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学科主题临床医学
Tauroursodeoxycholic acid suppresses endoplasmic reticulum stress in the chondrocytes of patients with osteoarthritis
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
2015-10-01
DOI10.3892/ijmm.2015.2295
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
WOS记录号WOS:000361134900020
项目编号30772198
资助机构National Natural Science Fundation of China
引用统计
被引频次:13[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/51040
专题北京大学第一临床医学院_骨科
北京大学第三临床医学院_成形外科
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
推荐引用方式
GB/T 7714
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.
APA Liu, Chao,Cao, Yongping,Yang, Xin,Shan, Pengcheng,&Liu, Heng.(2015).Tauroursodeoxycholic acid suppresses endoplasmic reticulum stress in the chondrocytes of patients with osteoarthritis.INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE,36(4),1081-1087.
MLA Liu, Chao,et al."Tauroursodeoxycholic acid suppresses endoplasmic reticulum stress in the chondrocytes of patients with osteoarthritis".INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE 36.4(2015):1081-1087.
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