Dong Ye1, Weihong Jian2, Jie Feng2, Xueqin Liao2. 1. Department of Orthopedics, The Third Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, 330000, China. Electronic address: dongye08@126.com. 2. Department of Orthopedics, The Third Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, 330000, China.
Abstract
OBJECTIVE: This study aimed to investigate the role of long noncoding RNA (lncRNA) ZFAS1 in the development of osteoarthritis (OA) as well as to explore the potential molecular mechanisms. MATERIAL AND METHODS: The expression of lncRNA ZFAS1 in OA chondrocytes was determined. After cell transfection, the effects of ZFAS1 overexpression on the viability, proliferation, apoptosis and migration of OA chondrocytes were detected. Additionally, the expression levels of Bcl-2, Bax, Caspase-3, and matrix metalloproteinases (MMP1 and MMP13) were determined. The expressions of Wnt3a signaling proteins, and the relationship between ZFAS1 and Wnt3a were detected as well. RESULTS: The expression of ZFAS1 was down-regulated in OA chondrocytes compared with normal chondrocytes. Overexpression of ZFAS1 promoted the viability, proliferation and migration, and inhibited apoptosis and matrix synthesis of OA chondrocytes. Additionally, overexpressed ZFAS1 significantly decreased Wnt3a factors. The effects of ZFAS1 on OA chondrocytes were achieved by regulating Wnt3a signaling. CONCLUSIONS: Our study demonstrates that ZFAS1 may promote chondrocyte proliferation, and migration, and decrease apoptosis and matrix synthesis in OA possible via targeting Wnt3a signaling. ZFAS1 provides a potential therapeutic target for OA treatment.
OBJECTIVE: This study aimed to investigate the role of long noncoding RNA (lncRNA) ZFAS1 in the development of osteoarthritis (OA) as well as to explore the potential molecular mechanisms. MATERIAL AND METHODS: The expression of lncRNA ZFAS1 in OA chondrocytes was determined. After cell transfection, the effects of ZFAS1 overexpression on the viability, proliferation, apoptosis and migration of OA chondrocytes were detected. Additionally, the expression levels of Bcl-2, Bax, Caspase-3, and matrix metalloproteinases (MMP1 and MMP13) were determined. The expressions of Wnt3a signaling proteins, and the relationship between ZFAS1 and Wnt3a were detected as well. RESULTS: The expression of ZFAS1 was down-regulated in OA chondrocytes compared with normal chondrocytes. Overexpression of ZFAS1 promoted the viability, proliferation and migration, and inhibited apoptosis and matrix synthesis of OA chondrocytes. Additionally, overexpressed ZFAS1 significantly decreased Wnt3a factors. The effects of ZFAS1 on OA chondrocytes were achieved by regulating Wnt3a signaling. CONCLUSIONS: Our study demonstrates that ZFAS1 may promote chondrocyte proliferation, and migration, and decrease apoptosis and matrix synthesis in OA possible via targeting Wnt3a signaling. ZFAS1 provides a potential therapeutic target for OA treatment.