Department of Joint Surgery, Qilu Hospital of Shandong University (Qingdao), Qingdao, P.R. China.
Eur Rev Med Pharmacol Sci. 2020 Nov;24(21):10984-10991. doi: 10.26355/eurrev_202011_23582.
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.
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.
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. MiR-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.
GAS5 is up-regulated in KOA serum, cartilage tissues and cells, and can induce chondrocyte apoptosis through down-regulating miR-137.
长链非编码 RNA(lncRNA)参与人类膝骨关节炎(KOA)的发病机制。生长停滞特异性 5(GAS5)是 lncRNA 的一个成员,但它在 KOA 的病理调节中的作用尚不清楚。本研究旨在探讨 GAS5 在 KOA 对软骨细胞凋亡及其他病理过程中的作用机制。
收集 2016 年 4 月至 2020 年 4 月期间我院收治的 35 例 KOA 患者和 30 例创伤截肢患者的血清和软骨组织。检测和分析 GAS5 和 miR-137 的表达。从 KOA 患者的软骨组织中提取软骨细胞,并通过转染调节基因。然后检测细胞凋亡、凋亡相关蛋白(caspase-3、Bax/Bcl-2)和增殖情况。验证 GAS5 与 miR-137 的靶向关系。
GAS5 在 KOA 患者的血清和软骨组织中呈上调表达,下调 GAS5 可抑制软骨细胞的凋亡过程并促进增殖。miR-137 在 KOA 患者的样本中下调,并受 GAS5 的负调控。GAS5 通过靶向下调 miR-137 诱导软骨细胞凋亡并抑制其增殖。
GAS5 在 KOA 血清、软骨组织和细胞中上调,可通过下调 miR-137 诱导软骨细胞凋亡。