D., additional

Published
2012
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37. 380 EFFECTOR MEMORY T LYMPHOCYTES ARE ASSOCIATED WITH CARDIOVASCULAR DISEASE IN HUMANS AND AORTIC ATHEROSCLEROSIS IN APOE AND LDL-R KNOCK-OUT ANIMALS

Author

Norata, G., primary, Ammirati E, E., additional, Banfi, M., additional, Vacchio, V., additional, Tramontana, S., additional, Garlaschelli, K., additional, Pelegatta, F., additional, Grigore, L., additional, Cianflone, D., additional, Maseri, A., additional, Catapano, A., additional, and Palini, A., additional

Published
2011
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38. Protein-energy wasting, inflammation and oxidative stress in CKD 5D

Author

Rosales, L., primary, Vega, O., additional, Usvyat, L., additional, Thijssen, S., additional, Levin, N., additional, Kotanko, P., additional, Miyamoto, T., additional, Witasp, A., additional, Rashid Qureshi, A., additional, Heimburger, O., additional, Barany, P., additional, Nordfors, L., additional, Lindholm, B., additional, Stenvinkel, P., additional, Jesus Carrero, J., additional, Kalousova, M., additional, Benakova, H., additional, Kubena, A. A., additional, Dusilova-Sulkova, S., additional, Tesar, V., additional, Zima, T., additional, Lee, Y. J., additional, Kim, M. S., additional, Song, B. G., additional, Cho, S., additional, Kim, S. R., additional, Stockler-Pinto, M., additional, Lobo, J., additional, Moraes, C., additional, Barros, A., additional, Farage, N., additional, Boaventura, G., additional, Mafra, D., additional, Malm, O., additional, Matsuda, S., additional, Akaike, N., additional, Kajiwara, K., additional, Tovbin, D., additional, Kesari, S., additional, Sola-Del Valle, D., additional, Barasch, J., additional, Douvdevani, A., additional, Zlotnik, M., additional, Abd Elkadir, A., additional, Storch, S., additional, Sarikaya, M., additional, Sari, F., additional, Gunes, J., additional, Eren, M., additional, Cetinkaya, R., additional, Hwang, J.-C., additional, Ma, T.-L., additional, Wang, C.-T., additional, Ogawa, H., additional, Nagaya, T., additional, Ota, Y., additional, Sarai, M., additional, Oda, O., additional, Biavo, B., additional, Uezima, C., additional, Costa, M. E., additional, Barros, C., additional, Martins, J. P., additional, Ribeiro Jr, E., additional, Tzanno-Martins, C., additional, Honda, H., additional, Kimata, N., additional, Wakai, K., additional, Akizawa, T., additional, Droulias, J., additional, Filliponi, V., additional, Argyropoulos, C., additional, Fischer, R., additional, Papakonstantinou, C., additional, Papadopoulos, C., additional, Kouvelis, A., additional, Zervas, G., additional, Dampolia, E., additional, Zerefos, N., additional, Valis, D., additional, Sarcina, C., additional, Baragetti, I., additional, Uboldi, P., additional, Buzzi, L., additional, Garlaschelli, K., additional, Ferrario, F., additional, Terraneo, V., additional, Norata, G. D., additional, Catapano, A. L., additional, Pozzi, C., additional, Conti, G., additional, Santoro, D., additional, Caccamo, D., additional, Condello, S., additional, Pazzano, D., additional, Savica, V., additional, Jentile, R., additional, Fede, C., additional, Bellinghieri, G., additional, Zortcheva, R., additional, Ikonomov, V., additional, Galunska, B., additional, Paskalev, D., additional, Dobreva, D., additional, Ivanova, D., additional, Tsunoda, M., additional, Ikee, R., additional, Sasaki, N., additional, Sato, N., additional, Hashimoto, N., additional, Korol, L., additional, Dudar, I., additional, Migal, L., additional, Gonchar, Y., additional, Seleznova, I., additional, Ischenko, V., additional, Erkmen Uyar, M., additional, Tutal, E., additional, Bal, Z., additional, Ahmed, N., additional, Sezer, S., additional, Fedak, D., additional, Kuzniewski, M., additional, Pawlica, D., additional, Kusnierz-Cabala, B., additional, Solnica, B., additional, Drozdz, M., additional, Janda, K., additional, Sulowicz, W., additional, Kopec, J., additional, Banach, M., additional, and Leal, V., additional

Published
2011
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43. Reply

Author

Baragetti, I., primary, Raselli, S., additional, Stucchi, A., additional, Terraneo, V., additional, Furiani, S., additional, Buzzi, L., additional, Garlaschelli, K., additional, Alberghini, E., additional, Catapano, A.L., additional, and Buccianti, G., additional

Published
2007
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47. Effect of the -420C/G variant of the resistin gene promoter on metabolic syndrome, obesity, myocardial infarction and kidney dysfunction.

