NDLI: βig-h3 Potentiates the Profibrogenic Effect of TGFβ Signaling on Connective Tissue Progenitor Cells Through the Negative Regulation of Master Chondrogenic Genes

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βig-h3 Potentiates the Profibrogenic Effect of TGFβ Signaling on Connective Tissue Progenitor Cells Through the Negative Regulation of Master Chondrogenic Genes

Content Provider	PubMed Central
Author	Lorda-diez, Carlos I. Montero, Juan A. Diaz-mendoza, Manuel J. Garcia-porrero, Juan A. Hurle, Juan M.
Copyright Year	2013
Abstract	Tendons and cartilage are specialized forms of connective tissues originated from common progenitor cells. Initial stages of differentiation of these tissues are characterized by the formation of cell aggregates, which share many molecular markers. Once differentiated, these cells retain considerable plasticity, and chondral metaplasia of tendon and fibrous connective tissues and eventual ossification often accompany degenerative diseases in the adult musculoskeletal system. While this fact is of great relevance for regenerative medicine and aging biology, its molecular basis remains to be elucidated. Gene expression analysis in several physiological and experimental paradigms suggests that differentiation of tendon and cartilage is regulated by a balance in the expression of chondrogenic versus tenogenic genes in the connective tissue cell precursors. Transforming growth factor β (TGFβ) may function both as a profibrogenic or as a prochondrogenic factor for embryonic limb mesoderm and mesenchymal stem cell cultures, but mice that are null for TGFβ 2 and 3 lack tendons. Here, we identify βig-h3 as a factor downstream TGFβ signaling regulated by Smad 2 and 3, which is highly expressed in the differentiating tendons and joint capsules. Furthermore, gain- and loss-of-function experiments using limb mesoderm micromass cultures show that βig-h3 downregulates the expression of cartilage master genes, including Sox9, type II collagen, and Hif-1α. Positive regulation of Sox9 and type II Collagen observed in micromass cultures grown under hypoxic conditions is prevented by exogenous administration of βIG-H3, and the antichondrogenic influence of βIG-H3 is lost after Hif-1α silencing with shRNA. Collectively, our findings indicate that βig-h3 promotes the fibrogenic influence of TGFβ signaling, neutralizing the prochondrogenic influence of the hypoxic-inducible factor 1 activated by the hypoxic microenvironment characteristic of limb mesenchymal aggregates.
Related Links	http://dx.doi.org/10.1089/ten.tea.2012.0188
Ending Page	457
Page Count	10
Starting Page	448
File Format	PDF
ISSN	19373341
e-ISSN	1937335X
Journal	Tissue Engineering. Part A
Issue Number	3-4
Volume Number	19
Language	English
Publisher	Mary Ann Liebert, Inc.
Publisher Date	2013-02-01
Access Restriction	Open
Rights Holder	Mary Ann Liebert, Inc.
Subject Keyword	Biochemistry Bioengineering Biomaterials Biomedical Engineering Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Biochemistry Biomaterials Bioengineering Biomedical Engineering

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