LncRNA GAS5 induces chondrocyte apoptosis by down-regulating miR-137
LncRNA GAS5 induces chondrocyte apoptosis by down-regulating miR-137
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DOI：
10.26355/eurrev_202011_23582
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发表时间：
2020-01-01
影响因子：
3.3
通讯作者：
Lin, J-X
中科院分区：
文献类型：
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作者：
Gao, S-T;Yu, Y-M;Lin, J-X
目的：长链非编码RNA （lncRNA）参与人膝骨关节炎（KOA）的发病机制。生长抑制特异性5 （GAS5）是lncRNA成员，但其在KOA病理调控中的作用尚不清楚。本研究旨在探讨KOA中GAS5对软骨细胞凋亡等病理过程的影响机制。患者与方法：收集我院2016年4月至2020年4月收治的35例KOA患者和30例外伤性截肢患者的血清和软骨组织。检测并分析GAS5和miR-137的表达。从KOA患者软骨组织中提取软骨细胞，转染基因进行调控。然后检测细胞凋亡、凋亡相关蛋白（caspase-3、Bax/Bcl-2）及增殖情况。验证GAS5与miR-137的靶向关系。结果：KOA患者血清和软骨组织中GAS5表达上调，下调GAS5可抑制软骨细胞凋亡过程，促进软骨细胞增殖。tvliR-137在KOA患者样本中下调，而GAS5负向调节。GAS5通过靶向下调miR-137诱导软骨细胞凋亡，抑制其增殖。结论：GAS5在KOA血清、软骨组织和细胞中表达上调，并可通过下调miR-137诱导软骨细胞凋亡。
OBJECTIVE: Long non-coding RNA (lncRNA) participates in the pathogenesis of human knee osteoarthritis (KOA). Growth arrest specificity 5 (GAS5) is a member lncRNA, but its role in pathological regulation of KOA is still unknown. This study aims to explore the mechanism of GAS5 in KOA on chondrocyte apoptosis and other pathological processes.PATIENTS AND METHODS: The serum and cartilage tissues were collected from 35 patients with KOA and 30 patients with traumatic amputation admitted to our hospital from April 2016 to April 2020. The expressions of GAS5 and miR-137 were detected and analyzed. Chondrocytes were extracted from cartilage tissues of KOA patients, and the genes were regulated by transfection. Then, the cells were detected, including apoptosis, apoptosis-related proteins (caspase-3, Bax/Bcl-2), and proliferation. The targeting relationship between GAS5 and miR-137 was verified.RESULTS: GAS5 was up-regulated in serum and cartilage tissues of KOA patients, and down-regulation of GAS5 could inhibit the apoptosis process of chondrocytes and promote proliferation. tvliR-137 was down-regulated in samples of KOA patients and was negatively regulated by GAS5. GAS5 induced apoptosis of chondrocytes and inhibited its proliferation through targeted down-regulating miR-137.CONCLUSIONS: GAS5 is up-regulated in KOA serum, cartilage tissues and cells, and can induce chondrocyte apoptosis through down-regulating miR-137.