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Dysregulated miR-127-5p contributes to type II collagen degradation by targeting matrix metalloproteinase-13 in human intervertebral disc degeneration.
Biochimie. 2017 Aug; 139:74-80.B

Abstract

BACKGROUND

Intervertebral disc degeneration (IDD) is a chronic disease associated with the degradation of extracellular matrix (ECM). Matrix metalloproteinase (MMP)-13 is a major enzyme that mediates the degradation of ECM components. MMP-13 has been predicted to be a potential target of miR-127-5p. However, the exact function of miR-127-5p in IDD is still unclear.

OBJECTIVE

We designed this study to evaluate the correlation between miR-127-5p level and the degeneration of human intervertebral discs and explore the potential mechanisms.

METHODS

miR-127-5p levels and MMP-13 mRNA levels were detected by quantitative real-time polymerase chain reaction (qPCR). To determine whether MMP-13 is a target of miR-127-5p, dual luciferase reporter assays were performed. miR-127-5p mimic and miR-127-5p inhibitor were used to overexpress or downregulate miR-127-5p expression in human NP cells, respectively. Small interfering RNA (siRNA) was used to knock down MMP-13 expression in human NP cells. Type II collagen expression in human NP cells was detected by qPCR, western blotting, and immunofluorescence staining.

RESULTS

We confirmed that miR-127-5p was significantly downregulated in nucleus pulposus (NP) tissue of degenerative discs and its expression was inversely correlated with MMP-13 mRNA levels. We reveal that MMP-13 may act as a target of miR-127-5p. Expression of miR-127-5p was inversely correlated with type II collagen expression in human NP cells. Moreover, suppression of MMP-13 expression by siRNA blocked downstream signaling and increased type II collagen expression.

CONCLUSION

Dysregulated miR-127-5p contributed to the degradation of type II collagen by targeting MMP-13 in human IDD. Our findings highlight that miR-127-5p may serve as a new therapeutic target in IDD.

Authors+Show Affiliations

Department of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan 430022, China.Department of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan 430022, China.Department of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan 430022, China.Department of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan 430022, China.Department of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan 430022, China.Department of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan 430022, China.Department of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan 430022, China.Department of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan 430022, China.Department of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan 430022, China.Department of Orthopaedics, Wuhan No.1 Hospital, 215 Zhongshan Avenue, Wuhan 430022, China.Department of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan 430022, China.Department of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan 430022, China.Department of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan 430022, China. Electronic address: yangcao1971@sina.com.

Pub Type(s)

Comparative Study
Journal Article

Language

eng

PubMed ID

28559201

Citation

Hua, Wen-Bin, et al. "Dysregulated miR-127-5p Contributes to Type II Collagen Degradation By Targeting Matrix Metalloproteinase-13 in Human Intervertebral Disc Degeneration." Biochimie, vol. 139, 2017, pp. 74-80.
Hua WB, Wu XH, Zhang YK, et al. Dysregulated miR-127-5p contributes to type II collagen degradation by targeting matrix metalloproteinase-13 in human intervertebral disc degeneration. Biochimie. 2017;139:74-80.
Hua, W. B., Wu, X. H., Zhang, Y. K., Song, Y., Tu, J., Kang, L., Zhao, K. C., Li, S., Wang, K., Liu, W., Shao, Z. W., Yang, S. H., & Yang, C. (2017). Dysregulated miR-127-5p contributes to type II collagen degradation by targeting matrix metalloproteinase-13 in human intervertebral disc degeneration. Biochimie, 139, 74-80. https://doi.org/10.1016/j.biochi.2017.05.018
Hua WB, et al. Dysregulated miR-127-5p Contributes to Type II Collagen Degradation By Targeting Matrix Metalloproteinase-13 in Human Intervertebral Disc Degeneration. Biochimie. 2017;139:74-80. PubMed PMID: 28559201.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Dysregulated miR-127-5p contributes to type II collagen degradation by targeting matrix metalloproteinase-13 in human intervertebral disc degeneration. AU - Hua,Wen-Bin, AU - Wu,Xing-Huo, AU - Zhang,Yu-Kun, AU - Song,Yu, AU - Tu,Ji, AU - Kang,Liang, AU - Zhao,Kang-Cheng, AU - Li,Shuai, AU - Wang,Kun, AU - Liu,Wei, AU - Shao,Zeng-Wu, AU - Yang,Shu-Hua, AU - Yang,Cao, Y1 - 2017/05/27/ PY - 2017/01/16/received PY - 2017/05/25/accepted PY - 2017/6/1/pubmed PY - 2017/9/13/medline PY - 2017/6/1/entrez KW - Intervertebral disc degeneration KW - Matrix metalloproteinase-13 KW - MicroRNA KW - Nucleus pulposus KW - Type II collagen KW - miR-127-5p SP - 74 EP - 80 JF - Biochimie JO - Biochimie VL - 139 N2 - BACKGROUND: Intervertebral disc degeneration (IDD) is a chronic disease associated with the degradation of extracellular matrix (ECM). Matrix metalloproteinase (MMP)-13 is a major enzyme that mediates the degradation of ECM components. MMP-13 has been predicted to be a potential target of miR-127-5p. However, the exact function of miR-127-5p in IDD is still unclear. OBJECTIVE: We designed this study to evaluate the correlation between miR-127-5p level and the degeneration of human intervertebral discs and explore the potential mechanisms. METHODS: miR-127-5p levels and MMP-13 mRNA levels were detected by quantitative real-time polymerase chain reaction (qPCR). To determine whether MMP-13 is a target of miR-127-5p, dual luciferase reporter assays were performed. miR-127-5p mimic and miR-127-5p inhibitor were used to overexpress or downregulate miR-127-5p expression in human NP cells, respectively. Small interfering RNA (siRNA) was used to knock down MMP-13 expression in human NP cells. Type II collagen expression in human NP cells was detected by qPCR, western blotting, and immunofluorescence staining. RESULTS: We confirmed that miR-127-5p was significantly downregulated in nucleus pulposus (NP) tissue of degenerative discs and its expression was inversely correlated with MMP-13 mRNA levels. We reveal that MMP-13 may act as a target of miR-127-5p. Expression of miR-127-5p was inversely correlated with type II collagen expression in human NP cells. Moreover, suppression of MMP-13 expression by siRNA blocked downstream signaling and increased type II collagen expression. CONCLUSION: Dysregulated miR-127-5p contributed to the degradation of type II collagen by targeting MMP-13 in human IDD. Our findings highlight that miR-127-5p may serve as a new therapeutic target in IDD. SN - 1638-6183 UR - https://www.unboundmedicine.com/medline/citation/28559201/Dysregulated_miR_127_5p_contributes_to_type_II_collagen_degradation_by_targeting_matrix_metalloproteinase_13_in_human_intervertebral_disc_degeneration_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0300-9084(17)30142-6 DB - PRIME DP - Unbound Medicine ER -