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Title: Reversible differentiation of myofibroblasts by MyoD

Abstract

Myofibroblasts participate in tissue repair processes in diverse mammalian organ systems. The deactivation of myofibroblasts is critical for termination of the reparative response and restoration of tissue structure and function. The current paradigm on normal tissue repair is the apoptotic clearance of terminally differentiated myofibroblasts; while, the accumulation of activated myofibroblasts is associated with progressive human fibrotic disorders. The capacity of myofibroblasts to undergo de-differentiation as a potential mechanism for myofibroblast deactivation has not been examined. In this report, we have uncovered a role for MyoD in the induction of myofibroblast differentiation by transforming growth factor-{beta}1 (TGF-{beta}1). Myofibroblasts demonstrate the capacity for de-differentiation and proliferation by modulation of endogenous levels of MyoD. We propose a model of reciprocal signaling between TGF-{beta}1/ALK5/MyoD and mitogen(s)/ERK-MAPK/CDKs that regulate myofibroblast differentiation and de-differentiation, respectively. Our studies provide the first evidence for MyoD in controlling myofibroblast activation and deactivation. Restricted capacity for de-differentiation of myofibroblasts may underlie the progressive nature of recalcitrant human fibrotic disorders.

Authors:
; ; ;
Publication Date:
OSTI Identifier:
22212162
Resource Type:
Journal Article
Journal Name:
Experimental Cell Research
Additional Journal Information:
Journal Volume: 317; Journal Issue: 13; Other Information: Copyright (c) 2011 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0014-4827
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; ANIMAL TISSUES; BIOLOGICAL REPAIR; CELL PROLIFERATION; CLEARANCE; FIBROBLASTS; FIBROSIS; GROWTH FACTORS

Citation Formats

Hecker, Louise, Jagirdar, Rajesh, Jin, Toni, and Thannickal, Victor J., E-mail: vjthan@uab.edu. Reversible differentiation of myofibroblasts by MyoD. United States: N. p., 2011. Web. doi:10.1016/J.YEXCR.2011.03.016.
Hecker, Louise, Jagirdar, Rajesh, Jin, Toni, & Thannickal, Victor J., E-mail: vjthan@uab.edu. Reversible differentiation of myofibroblasts by MyoD. United States. doi:10.1016/J.YEXCR.2011.03.016.
Hecker, Louise, Jagirdar, Rajesh, Jin, Toni, and Thannickal, Victor J., E-mail: vjthan@uab.edu. Mon . "Reversible differentiation of myofibroblasts by MyoD". United States. doi:10.1016/J.YEXCR.2011.03.016.
@article{osti_22212162,
title = {Reversible differentiation of myofibroblasts by MyoD},
author = {Hecker, Louise and Jagirdar, Rajesh and Jin, Toni and Thannickal, Victor J., E-mail: vjthan@uab.edu},
abstractNote = {Myofibroblasts participate in tissue repair processes in diverse mammalian organ systems. The deactivation of myofibroblasts is critical for termination of the reparative response and restoration of tissue structure and function. The current paradigm on normal tissue repair is the apoptotic clearance of terminally differentiated myofibroblasts; while, the accumulation of activated myofibroblasts is associated with progressive human fibrotic disorders. The capacity of myofibroblasts to undergo de-differentiation as a potential mechanism for myofibroblast deactivation has not been examined. In this report, we have uncovered a role for MyoD in the induction of myofibroblast differentiation by transforming growth factor-{beta}1 (TGF-{beta}1). Myofibroblasts demonstrate the capacity for de-differentiation and proliferation by modulation of endogenous levels of MyoD. We propose a model of reciprocal signaling between TGF-{beta}1/ALK5/MyoD and mitogen(s)/ERK-MAPK/CDKs that regulate myofibroblast differentiation and de-differentiation, respectively. Our studies provide the first evidence for MyoD in controlling myofibroblast activation and deactivation. Restricted capacity for de-differentiation of myofibroblasts may underlie the progressive nature of recalcitrant human fibrotic disorders.},
doi = {10.1016/J.YEXCR.2011.03.016},
journal = {Experimental Cell Research},
issn = {0014-4827},
number = 13,
volume = 317,
place = {United States},
year = {2011},
month = {8}
}