LncRNA GAS5 induces chondrocyte apoptosis by down-regulating miR-137

S.-T. Gao, Y.-M. Yu, L.-P. Wan, Z.-M. Liu, J.-X. Lin

Department of Joint Surgery, Qilu Hospital of Shandong University (Qingdao), Qingdao, P.R. China. linjunxine@126.com

---

• Orthopedics

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. 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.

CONCLUSIONS: GAS5 is up-regulated in KOA serum, cartilage tissues and cells, and can induce chondrocyte apoptosis through down-regulating miR-137.

Free PDF Download