Tags

Type your tag names separated by a space and hit enter

MiR-210 facilitates ECM degradation by suppressing autophagy via silencing of ATG7 in human degenerated NP cells.
Biomed Pharmacother. 2017 Sep; 93:470-479.BP

Abstract

Intervertebral disc degeneration (IDD) is thought to be the most common cause of low back pain. Dysregulation of microRNAs (miRNAs) is involved in the development of IDD. The aim of this study was to explore the influence of miR-210 on type II collagen (Col II) and aggrecan expression and possible mechanisms in human degenerated nucleus pulposus (NP) cells. Our results showed that miR-210 levels were significantly increased in degenerated NP tissues compared with healthy controls, and positively correlated with disc degeneration grade. By gain-of-function and loss-of-function studies in human degenerated NP cells, miR-210 was shown to inhibit autophagy and then upregulate MMP-3 and MMP-13 expression, leading to increased degradation of Col II and aggrecan. Autophagy-related gene 7 (ATG7) was identified as a direct target of miR-210. Knockdown of ATG7 by small interfering RNA (siRNA) abrogated the effects of miR-210 inhibitor on MMP-3, MMP-13, Col II and aggrecan expression. Taken together, these results suggest that miR-210 inhibits autophagy via silencing of ATG7, leading to increased Col II and aggrecan degradation in human degenerated NP cells.

Authors+Show Affiliations

Department of Spine Surgery, The First Affiliated Hospital, University of South China, Hengyang, Hunan 421001, China.School of Nursing, Hunan Polytechnic of Environment and Biology, Hengyang, Hunan 421001, China.Department of Hand Microsurgery, The First Affiliated Hospital, University of South China, Hengyang, Hunan 421001, China.Department of Spine Surgery, The First Affiliated Hospital, University of South China, Hengyang, Hunan 421001, China.Department of Spine Surgery, The First Affiliated Hospital, University of South China, Hengyang, Hunan 421001, China.Department of Spine Surgery, The First Affiliated Hospital, University of South China, Hengyang, Hunan 421001, China.Department of Hand Microsurgery, The First Affiliated Hospital, University of South China, Hengyang, Hunan 421001, China.Department of Spine Surgery, The First Affiliated Hospital, University of South China, Hengyang, Hunan 421001, China.Department of Spine Surgery, The First Affiliated Hospital, University of South China, Hengyang, Hunan 421001, China.Department of Spine Surgery, The First Affiliated Hospital, University of South China, Hengyang, Hunan 421001, China. Electronic address: wwwwjj167@qq.com.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

28667916

Citation

Wang, Cheng, et al. "MiR-210 Facilitates ECM Degradation By Suppressing Autophagy Via Silencing of ATG7 in Human Degenerated NP Cells." Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie, vol. 93, 2017, pp. 470-479.
Wang C, Zhang ZZ, Yang W, et al. MiR-210 facilitates ECM degradation by suppressing autophagy via silencing of ATG7 in human degenerated NP cells. Biomed Pharmacother. 2017;93:470-479.
Wang, C., Zhang, Z. Z., Yang, W., Ouyang, Z. H., Xue, J. B., Li, X. L., Zhang, J., Chen, W. K., Yan, Y. G., & Wang, W. J. (2017). MiR-210 facilitates ECM degradation by suppressing autophagy via silencing of ATG7 in human degenerated NP cells. Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie, 93, 470-479. https://doi.org/10.1016/j.biopha.2017.06.048
Wang C, et al. MiR-210 Facilitates ECM Degradation By Suppressing Autophagy Via Silencing of ATG7 in Human Degenerated NP Cells. Biomed Pharmacother. 2017;93:470-479. PubMed PMID: 28667916.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - MiR-210 facilitates ECM degradation by suppressing autophagy via silencing of ATG7 in human degenerated NP cells. AU - Wang,Cheng, AU - Zhang,Zi-Zhen, AU - Yang,Wei, AU - Ouyang,Zhi-Hua, AU - Xue,Jing-Bo, AU - Li,Xue-Lin, AU - Zhang,Jian, AU - Chen,Wen-Kang, AU - Yan,Yi-Guo, AU - Wang,Wen-Jun, Y1 - 2017/06/28/ PY - 2017/03/16/received PY - 2017/06/02/revised PY - 2017/06/12/accepted PY - 2017/7/2/pubmed PY - 2018/5/1/medline PY - 2017/7/2/entrez KW - ATG7 KW - Autophagy KW - ECM KW - IDD KW - miR-210 SP - 470 EP - 479 JF - Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie JO - Biomed. Pharmacother. VL - 93 N2 - Intervertebral disc degeneration (IDD) is thought to be the most common cause of low back pain. Dysregulation of microRNAs (miRNAs) is involved in the development of IDD. The aim of this study was to explore the influence of miR-210 on type II collagen (Col II) and aggrecan expression and possible mechanisms in human degenerated nucleus pulposus (NP) cells. Our results showed that miR-210 levels were significantly increased in degenerated NP tissues compared with healthy controls, and positively correlated with disc degeneration grade. By gain-of-function and loss-of-function studies in human degenerated NP cells, miR-210 was shown to inhibit autophagy and then upregulate MMP-3 and MMP-13 expression, leading to increased degradation of Col II and aggrecan. Autophagy-related gene 7 (ATG7) was identified as a direct target of miR-210. Knockdown of ATG7 by small interfering RNA (siRNA) abrogated the effects of miR-210 inhibitor on MMP-3, MMP-13, Col II and aggrecan expression. Taken together, these results suggest that miR-210 inhibits autophagy via silencing of ATG7, leading to increased Col II and aggrecan degradation in human degenerated NP cells. SN - 1950-6007 UR - https://www.unboundmedicine.com/medline/citation/28667916/MiR_210_facilitates_ECM_degradation_by_suppressing_autophagy_via_silencing_of_ATG7_in_human_degenerated_NP_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0753-3322(17)31229-5 DB - PRIME DP - Unbound Medicine ER -