Fibronectin-mediated adhesion rescues cell cycle arrest induced by fibroblast growth factor-1 by decreased expression of P21cip/waf in human chondrocytes |
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Authors: | Jun-Hyeog Jang Chong-Pyoung Chung |
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Affiliation: | (1) Department of Biochemistry, Inha University College of Medicine, Jung-Gu, 400-712 Incheon, Korea;(2) Intellectual Biointerface Engineering Center and Department of Periodontology, Seoul National University College of Dentistry, 110-768 Seoul, Korea |
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Abstract: | Summary In chondrocytes, fibroblast growth factors (FGFs) inhibit chondrocytes proliferation by upregulation of the cell cycle inhibitor p21cip/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 p21cip/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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Keywords: | chondrocytes extracellular matrix FGF-1 fibronectin p21 |
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