Author

Norata GD, Ongari M, Garlaschelli K, Tibolla G, Grigore L, Raselli S, Vettoretti S, Baragetti I, Noto D, Cefalù AB, Buccianti G, Averna M, and Catapano AL

Abstract

Objective. Resistin is an adipokine that has been suggested to be correlated with markers of inflammation and to be predictive of coronary atherosclerosis and type II diabetes in humans. A common single nucleotide polymorphism (SNP) (-420C/G) in the promoter of resistin is associated with increased resistin plasma levels and susceptibility to type II diabetes. The aim of this study was to investigate the association of the -420C/G polymorphism with metabolic syndrome, obesity, myocardial infarction and kidney disease. Design and results. First we studied 1542 subjects from the PLIC study (a population based cohort). GG carriers showed an higher prevalence of obesity and metabolic syndrome as well as increased plasma triglycerides levels, BMI, systolic and diastolic blood pressure and cardiovascular risk according to Framingham algorithm (P < 0.05 for all). Next we investigated the presence of the -420C/G resistin polymorphism in a case-control study that included 300 subject with myocardial infarction and 300 age and sex matched controls and then we studied the role of the -420C/G SNP in 88 patients with mild to moderate renal dysfunction. No statistically significant differences in allele frequencies between the PLIC study, the myocardial infarction (MI) cases and the subjects with renal dysfunction were observed. Pro-inflammatory gene expression profiling of peripheral blood mononuclear cells failed to detect any difference between wild type subjects and carriers of the rare allele. Conclusion. Our data suggest that the presence of the -420C/G SNP of the resistin gene is associated with increased obesity and metabolic syndrome, although it is not different in subjects at high cardiovascular risk such as patients with myocardial infarction or patients with renal dysfunction compared with controls. [ABSTRACT FROM AUTHOR]

Published
2007
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50. Disease trends over time and CD4+CCR5+T-cells expansion predict carotid atherosclerosis development in patients with systemic lupus erythematosus

Author

Giuseppe A. Ramirez, Angelo A. Manfredi, Alvise Berti, Enrico Ammirati, Alberico L. Catapano, Martina Berteotti, Paolo G. Camici, Marco Magnoni, Enrica Bozzolo, Katia Garlaschelli, Isabella Scotti, Liliana Grigore, Andrea Baragetti, Giuseppe Danilo Norata, Baragetti, A., Ramirez, G. A., Magnoni, M., Garlaschelli, K., Grigore, L., Berteotti, M., Scotti, I., Bozzolo, E., Berti, A., Camici, P. G., Catapano, A. L., Manfredi, A. A., Ammirati, E., and Norata, G. D.

Subjects
medicine.medical_specialty, T cell, Endocrinology, Diabetes and Metabolism, Population, Adaptive immunity, Medicine (miscellaneous), Disease, Systemic lupus erythematosu, 030204 cardiovascular system & hematology, CXCR3, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, Nutrition and Dietetic, Medicine, skin and connective tissue diseases, education, Prospective cohort study, 030203 arthritis & rheumatology, education.field_of_study, Nutrition and Dietetics, business.industry, Vascular disease, Incidence (epidemiology), Carotid atherosclerosi, medicine.disease, medicine.anatomical_structure, Predictive value of tests, Immunology, Cardiology, business, Cardiology and Cardiovascular Medicine
Abstract

Background and Aim Patients with Systemic Lupus Erythematosus (SLE) present increased cardiovascular mortality compared to the general population. Few studies have assessed the long-term development and progression of carotid atherosclerotic plaque in SLE patients. Our aim was to investigate the association of clinical and laboratory markers of disease activity and classical cardiovascular risk factors (CVRF) with carotid atherosclerosis development in SLE patients in a prospective 5-year study. Methods and results Clinical history and information on principal CVRFs were collected at baseline and after 5 years in 40 SLE patients (36 women, mean age 42 ± 9 years; 14.4 ± 7 years of mean disease duration) and 50 age-matched controls. Carotid Doppler ultrasonography was employed to quantify the atherosclerotic burden at baseline and at follow up. Clinimetrics were applied to assess SLE activity over time (SLEDAI). The association between basal circulating T cell subsets (including CD4+CCR5+; CD4+CXCR3+; CD4+HLADR+; CD4+CD45RA+RO−, CD4+CD45RO+RA− and their subsets) and atherosclerosis development was evaluated. During the 5-year follow up, 32% of SLE patients, developed carotid atherosclerosis compared to 4% of controls. Furthermore, considering SLEDAI changes over time, patients within the highest tertile were those with increased incidence of carotid atherosclerosis independently of CVRF. In addition, increased levels of CD4+CCR5+ T cells were independently associated with the development of carotid atherosclerosis in SLE patients. Conclusion Serial clinical evaluations over time, rather than a single point estimation of disease activity or CVRF burden, are required to define the risk of carotid atherosclerosis development in SLE patients. Specific T cell subsets are associated with long-term atherosclerotic progression and may further be of help in predicting vascular disease progression.

Published
2018

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