dysfunction of collagen synthesis and secretion in chondrocytes induced by wisp3 mutation

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ID: 227788
2013
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Abstract
Wisp3 gene mutation was shown to cause spondyloepiphyseal dysplasia tarda with progressive arthropathy (SRDT-PA), but the underlying mechanism is not clear. To clarify this mechanism, we constructed the wild and mutated Wisp3 expression vectors and transfected into human chondrocytes lines C-20/A4; Wisp3 proteins subcellular localization, cell proliferation, cell apoptosis, and Wisp3-mediated gene expression were determined, and dynamic secretion of collagen in transfected chondrocytes was analyzed by 14C-proline incorporation experiment. Mutated Wisp3 protein increased proliferation activity, decreased apoptosis of C-20/A4 cells, and aggregated abnormally in cytoplasm. Expression of collagen II was also downregulated in C-20/A4 cells transfected with mutated Wisp3. Wild type Wisp3 transfection increased intracellular collagen content and extracellular collagen secretion, but the mutated Wisp3 lost this function, and the peak phase of collagen secretion was delayed in mutated Wisp3 transfected cells. Thus abnormal protein distribution, cell proliferation, collagen synthesis, and secretion in Wisp3 mutated chondrocytes might contribute to the pathogenesis of SEDT-PA.
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wang2013internationaldysfunction Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Min Wang;Xiao-Fei Man;Ya-Qing Liu;Er-Yuan Liao;Zhi-Feng Shen;Xiang-Hang Luo;Li-Juan Guo;Xian-Ping Wu;Hou-De Zhou
Journal zhonghua wei zhong bing ji jiu yi xue
Year 2013
DOI
10.1155/2013/679763
URL
http://dx.doi.org/10.1155/2013/679763
Keywords
clinical endocrinology diseases of the endocrine glands

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