Open AccessMicroRNA‐93 regulates collagen loss by targeting MMP3 in human nucleus pulposus cells
Author(s) -
Jing Wanli,
Jiang Wenxue
Publication year - 2015
Publication title -
cell proliferation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.647
H-Index - 74
eISSN - 1365-2184
pISSN - 0960-7722
DOI - 10.1111/cpr.12176
Subject(s) - mmp3 , microrna , intervertebral disc , nucleus , blot , type ii collagen , degeneration (medical) , gene expression , matrix metalloproteinase , microbiology and biotechnology , degenerative disc disease , chemistry , cell , cartilage , pathology , biology , gene , medicine , anatomy , biochemistry , alternative medicine
Objectives Degenerated disc disease is one of the most common medical conditions in patients suffering from low back pain. Recent studies have shown that micro RNA s can regulate cell function in many pathological conditions. The aim of this study was to investigate expression and role of miR‐93 in disc degeneration. Materials and methods Quantitative RT ‐ PCR was employed to investigate level of miR‐93 in degenerative nucleus pulposus ( NP ) tissues. Then, functional analysis of miR‐93 in regulating collagen II expression was performed. Subsequently, western blotting and luciferase reporter assay were used to detect the target gene. Results We showed that miR‐93 was significantly down‐regulated in degenerative NP tissues and its levels were associated with grade of disc degeneration. Overexpression of miR‐93 stimulated type II collagen expression in NP cells. Moreover, MMP 3 was identified as a putative target of miR‐93. MiR‐93 inhibited MMP 3 expression by directly targeting its 3′UTR, and this was abolished by miR‐93 binding site mutations. Additionally, restoration of MMP 3 in miR‐93‐overexpressed NP cells reversed effects of type II collagen expression. Expression of MMP 3 inversely correlated with miR‐93 expression in degenerative NP tissues. Conclusions Taken together, we demonstrated that miR‐93 contributed to abnormal NP cell type II collagen expression by targeting MMP 3, involved in intervertebral disc degeneration.