Modulation of MMP-2 and MMP-9 through connected pathways and growth factors is critical for extracellular matrix balance of intra-articular ligaments

2017 ◽  
Vol 12 (1) ◽  
pp. e550-e565 ◽  
Author(s):  
Jing Xie ◽  
Chun-Li Wang ◽  
Wenbin Yang ◽  
Jue Wang ◽  
Cheng Chen ◽  
...  
2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Pawel Olczyk ◽  
Łukasz Mencner ◽  
Katarzyna Komosinska-Vassev

Wound healing is the physiologic response to tissue trauma proceeding as a complex pathway of biochemical reactions and cellular events, secreted growth factors, and cytokines. Extracellular matrix constituents are essential components of the wound repair phenomenon. Firstly, they create a provisional matrix, providing a structural integrity of matrix during each stage of healing process. Secondly, matrix molecules regulate cellular functions, mediate the cell-cell and cell-matrix interactions, and serve as a reservoir and modulator of cytokines and growth factors’ action. Currently known mechanisms, by which extracellular matrix components modulate each stage of the process of soft tissue remodeling after injury, have been discussed.


2012 ◽  
Vol 92 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Sandra G. Velleman ◽  
Jonghyun Shin ◽  
Xuehui Li ◽  
Yan Song

Velleman, S. G., Shin, J., Li, X. and Song, Y. 2012. Review: The skeletal muscle extracellular matrix: Possible roles in the regulation of muscle development and growth. Can. J. Anim. Sci. 92: 1–10. Skeletal muscle fibers are surrounded by an extrinsic extracellular matrix environment. The extracellular matrix is composed of collagens, proteoglycans, glycoproteins, growth factors, and cytokines. How the extracellular matrix influences skeletal muscle development and growth is an area that is not completely understood at this time. Studies on myogenesis have largely been directed toward the cellular components and overlooked that muscle cells secrete a complex extracellular matrix network. The extracellular matrix modulates muscle development by acting as a substrate for muscle cell migration, growth factor regulation, signal transduction of information from the extracellular matrix to the intrinsic cellular environment, and provides a cellular structural architecture framework necessary for tissue function. This paper reviews extracellular matrix regulation of muscle growth with a focus on secreted proteoglycans, cell surface proteoglycans, growth factors and cytokines, and the dynamic nature of the skeletal muscle extracellular matrix, because of its impact on the regulation of muscle cell proliferation and differentiation during myogenesis.


1994 ◽  
Vol 4 (8) ◽  
pp. 302-303 ◽  
Author(s):  
Pita Enriquez-Harris ◽  
John K. Heath

1995 ◽  
Vol 108 (6) ◽  
pp. 2153-2162 ◽  
Author(s):  
J.F. Talts ◽  
A. Weller ◽  
R. Timpl ◽  
M. Ekblom ◽  
P. Ekblom

We have here studied the composition and regulation of stromal extracellular matrix components in an experimental tumor model. Nude mice were inoculated with WCCS-1 cells, a human Wilms' tumor cell line. In the formed tumors the stroma was found to contain mesenchymal extracellular matrix proteins such as tenascin-C, fibulins-1 and 2 and fibronectin, but no nidogen. Nidogen was confined to basement membranes of tumor blood vessels. Since glucocorticoids have been shown to downregulate tenascin-C expression in vitro, we tested whether dexamethasone can influence biosynthesis of extracellular matrix components during tumor formation in vivo. A downregulation of tenascin-C mRNA and an upregulation of fibronectin mRNA expression by dexamethasone was noted. Transforming growth factor-beta 1 mRNA levels were unaffected by the dexamethasone treatment. Glucocorticoids can thus downregulate tenascin-C synthesis although local stimulatory growth factors are present. The competition between a negative and a positive extrinsic factor on synthesis of stromal extracellular matrix components was studied in a fibroblast/preadipocyte cell line. Transforming growth factor-beta 1 stimulated tenascin-C synthesis but did not affect fibronectin or fibulin-2 synthesis. Dexamethasone at high concentrations could completely suppress the effect of transforming growth factor-beta 1 on tenascin-C mRNA expression. Transforming growth factor-beta 1 could in turn overcome the downregulation of tenascin-C mRNA expression caused by a lower concentration of dexamethasone. We therefore suggest that the limited expression of tenascin-C in part is due to a continuous suppression by physiological levels of glucocorticoids, which can be overcome by local stimulatory growth factors when present in sufficient amounts.


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