Molecular analysis of the TGF-beta controlled gene expression program in chicken embryo dermal myofibroblasts

0423219 - ÚMG 2014 RIV NL eng J - Článek v odborném periodiku
Kosla, Jan - Dvořák, Michal - Čermák, Vladimír
Molecular analysis of the TGF-beta controlled gene expression program in chicken embryo dermal myofibroblasts.
Gene. Roč. 513, č. 1 (2013), s. 90-100. ISSN 0378-1119. E-ISSN 1879-0038
Grant CEP: GA AV ČR KAN200520801
Institucionální podpora: RVO:68378050
Klíčová slova: microarray * myofibroblastic phenotype * inhibition of TGF-beta signaling
Kód oboru RIV: EB - Genetika a molekulární biologie
Impakt faktor: 2.082, rok: 2013

The myofibroblast is a mesenchymal cell characterized by synthesis of the extracellular matrix, plus contractile and secretory activities. Myofibroblasts participate in physiological tissue repair, but can also cause devastating fibrosis. They are present in the tumor stroma of carcinomas and contribute to tumor growth and spreading. As myofibroblasts derive from various cell types and appear in a variety of tissues, there is marked variability in their phenotype. As regulatory mechanism of wound healing are likely conserved among vertebrates, detailed knowledge of these mechanisms in more distant species will help to distinguish general from specific phenomena. To provide this as yet missing comparison, we analyzed the impact of the chemical inhibition of TGF-beta signaling on gene expression in chicken embryo dermal myofibroblasts. We revealed genes previously reported in mammalian systems (e.g. SPON2, ASPN, COMP, LUM, HAS2, IL6, CXCL12,VEGFA) as well as novel TGF-beta dependent genes, among them PGF, VEGFC, PTN, FAM180A, FIBIN, ZIC1, ADCY2, RET, HHIP and DNER. Inhibition of TGF-beta signaling also induced multiple genes, including NPR3, AGTR2, MTUS1, SOD3 and NOV. We also analyzed the effects of long term inhibition, and found that it is not able to induce myofibroblast dedifferentiation. (c) 2012 Elsevier B.V. All rights reserved.
Trvalý link: http://hdl.handle.net/11104/0229369