31 results on '"Voellenkle, Christine"'
Search Results
2. Coding and Non-Coding Transcriptomic Landscape of Aortic Complications in Marfan Syndrome.
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Udugampolage, Nathasha Samali, Frolova, Svetlana, Taurino, Jacopo, Pini, Alessandro, Martelli, Fabio, and Voellenkle, Christine
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MARFAN syndrome ,THORACIC aneurysms ,TRANSCRIPTOMES ,CONGENITAL disorders ,AORTA - Abstract
Marfan syndrome (MFS) is a rare congenital disorder of the connective tissue, leading to thoracic aortic aneurysms (TAA) and dissection, among other complications. Currently, the most efficient strategy to prevent life-threatening dissection is preventive surgery. Periodic imaging applying complex techniques is required to monitor TAA progression and to guide the timing of surgical intervention. Thus, there is an acute demand for non-invasive biomarkers for diagnosis and prognosis, as well as for innovative therapeutic targets of MFS. Unraveling the intricate pathomolecular mechanisms underlying the syndrome is vital to address these needs. High-throughput platforms are particularly well-suited for this purpose, as they enable the integration of different datasets, such as transcriptomic and epigenetic profiles. In this narrative review, we summarize relevant studies investigating changes in both the coding and non-coding transcriptome and epigenome in MFS-induced TAA. The collective findings highlight the implicated pathways, such as TGF-β signaling, extracellular matrix structure, inflammation, and mitochondrial dysfunction. Potential candidates as biomarkers, such as miR-200c, as well as therapeutic targets emerged, like Tfam, associated with mitochondrial respiration, or miR-632, stimulating endothelial-to-mesenchymal transition. While these discoveries are promising, rigorous and extensive validation in large patient cohorts is indispensable to confirm their clinical relevance and therapeutic potential. [ABSTRACT FROM AUTHOR]
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- 2024
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- View/download PDF
3. circRNA-miRNA-mRNA Deregulated Network in Ischemic Heart Failure Patients
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Madè, Alisia, primary, Bibi, Alessia, additional, Garcia-Manteiga, Jose Manuel, additional, Tascini, Anna Sofia, additional, Piella, Santiago Nicolas, additional, Tikhomirov, Roman, additional, Voellenkle, Christine, additional, Gaetano, Carlo, additional, Leszek, Przemyslaw, additional, Castelvecchio, Serenella, additional, Menicanti, Lorenzo, additional, Martelli, Fabio, additional, and Greco, Simona, additional
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- 2023
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4. Hypoxia-induced miR-210 modulates the inflammatory response and fibrosis upon acute ischemia
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Zaccagnini Germana, Greco Simona, Longo Marialucia, Maimone Biagina, Voellenkle Christine, Fuschi Paola, Carrara Matteo, Creo Pasquale, Maselli Davide, Tirone Mario, Mazzone Massimiliano, Gaetano Carlo, Spinetti Gaia, and Martelli Fabio
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Cytology ,QH573-671 - Abstract
Abstract Hypoxia-induced miR-210 is a crucial component of the tissue response to ischemia, stimulating angiogenesis and improving tissue regeneration. Previous analysis of miR-210 impact on the transcriptome in a mouse model of hindlimb ischemia showed that miR-210 regulated not only vascular regeneration functions, but also inflammation. To investigate this event, doxycycline-inducible miR-210 transgenic mice (Tg-210) and anti-miR-210 LNA-oligonucleotides were used. It was found that global miR-210 expression decreased inflammatory cells density and macrophages accumulation in the ischemic tissue. To dissect the underpinning cell mechanisms, Tg-210 mice were used in bone marrow (BM) transplantation experiments and chimeric mice underwent hindlimb ischemia. MiR-210 overexpression in the ischemic tissue was sufficient to increase capillary density and tissue repair, and to reduce inflammation in the presence of Wt-BM infiltrating cells. Conversely, when Tg-210-BM cells migrated in a Wt ischemic tissue, dysfunctional angiogenesis, inflammation, and impaired tissue repair, accompanied by fibrosis were observed. The fibrotic regions were positive for α-SMA, Vimentin, and Collagen V fibrotic markers and for phospho-Smad3, highlighting the activation of TGF-β1 pathway. Identification of Tg-210 cells by in situ hybridization showed that BM-derived cells contributed directly to fibrotic areas, where macrophages co-expressing fibrotic markers were observed. Cell cultures of Tg-210 BM-derived macrophages exhibited a pro-fibrotic phenotype and were enriched with myofibroblast-like cells, which expressed canonical fibrosis markers. Interestingly, inhibitors of TGF-β type-1-receptor completely abrogated this pro-fibrotic phenotype. In conclusion, a context-dependent regulation by miR-210 of the inflammatory response was identified. miR-210 expression in infiltrating macrophages is associated to improved angiogenesis and tissue repair when the ischemic recipient tissue also expresses high levels of miR-210. Conversely, when infiltrating an ischemic tissue with mismatched miR-210 levels, macrophages expressing high miR-210 levels display a pro-fibrotic phenotype, leading to impaired tissue repair, fibrosis, and dysfunctional angiogenesis.
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- 2021
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5. Dysregulation of microRNA expression in diabetic skin
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Baldini, Enke, Testa, Erika, Voellenkle, Christine, De Domenico, Emanuela, Cianfarani, Francesca, Martelli, Fabio, Ulisse, Salvatore, and Odorisio, Teresa
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- 2020
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6. Correction: Hypoxia-induced miR-210 modulates the inflammatory response and fibrosis upon acute ischemia
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Zaccagnini, Germana, Greco, Simona, Longo, Marialucia, Maimone, Biagina, Voellenkle, Christine, Fuschi, Paola, Carrara, Matteo, Creo, Pasquale, Maselli, Davide, Tirone, Mario, Mazzone, Massimiliano, Gaetano, Carlo, Spinetti, Gaia, and Martelli, Fabio
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- 2021
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7. CircANKRD12 Is Induced in Endothelial Cell Response to Oxidative Stress
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Voellenkle, Christine, primary, Fuschi, Paola, additional, Mutoli, Martina, additional, Carrara, Matteo, additional, Righini, Paolo, additional, Nano, Giovanni, additional, Gaetano, Carlo, additional, and Martelli, Fabio, additional
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- 2022
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8. miR-210 hypoxamiR in Angiogenesis and Diabetes
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Zaccagnini, Germana, primary, Greco, Simona, additional, Voellenkle, Christine, additional, Gaetano, Carlo, additional, and Martelli, Fabio, additional
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- 2022
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9. Increased BACE1-AS long noncoding RNA and β-amyloid levels in heart failure
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Greco, Simona, Zaccagnini, Germana, Fuschi, Paola, Voellenkle, Christine, Carrara, Matteo, Sadeghi, Iman, Bearzi, Claudia, Maimone, Biagina, Castelvecchio, Serenella, Stellos, Konstantinos, Gaetano, Carlo, Menicanti, Lorenzo, and Martelli, Fabio
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- 2017
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10. Hypoxia-Induced miR-210 Is Necessary for Vascular Regeneration upon Acute Limb Ischemia
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Zaccagnini, Germana, primary, Maimone, Biagina, additional, Fuschi, Paola, additional, Longo, Marialucia, additional, Da Silva, Daniel, additional, Carrara, Matteo, additional, Voellenkle, Christine, additional, Perani, Laura, additional, Esposito, Antonio, additional, Gaetano, Carlo, additional, and Martelli, Fabio, additional
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- 2019
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11. Dysregulation of Circular RNAs in Myotonic Dystrophy Type 1
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Renna, Laura Valentina, Sain, Simona Baghai, Voellenkle, Christine, Perfetti, Alessandra, Carrara, Matteo, Fuschi, Paola, Renna, Laura, Longo, Marialucia, Sain, Simona, Cardani, Rosanna, Valaperta, Rea, Silvestri, Gabriella, Legnini, Ivano, Bozzoni, Irene, Furling, Denis, Gaetano, Carlo, Falcone, Germana, Meola, Giovanni, Martelli, Fabio, Istituti di Ricovero e Cura a Carattere Scientifico (IRCCS), IRCCS San Raffaele Scientific Institute [Milan, Italie], Fondazione 'Policlinico Universitario A. Gemelli' [Rome], Università degli Studi di Roma 'La Sapienza' = Sapienza University [Rome], Department of Biology and Biotechnology 'Charles Darwin', Institut Pasteur, Fondation Cenci Bolognetti - Istituto Pasteur Italia, Fondazione Cenci Bolognetti, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Università degli Studi di Roma 'La Sapienza' = Sapienza University [Rome], Institut de Myologie, Centre National de la Recherche Scientifique (CNRS)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Association française contre les myopathies (AFM-Téléthon)-Sorbonne Université (SU), Centre de Recherche en Myologie, Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), University of Milan, This study was supported by: Telethon-Italy (no. GGP14092) and AFM-Telethon (no. 18477) to F.M. and G.F., Ministero della Salute (Ricerca Corrente, 5 × 1000, RF-2011-02347907, and PE-2011-02348537) to F.M., ERC-2013 (AdG 340172–MUNCODD), Telethon-Italy (GGP16213), and Fondazione Roma (2015-2017) to I.B., FMM-Fondazione Malattie Miotoniche (2017-18) to R.C., and Ministero della Salute (5 × 1000) to S.B.S., We thank the platform for the immortalization of human cells of the Institut de Myologie, Paris, France, for providing DM1 and control myogenic cell lines, as well as Michele Cavalli (Biomedical Sciences for Health, University of Milan and IRCCS Policlinico San Donato, Milan, Italy) for his support in clinical data collection., and Centre de recherche en Myologie – U974 SU-INSERM
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Male ,[SDV]Life Sciences [q-bio] ,Myotonic dystrophy ,Settore MED/03 - GENETICA MEDICA ,Polymerase Chain Reaction ,lcsh:Chemistry ,Exon ,0302 clinical medicine ,MESH: Alternative Splicing/genetics ,lcsh:QH301-705.5 ,Spectroscopy ,alternative splicing ,circular RNA ,muscular dystrophies ,0303 health sciences ,MESH: Gene Expression Regulation ,MESH: Muscle, Skeletal/pathology ,General Medicine ,MESH: Case-Control Studies ,Computer Science Applications ,MESH: Reproducibility of Results ,medicine.anatomical_structure ,RNA splicing ,Female ,MESH: RNA/blood ,Adult ,musculoskeletal diseases ,Biology ,Article ,Catalysis ,Cell Line ,Inorganic Chemistry ,03 medical and health sciences ,MESH: RNA/genetics ,Circular RNA ,microRNA ,medicine ,Humans ,MESH: Myotonic Dystrophy/genetics ,Physical and Theoretical Chemistry ,Muscle, Skeletal ,Molecular Biology ,Gene ,030304 developmental biology ,MESH: Humans ,MESH: Myotonic Dystrophy/blood ,Organic Chemistry ,Alternative splicing ,Reproducibility of Results ,Skeletal muscle ,MESH: Adult ,MESH: Polymerase Chain Reaction ,RNA, Circular ,medicine.disease ,Molecular biology ,MESH: Male ,MESH: Cell Line ,Gene Expression Regulation ,lcsh:Biology (General) ,lcsh:QD1-999 ,Case-Control Studies ,MESH: Muscle, Skeletal/metabolism ,RNA ,MESH: Female ,030217 neurology & neurosurgery - Abstract
Circular RNAs (circRNAs) constitute a recently re-discovered class of non-coding RNAs functioning as sponges for miRNAs and proteins, affecting RNA splicing and regulating transcription. CircRNAs are generated by &ldquo, back-splicing&rdquo, which is the linking covalently of 3&prime, and 5&prime, ends of exons. Thus, circRNA levels might be deregulated in conditions associated with altered RNA-splicing. Significantly, growing evidence indicates their role in human diseases. Specifically, myotonic dystrophy type 1 (DM1) is a multisystemic disorder caused by expanded CTG repeats in the DMPK gene which results in abnormal mRNA-splicing. In this investigation, circRNAs expressed in DM1 skeletal muscles were identified by analyzing RNA-sequencing data-sets followed by qPCR validation. In muscle biopsies, out of nine tested, four transcripts showed an increased circular fraction: CDYL, HIPK3, RTN4_03, and ZNF609. Their circular fraction values correlated with skeletal muscle strength and with splicing biomarkers of disease severity, and displayed higher values in more severely affected patients. Moreover, Receiver-Operating-Characteristics curves of these four circRNAs discriminated DM1 patients from controls. The identified circRNAs were also detectable in peripheral-blood-mononuclear-cells (PBMCs) and the plasma of DM1 patients, but they were not regulated significantly. Finally, increased circular fractions of RTN4_03 and ZNF609 were also observed in differentiated myogenic cell lines derived from DM1 patients. In conclusion, this pilot study identified circRNA dysregulation in DM1 patients.
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- 2019
12. Dysregulation of circular RNAs in myotonic dystrophy type 1
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Voellenkle, Christine, primary, Perfetti, Alessandra, additional, Carrara, Matteo, additional, Fuschi, Paola, additional, Renna, Laura Valentina, additional, Longo, Marialucia, additional, Cardani, Rosanna, additional, Valaperta, Rea, additional, Silvestri, Gabriella, additional, Legnini, Ivano, additional, Bozzoni, Irene, additional, Furling, Denis, additional, Gaetano, Carlo, additional, Falcone, Germana, additional, Meola, Giovanni, additional, and Martelli, Fabio, additional
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- 2018
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13. Implication of long noncoding RNAs in the endothelial cell response to hypoxia revealed by RNA-sequencing
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Voellenkle, Christine, Garcia-Manteiga, Jose Manuel, Pedrott, Simona, De Toma, Ilario, Da Silva, Daniel, Maimone, Biagina, Greco, Simona, Fasanaro, Pasquale, Creo, Pasquale, Zaccagnini, Germana, Gaetano, Carlo, and Martelli, Fabio
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embryonic structures ,ddc:610 - Abstract
Long noncoding RNAs (lncRNAs) are non-protein coding RNAs regulating gene expression. Although for some lncRNAs a relevant role in hypoxic endothelium has been shown, the regulation and function of lncRNAs is still largely unknown in the vascular physio-pathology. Taking advantage of next-generation sequencing techniques, transcriptomic changes induced by endothelial cell exposure to hypoxia were investigated. Paired-end sequencing of polyadenylated RNA derived from human umbilical vein endothelial cells (HUVECs) exposed to 1% O2 or normoxia was performed. Bioinformatics analysis identified ≈2000 differentially expressed genes, including 122 lncRNAs. Extensive validation was performed by both microarray and qPCR. Among the validated lncRNAs, H19, MIR210HG, MEG9, MALAT1 and MIR22HG were also induced in a mouse model of hindlimb ischemia. To test the functional relevance of lncRNAs in endothelial cells, knockdown of H19 expression was performed. H19 inhibition decreased HUVEC growth, inducing their accumulation in G1 phase of the cell cycle; accordingly, p21 (CDKN1A) expression was increased. Additionally, H19 knockdown also diminished HUVEC ability to form capillary like structures when plated on matrigel. In conclusion, a high-confidence signature of lncRNAs modulated by hypoxia in HUVEC was identified and a significant impact of H19 lncRNA was shown.
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- 2017
14. Dysregulation of MicroRNA biogenesis in diabetic skin
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Baldini, Enke, Testa, Erika, Cianfarani, Francesca, Voellenkle, Christine, Martelli, Fabio, Ulisse, Salvatore, and Odorisio, Teresa
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Ago 2 ,Diabetes ,MicroRNA ,Exportin 5 ,MicroRNA, Diabetes, Skin, Drosha, Dicer, DCGR8, Exportin 5, Ago 2 ,DCGR8 ,Skin ,Drosha ,Dicer - Published
- 2017
15. Central role of the p53 pathway in the noncoding-RNA response to oxidative stress
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Fuschi, Paola, primary, Carrara, Matteo, additional, Voellenkle, Christine, additional, Garcia-Manteiga, Jose Manuel, additional, Righini, Paolo, additional, Maimone, Biagina, additional, Sangalli, Elena, additional, Villa, Francesco, additional, Specchia, Claudia, additional, Picozza, Mario, additional, Nano, Giovanni, additional, Gaetano, Carlo, additional, Spinetti, Gaia, additional, Puca, Annibale A., additional, Magenta, Alessandra, additional, and Martelli, Fabio, additional
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- 2017
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16. MOESM2 of Long noncoding RNA dysregulation in ischemic heart failure
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Greco, Simona, Zaccagnini, Germana, Perfetti, Alessandra, Fuschi, Paola, Valaperta, Rea, Voellenkle, Christine, Castelvecchio, Serenella, Gaetano, Carlo, Finato, Nicoletta, Beltrami, Antonio, Menicanti, Lorenzo, and Martelli, Fabio
- Abstract
Additional file 2: Figure S1. Cardiac hypertrophy of non end-stage patients. Sections were derived from FFPE LV biopsies of controls (A) and HF patients (B). Hematoxylin and eosin staining showed a clear cardiomyocyte hypertrophy. Representative pictures are shown (HF n=16; CTR n=4; calibration bar=100 µm; magnification 20X). The bar graphs show the RT-qPCR measurement of MYH6 and NPPA hypertrophy markers, that are down- and up-regulated as expected (HF=10; CTR=5; **p≤0.01; *** p≤0.001) (C and D). Figure S2: Quality control of RNA extracted from heart biopsies of patients and controls. Total RNA was extracted from LV samples derived from non end-stage HF (n=18, panel A), end-stage HF (n=11, panel B) or controls (n=17, panel C). Integrity and amount of RNAs were measured by Bioanalyzer electrophoresis. Representative patterns and RNA Integrity Numbers (RIN) are shown. Figure S3: LncRNAs profiling in non end-stage HF patients. (A) Profiling of lncRNAs by RT-qPCR in 13 HF patients and 12 age-and sex-matched controls. (B) Validation of significantly deregulated lncRNAs in 18 HF and 17 controls. The bar graph (A) and table (B) shows the average fold change values with respect to controls (*p≤0.05, **p≤0.01; *** p≤0.001). Figure S4: Transverse aortic constriction induces cardiac hypertrophy. LV pressure overload was induced by TAC in C57BL/6J mice and cardiac hypertrophy markers were measured by RT-qPCR, 7 days after surgery. As expected atp2a2 was down- modulated and nppa, nppb and acta were increased (TAC=10; CTR=8; *p≤0.05, **p≤0.01). Figure S5: Mouse-human genomic alignment of HF lncRNAs. Gene locations from GRCh38.p5 (GCA_000001405.20) and from GRCm38.p4 (GCA_000001635.6) human and mouse genome assemblies, respectively, were used to compare the lncRNA sequence alignment in human and mouse by using Clustal Omega (http://www.ebi.ac.uk/Tools/msa/clustalo/). The percentage of identity is indicated. Figure S6: LncRNA/mRNA correlation analysis in HF. HF lncRNAs levels correlated to the levels of the mRNA expressed in the same samples. The bar graph indicates the number of transcripts significantly correlated for each lncRNA, either positively (white) or negatively (black). Figure S7: Venn’s diagram of enriched pathways in common between LV and PBMCs in HF patients GSE26887, GSE9128 and GSE1869 GEO datasets. The comparison of the 89, 99 and 53 enriched pathways of GSE26887, GSE9128 and GSE1869 datasets, respectively, identified 43 enriched pathways in common. Transcriptomic changes observed in LV and PBMCs of HF patients were determined in the following GEO datasets: for LV, GSE26887, and for PBMCs, GSE9128 and GSE1869. Common deregulated pathways were plotted as a Venn’s diagram.
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- 2016
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17. p75(NTR)-dependent activation of NF-κB regulates microRNA-503 transcription and pericyte-endothelial crosstalk in diabetes after limb ischaemia
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Caporali, Andrea, Meloni, Marco, Nailor, Audrey, Mitić, Tijana, Shantikumar, Saran, Riu, Federica, Sala-Newby, Graciela B., Rose, Lorraine, Besnier, Marie, Katare, Rajesh, Voellenkle, Christine, Verkade, Paul, Martelli, Fabio, Madeddu, Paolo, and Emanueli, Costanza
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Diabetes ,miRNAs ,Transcription ,Cell signalling - Abstract
The communication between vascular endothelial cells (ECs) and pericytes in themicrovasculature is fundamental for vascular growth and homeostasis; however, these processes are disrupted by diabetes. Here we show that modulation of p75(NTR) expression in ECs exposed to high glucose activates transcription of miR-503, which negatively affects pericyte function. p75(NTR) activates NF-kB to bind the miR-503 promoter and upregulate miR-503 expression in ECs. NF-kB further induces activation of Rho kinase and shedding of endothelial microparticles carrying miR-503, which transfer miR-503 from ECs to vascular pericytes. Theintegrin-mediated uptake of miR-503 in the recipient pericytes reduces expression of EFNB2 and VEGFA, resulting in impaired migration and proliferation. We confirm operation of the above mechanisms in mouse models of diabetes, in which EC-derived miR-503 reduces pericyte coverage of capillaries, increased permeability and impaired post-ischemic angiogenesis in limb muscles. Collectively, our data demonstrate that miR-503 regulates pericyte-endothelial crosstalk in microvascular diabetic complications.
- Published
- 2015
18. The expression of the BPIFB4 and CXCR4 associates with sustained health in long-living individuals from Cilento-Italy
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Spinetti, Gaia, primary, Sangalli, Elena, additional, Specchia, Claudia, additional, Villa, Francesco, additional, Spinelli, Chiara, additional, Pipolo, Rita, additional, Carrizzo, Albino, additional, Greco, Simona, additional, Voellenkle, Christine, additional, Vecchione, Carmine, additional, Madeddu, Paolo, additional, Martelli, Fabio, additional, and Puca, Annibale Alessandro, additional
- Published
- 2017
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19. Long noncoding RNA dysregulation in ischemic heart failure
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Greco, Simona, primary, Zaccagnini, Germana, additional, Perfetti, Alessandra, additional, Fuschi, Paola, additional, Valaperta, Rea, additional, Voellenkle, Christine, additional, Castelvecchio, Serenella, additional, Gaetano, Carlo, additional, Finato, Nicoletta, additional, Beltrami, Antonio Paolo, additional, Menicanti, Lorenzo, additional, and Martelli, Fabio, additional
- Published
- 2016
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20. microRNAs in ischaemic cardiovascular diseases
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Greco, Simona, primary, Zaccagnini, Germana, additional, Voellenkle, Christine, additional, and Martelli, Fabio, additional
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- 2016
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21. Profiling and Discovery of microRNAs Expressed in Hypoxic Endothelial Cells by Massively Parallel Sequencing
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Voellenkle Christine 2, van Rooij Jeroen 2, Guffanti Alessandro 3, Brini Elena 3, Fasanaro Pasquale 1, Isaia Eleonora 2, Croft Larry 4, David Matei 5, Capogrossi Maurizio C. 1, Moles Anna 3, Felsani Armando 3, and Martelli Fabio 1
- Published
- 2010
22. Transcriptional Profiling of Hmgb1-Induced Myocardial Repair Identifies a Key Role for Notch Signaling
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Limana, Federica, primary, Esposito, Grazia, additional, Fasanaro, Pasquale, additional, Foglio, Eleonora, additional, Arcelli, Diego, additional, Voellenkle, Christine, additional, Di Carlo, Anna, additional, Avitabile, Daniele, additional, Martelli, Fabio, additional, Antonio Russo, Matteo, additional, Pompilio, Giulio, additional, Germani, Antonia, additional, and Capogrossi, Maurizio C, additional
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- 2013
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23. ROD1 Is a Seedless Target Gene of Hypoxia-Induced miR-210
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Fasanaro, Pasquale, primary, Romani, Sveva, additional, Voellenkle, Christine, additional, Maimone, Biagina, additional, Capogrossi, Maurizio C., additional, and Martelli, Fabio, additional
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- 2012
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24. Deep-sequencing of endothelial cells exposed to hypoxia reveals the complexity of known and novel microRNAs
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Voellenkle, Christine, primary, van Rooij, Jeroen, additional, Guffanti, Alessandro, additional, Brini, Elena, additional, Fasanaro, Pasquale, additional, Isaia, Eleonora, additional, Croft, Larry, additional, David, Matei, additional, Capogrossi, Maurizio C., additional, Moles, Anna, additional, Felsani, Armando, additional, and Martelli, Fabio, additional
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- 2012
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25. ChIP-on-Chip Analysis of In Vivo Mutant p53 Binding To Selected Gene Promoters
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Dell'Orso, Stefania, primary, Fontemaggi, Giulia, additional, Stambolsky, Perry, additional, Goeman, Frauke, additional, Voellenkle, Christine, additional, Levrero, Massimo, additional, Strano, Sabrina, additional, Rotter, Varda, additional, Oren, Moshe, additional, and Blandino, Giovanni, additional
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- 2011
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26. MicroRNA signatures in peripheral blood mononuclear cells of chronic heart failure patients
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Voellenkle, Christine, primary, van Rooij, Jeroen, additional, Cappuzzello, Claudia, additional, Greco, Simona, additional, Arcelli, Diego, additional, Di Vito, Luca, additional, Melillo, Guido, additional, Rigolini, Roberta, additional, Costa, Elena, additional, Crea, Filippo, additional, Capogrossi, Maurizio C., additional, Napolitano, Monica, additional, and Martelli, Fabio, additional
- Published
- 2010
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27. Hypoxia-Induced miR-210 Is Necessary for Vascular Regeneration upon Acute Limb Ischemia.
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Zaccagnini, Germana, Maimone, Biagina, Fuschi, Paola, Longo, Marialucia, Da Silva, Daniel, Carrara, Matteo, Voellenkle, Christine, Perani, Laura, Esposito, Antonio, Gaetano, Carlo, and Martelli, Fabio
- Subjects
VENTRICULAR remodeling ,ISCHEMIA ,PERIPHERAL vascular diseases ,MYOCARDIAL infarction ,LIFE expectancy ,TRANSGENIC mice - Abstract
Critical limb ischemia is the most serious form of peripheral artery disease, characterized by severe functional consequences, difficult clinical management and reduced life expectancy. The goal of this study was to investigate the miR-210 role in the neo-angiogenic response after acute limb ischemia. Complementary approaches were used in a mouse model of hindlimb ischemia: miR-210 loss-of-function was obtained by administration of LNA-oligonucleotides anti-miR-210; for miR-210 gain-of-function, a doxycycline-inducible miR-210 transgenic mouse was used. We tested miR-210 ability to stimulate vascular regeneration following ischemia. We found that miR-210 was necessary and sufficient to stimulate blood perfusion recovery, as well as arteriolar and capillary density increase, in the ischemic muscle. To clarify the molecular events underpinning miR-210 pro-angiogenic action, the transcriptomic changes in ischemic muscles upon miR-210 blocking were analyzed. We found that miR-210 impacted the transcriptome significantly, regulating pathways and functions linked to vascular regeneration. In agreement with a pro-angiogenic role, miR-210 also improved cardiac function and left ventricular remodeling after myocardial infarction. Moreover, miR-210 blocking decreased capillary density in a Matrigel plug assay, indicating that miR-210 is necessary for angiogenesis independently of ischemia. Collectively, these data indicate that miR-210 plays a pivotal role in promoting vascular regeneration. [ABSTRACT FROM AUTHOR]
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- 2020
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- View/download PDF
28. Dysregulation of Circular RNAs in Myotonic Dystrophy Type 1.
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Voellenkle, Christine, Perfetti, Alessandra, Carrara, Matteo, Fuschi, Paola, Renna, Laura Valentina, Longo, Marialucia, Sain, Simona Baghai, Cardani, Rosanna, Valaperta, Rea, Silvestri, Gabriella, Legnini, Ivano, Bozzoni, Irene, Furling, Denis, Gaetano, Carlo, Falcone, Germana, Meola, Giovanni, and Martelli, Fabio
- Subjects
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CIRCULAR RNA , *MYOTONIA atrophica , *MICRORNA , *RNA sequencing , *SKELETAL muscle - Abstract
Circular RNAs (circRNAs) constitute a recently re-discovered class of non-coding RNAs functioning as sponges for miRNAs and proteins, affecting RNA splicing and regulating transcription. CircRNAs are generated by "back-splicing", which is the linking covalently of 3′- and 5′-ends of exons. Thus, circRNA levels might be deregulated in conditions associated with altered RNA-splicing. Significantly, growing evidence indicates their role in human diseases. Specifically, myotonic dystrophy type 1 (DM1) is a multisystemic disorder caused by expanded CTG repeats in the DMPK gene which results in abnormal mRNA-splicing. In this investigation, circRNAs expressed in DM1 skeletal muscles were identified by analyzing RNA-sequencing data-sets followed by qPCR validation. In muscle biopsies, out of nine tested, four transcripts showed an increased circular fraction: CDYL, HIPK3, RTN4_03, and ZNF609. Their circular fraction values correlated with skeletal muscle strength and with splicing biomarkers of disease severity, and displayed higher values in more severely affected patients. Moreover, Receiver-Operating-Characteristics curves of these four circRNAs discriminated DM1 patients from controls. The identified circRNAs were also detectable in peripheral-blood-mononuclear-cells (PBMCs) and the plasma of DM1 patients, but they were not regulated significantly. Finally, increased circular fractions of RTN4_03 and ZNF609 were also observed in differentiated myogenic cell lines derived from DM1 patients. In conclusion, this pilot study identified circRNA dysregulation in DM1 patients. [ABSTRACT FROM AUTHOR]
- Published
- 2019
- Full Text
- View/download PDF
29. p75NTR-dependent activation of NF-κB regulates microRNA-503 transcription and pericyte-endothelial crosstalk in diabetes after limb ischaemia.
- Author
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Caporali, Andrea, Meloni, Marco, Nailor, Audrey, Mitić, Tijana, Shantikumar, Saran, Riu, Federica, Sala-Newby, Graciela B., Rose, Lorraine, Besnier, Marie, Katare, Rajesh, Voellenkle, Christine, Verkade, Paul, Martelli, Fabio, Madeddu, Paolo, and Emanueli, Costanza
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- 2015
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30. Time-controlled and muscle-specific CRISPR/Cas9-mediated deletion of CTG-repeat expansion in the DMPK gene.
- Author
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Cardinali B, Provenzano C, Izzo M, Voellenkle C, Battistini J, Strimpakos G, Golini E, Mandillo S, Scavizzi F, Raspa M, Perfetti A, Baci D, Lazarevic D, Garcia-Manteiga JM, Gourdon G, Martelli F, and Falcone G
- Abstract
CRISPR/Cas9-mediated therapeutic gene editing is a promising technology for durable treatment of incurable monogenic diseases such as myotonic dystrophies. Gene-editing approaches have been recently applied to in vitro and in vivo models of myotonic dystrophy type 1 (DM1) to delete the pathogenic CTG-repeat expansion located in the 3' untranslated region of the DMPK gene. In DM1-patient-derived cells removal of the expanded repeats induced beneficial effects on major hallmarks of the disease with reduction in DMPK transcript-containing ribonuclear foci and reversal of aberrant splicing patterns. Here, we set out to excise the triplet expansion in a time-restricted and cell-specific fashion to minimize the potential occurrence of unintended events in off-target genomic loci and select for the target cell type. To this aim, we employed either a ubiquitous promoter-driven or a muscle-specific promoter-driven Cas9 nuclease and tetracycline repressor-based guide RNAs. A dual-vector approach was used to deliver the CRISPR/Cas9 components into DM1 patient-derived cells and in skeletal muscle of a DM1 mouse model. In this way, we obtained efficient and inducible gene editing both in proliferating cells and differentiated post-mitotic myocytes in vitro as well as in skeletal muscle tissue in vivo ., Competing Interests: The authors declare no competing interests., (© 2021 The Authors.)
- Published
- 2021
- Full Text
- View/download PDF
31. ChIP-on-chip analysis of in vivo mutant p53 binding to selected gene promoters.
- Author
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Dell'Orso S, Fontemaggi G, Stambolsky P, Goeman F, Voellenkle C, Levrero M, Strano S, Rotter V, Oren M, and Blandino G
- Subjects
- Amino Acid Sequence, Binding Sites genetics, Cell Line, Tumor, Chromatin metabolism, Chromatin Immunoprecipitation, Consensus Sequence genetics, DNA-Binding Proteins genetics, Humans, Mutant Proteins genetics, NF-kappa B metabolism, Protein Binding physiology, Transcription Factors genetics, Transcription Factors metabolism, Transcription, Genetic genetics, Tumor Suppressor Protein p53 genetics, p300-CBP Transcription Factors metabolism, DNA-Binding Proteins metabolism, Mutant Proteins metabolism, Oligonucleotide Array Sequence Analysis, Promoter Regions, Genetic, Tumor Suppressor Protein p53 metabolism
- Abstract
Growing evidence shows that mutant p53 proteins, which are present in many human tumors, gain oncogenic activities that can actively contribute to tumorigenesis. Mutant p53 proteins have been extensively shown to affect the expression of several genes involved in various aspects of cancer biology. We show here the ChIP-on-chip analysis of mutant p53 binding to a set of 154 promoters, composed of both validated and putative mutant p53 target genes. By using the chromatin obtained from mutant p53R175H-immunoprecipitation in proliferating SKBr3 breast cancer cells, we found that mutant p53 binds to 40 of the 154 promoters analyzed. siRNA-mediated mutant p53 knock-down modulates the transcript abundance of some of these target genes. Two-thirds of the mutant p53-bound promoters were also engaged by either p300 or PCAF acetyl-transferases, strongly indicating the presence of transcriptionally active complexes. We also found that NF-kB binding sites are overrepresented among the mutant p53-bound promoters; a ChIP-on-chip analysis confirmed that NF-kB p65 binds to 27 of the mutant p53-bound promoters, indicating that mutant p53 could influence the transcriptional output of these NF-kB target genes.
- Published
- 2011
- Full Text
- View/download PDF
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