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学科主题: 临床医学
题名:
Tauroursodeoxycholic acid suppresses endoplasmic reticulum stress in the chondrocytes of patients with osteoarthritis
作者: Liu, Chao1,2; Cao, Yongping2; Yang, Xin2; Shan, Pengcheng2; Liu, Heng2
关键词: chondrocyte ; osteoarthritis ; endoplasmic reticulum stress ; tauroursodeoxycholic acid ; tunicamycin
刊名: INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
发表日期: 2015-10-01
DOI: 10.3892/ijmm.2015.2295
卷: 36, 期:4, 页:1081-1087
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Medicine, Research & Experimental
研究领域[WOS]: Research & Experimental Medicine
关键词[WOS]: CELL-DEATH ; INDUCED APOPTOSIS ; NITRIC-OXIDE ; MOUSE MODEL ; ER STRESS ; CARTILAGE ; CHOP/GADD153 ; SIGNALS ; GROWTH ; ROLES
英文摘要:

The main pathogenic events in osteoarthritis (OA) include loss and abnormal remodeling of cartilage extracellular matrix. The present study aimed to evaluate the protective effect of tauroursodeoxycholic acid on chondrocyte apoptosis induced by endoplasmic reticulum (ER) stress. Articular cartilage tissues were collected from 18 patients who underwent total knee arthroplasty and were analyzed histologically. Subsequently, chondrocyte apoptosis was assessed by TUNEL. Quantitative polymerase chain reaction and western blot analysis were employed to evaluate gene and protein expression, respectively, of ER stress markers, including glucose-regulated protein 78 (GRP78), growth arrest and DNA-damage-inducible gene 153 (GADD153) and caspase-12 along with type II collagen. Chondrocytes obtained from osteoarthritis patients at different stages were cultured in three conditions including: No treatment (CON group), tunicamycin treatment to induce ER stress (ERS group) and tauroursodeoxycholic acid treatment after 4 h of tunicamycin (TDA group); and cell proliferation, apoptosis, function and ER stress level were assessed. Degradation of cartilage resulted in histological damage with more apoptotic cartilage cells observed. Of note, GRP78, GADD153 and caspase-12 mRNA and protein expression increased gradually from grade I to III cartilage tissue, while type II collagen expression decreased. Tunicamycin induced ER stress, as shown by a high expression of ER stress markers, reduced cell proliferation, increased apoptosis and decreased synthesis of type II collagen. Notably, tauroursodeoxycholic acid treatment resulted in the improvement of tunicamycin-induced ER stress. These results indicated that ER stress is highly involved in the tunicamycin-induced apoptosis in chondrocytes, which can be prevented by tauroursodeoxycholic acid.

语种: 英语
所属项目编号: 30772198
项目资助者: National Natural Science Fundation of China
WOS记录号: WOS:000361134900020
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/51040
Appears in Collections:北京大学第一临床医学院_骨科_期刊论文

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作者单位: 1.Third Mil Med Univ, Xinqiao Hosp, Dept Orthoped, Chongqing 400037, Peoples R China
2.Peking Univ, Hosp 1, Dept Orthoped, Beijing 100034, Peoples R China

Recommended Citation:
Liu, Chao,Cao, Yongping,Yang, Xin,et al. Tauroursodeoxycholic acid suppresses endoplasmic reticulum stress in the chondrocytes of patients with osteoarthritis[J]. INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE,2015,36(4):1081-1087.
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