LncRNA-UCA1 enhances MMP-13 expression by inhibiting miR- 204-5p in human chondrocytes
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Guodong Wang1,*, Xianmin Bu2,*, Yuanmin Zhang1,*, Xiaowei Zhao1, Ying Kong1, Longfei Ma1, Shuaishuai Niu1, Bin Wu1 and Chunyang Meng1
1Department of Orthopaedics, Affiliated Hospital of Jining Medical University, Jining, Shandong, China
2Department of Pathology, Shandong Jining No.1 People's Hospital, Jining, Shandong, China
*These authors contributed equally to this work
Chunyang Meng, email: [email protected]
Keywords: osteoarthritis, long noncoding RNAs, UCA1, miR-204-5p, MMP-13
Received: June 02, 2017 Accepted: July 25, 2017 Published: August 10, 2017
Osteoarthritis (OA) is a common degenerative disease characterized by degeneration of articular cartilage. Increasing studies showed that long noncoding RNAs (lncRNAs) play important roles in the cartilage damage. However, little is known about the role of UCA1 in the osteoarthritis. The expression level of UCA1 was upregulated in the OA cartilage. Overexpression of UCA1 suppressed the miR-204-5p expression in the chondrocytes. The expression of miR-204-5p was downregulated in the OA cartilage. Moreover, the expression of miR-204-5p was negatively correlated with the UCA1 expression in the OA cartilage. Elevated expression of UCA1 promoted the chondrocytes cell proliferation and overexpression of miR-204-5p suppressed chondrocytes cell proliferation. In addition, overexpression of UCA1 decreased the expression of the type II collagen and type IV collagen expression in the chondrocytes. Elevated expression of miR-204-5p promoted the type II collagen and type IV collagen expression in the chondrocytes. We idetified MMP-13 was a direct target gene of miR-204-5p in the chondrocytes. Overexpression of UCA1 enhanced the MMP-13 expression in the chondrocytes. Elevated expression of UCA1 regulated the chondrocytes cell proliferation and collagen expression through inhibiting the miR-204-5p expression.These results suggested that UCA1 played as an important regulator of survival and matrix synthesis of chondrocytes partly through suppressing the miR-204-5p expression.
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