Please use this identifier to cite or link to this item:
|標題:||Arsenic induces cell apoptosis in cultured osteoblasts through endoplasmic reticulum stress||作者:||Tang, C.H.
|關鍵字:||Arsenic;Osteoporosis;Osteoblast;GRP78;ER;glucose-regulated proteins;internal cancers;death;bone;activation;osteoporosis;expression;induction;pathogenesis;depletion||Project:||Toxicology and Applied Pharmacology||期刊/報告no：:||Toxicology and Applied Pharmacology, Volume 241, Issue 2, Page(s) 173-181.||摘要:||
Osteoporosis is characterized by low bone mass resulting from an imbalance between bone resorption by osteoclasts and bone formation by osteoblasts. Therefore, decreased bone formation by osteoblasts may lead to the development of osteoporosis, and rate of apoptosis is responsible for the regulation of bone formation. Arsenic (As) exists ubiquitously ill our environment and increases the risk of neurotoxicity, liver injury, peripheral vascular disease and cancer. However, the effect of As on apoptosis of osteoblasts is mostly unknown. Here, we found that As induced cell apoptosis in osteoblastic cell lines (including hFOB, MC3T3-E1 and MG-63) and mouse bone marrow stromal cells (M2-10B4). As also induced upregulation of Bax and Bak, downregulation of Bcl-2 and dysfunction of mitochondria in osteoblasts. As also triggered endoplasmic reticulum (ER) stress, as indicated by changes in cytosolic-calcium levels. We found that As increased the expression and activities Of glucose-regulated protein 78 (GRP78) and calpain. Transfection of cells with GRP78 or calpain siRNA reduced As-mediated cell apoptosis in osteoblasts. Therefore, our results suggest that As increased cell apoptosis in Cultured osteoblasts and increased the risk of osteoporosis. (C) 2009 Elsevier Inc. All Fights reserved.
|Appears in Collections:||期刊論文|
Show full item record
TAIR Related Article
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.