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Fibronectin-Mediated Adhesion Rescues Cell Cycle Arrest Induced by Fibroblast Growth Factor-1 by Decreased Expression of $P21^{cip/waf}$ in Human Chondrocytes

Jun-Hyeog Jang and Chong-Pyoung Chung
In Vitro Cellular & Developmental Biology. Animal
Vol. 41, No. 5/6 (May - Jun., 2005), pp. 126-129
Stable URL: http://www.jstor.org/stable/4295606
Page Count: 4
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Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Fibronectin-Mediated Adhesion Rescues Cell Cycle Arrest Induced by Fibroblast Growth Factor-1 by Decreased Expression of $P21^{cip/waf}$ in Human Chondrocytes
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Abstract

In chondrocytes, fibroblast growth factors (FGFs) inhibit chondrocytes proliferation by upregulation of the cell cycle inhibitor $p21^{cip/waf}$. In this report, we first investigated the roles of fibronectin (FN)-mediated cell adhesion in the modulation of FGF-1's antiproliferative function in chondrocytes. In this study, we found that FN-mediated signaling could rescue cell cycle arrest induced by FGF-1 in primary human chondrocytes. This prevention of cell cycle arrest induced by FGF-1 was due to the suppression of the cell cycle inhibitor $p21^{cif/waf}$ expression on adhesion to FN and its downstream activation of signaling pathways. Finally, we showed that this rescue induced by FN-mediated adhesion is dependent on the extracellular regulated kinase (ERK) signaling pathway. Taken together, these studies support that, despite FGF-FGF receptor's growth-inhibitory function, the FN-mediated signaling can collaborate to compensate for its negative effect on chondrocytes proliferation, providing evidence for cross talk between signals emerging from these cell surface molecules in chondrocyte.

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