miR-21-5p protects IL-1β-induced human chondrocytes from degradation

Abstract Objective Osteoarthritis (OA) is a prevalent degenerative disease caused by various factors. MicroRNAs are important regulators in OA. MiR-21-5p expression is decreased in OA cartilage, but the effects of modulating miR-21-5p on cartilage regeneration are unknown. Therefore, our aim was to...

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Main Authors: Hai Zhu, Xin Yan, Meng Zhang, Feng Ji, Shouguo Wang
Format: Article
Language:English
Published: BMC 2019-05-01
Series:Journal of Orthopaedic Surgery and Research
Subjects:
Online Access:http://link.springer.com/article/10.1186/s13018-019-1160-7
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author Hai Zhu
Xin Yan
Meng Zhang
Feng Ji
Shouguo Wang
author_facet Hai Zhu
Xin Yan
Meng Zhang
Feng Ji
Shouguo Wang
author_sort Hai Zhu
collection DOAJ
description Abstract Objective Osteoarthritis (OA) is a prevalent degenerative disease caused by various factors. MicroRNAs are important regulators in OA. MiR-21-5p expression is decreased in OA cartilage, but the effects of modulating miR-21-5p on cartilage regeneration are unknown. Therefore, our aim was to investigate the effects of miR-21-5p on cartilage metabolism of OA chondrocytes. Design We used IL-1β (10 ng/ml) to mimic OA chondrocytes. OA chondrocytes were transfected with miR-21-5p, the gene expression of COL2A1, MMP13, and ADAMTS5 was detected by qPCR. At the same time, COL2A1, MMP13, and ADAMTS5 were analyzed at the protein level by Western blot. CCK8 measured the cell’s viability and SA-β-gal detected the cell’s senescence. