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001-es BibID:	BIBFORM101829
035-os BibID:	(cikkazonosító)e24568
Első szerző:	Kwiecinski, Monika
Cím:	Hepatocyte Growth Factor (HGF) Inhibits Collagen I and IV Synthesis in Hepatic Stellate Cells by miRNA-29 Induction / Monika Kwiecinski, Andrea Noetel, Natalia Elfimova, Jonel Trebicka, Stephanie Schievenbusch, Ingo Strack, Levente Molnar, Melanie von Brandenstein, Ulrich Töx, Roswitha Nischt, Oliver Coutelle, Hans Peter Dienes, Margarete Odenthal
Dátum:	2011
ISSN:	1932-6203
Megjegyzések:	Background:In chronic liver disease, hepatic stellate cells (HSC) transdifferentiate into myofibroblasts, promotingextracellular matrix (ECM) synthesis and deposition. Stimulation of HSC by transforming growth factor-b(TGF-b) is a crucialevent in liver fibrogenesis due to its impact on myofibroblastic transition and ECM induction. In contrast, hepatocyte growthfactor (HGF), exerts antifibrotic activities. Recently, miR-29 has been reported to be involved in ECM synthesis. We thereforestudied the influence of HGF and TGF-bon the miR-29 collagen axis in HSC.Methodology:HSC, isolated from rats, were characterized for HGF and Met receptor expression by Real-Time PCR andWestern blotting during culture induced myofibroblastic transition. Then, the levels of TGF-b, HGF, collagen-I and -IV mRNA,in addition to miR-29a and miR-29b were determined after HGF and TGF-bstimulation of HSC or after experimental fibrosisinduced by bile-duct obstruction in rats. The interaction of miR-29 with 39-untranslated mRNA regions (UTR) was analyzedby reporter assays. The repressive effect of miR-29 on collagen synthesis was studied in HSC treated with miR-29-mimicks byReal-Time PCR and immunoblotting.Principal Findings:The 39-UTR of the collagen-1 and24 subtypes were identified to bind miR-29. Hence, miR-29a/boverexpression in HSC resulted in a marked reduction of collagen-I and -IV synthesis. Conversely, a decrease in miR-29 levelsis observed during collagen accumulation upon experimental fibrosis, in vivo, and after TGF-bstimulation of HSC, in vitro.Finally, we show that during myofibroblastic transition and TGF-bexposure the HGF-receptor, Met, is upregulated in HSC.Thus, whereas TGF-bstimulation leads to a reduction in miR-29 expression and de-repression of collagen synthesis,stimulation with HGF was definitely associated with highly elevated miR-29 levels and markedly repressed collagen-I and -IVsynthesis.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk
Megjelenés:	Plos One. - 6 : 9 (2011), p. 1-13. -
További szerzők:	Noetel, Andrea Elfimova, Natalia Trebica, Jonel Schievenbusch, Stephanie Strack, Ingo Molnár Levente (1986-) Brandenstein, Melanie von Töx, Ulrich Nischt, Roswitha Coutelle, Oliver Dienes, Hans Peter Odenthal, Margarete
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