Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài:Tumor necrosis factor alpha and epidermal growth factor act additively to inhibit matrix gene expression by chondrocyte. | Available online http content 7 1 R1 27 Research article Tumor necrosis factor alpha and epidermal growth factor act additively to inhibit matrix gene expression by chondrocyte Aaron R Klooster and Suzanne M Bernier Open Access CIHR Group in Skeletal Development and Remodeling Department of Anatomy and Cell Biology The University of Western Ontario London Ontario Canada Corresponding author Suzanne M Bernier smbernie@ Received 26 Jul 2004 Revisions requested 23 Sep 2004 Revisions received 8 Oct 2004 Accepted 22 Oct 2004 Published 29 Nov 2004 Arthritis Res Ther 2005 7 R127-R138 DOI ar1464 2004 Klooster and Bernier. licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is cited. Abstract The failure of chondrocytes to replace the lost extracellular matrix contributes to the progression of degenerative disorders of cartilage. Inflammatory mediators present in the joint regulate the breakdown of the established matrix and the synthesis of new extracellular matrix molecules. In the present study we investigated the effects of tumor necrosis factor alpha TNF-a and epidermal growth factor EGF on chondrocyte morphology and matrix gene expression. Chondrocytes were isolated from distal femoral condyles of neonatal rats. Cells in primary culture displayed a cobblestone appearance. EGF but not TNF-a increased the number of cells exhibiting an elongated morphology. TNF-a potentiated the effect of EGF on chondrocyte morphology. Individually TNF-a and EGF diminished levels of aggrecan and type II collagen mRNA. In combination the effects of TNF-a and EGF were additive indicating the involvement of discrete signaling pathways. Cell viability was not compromised by TNF-a or by EGF alone or in combination. EGF alone did not .
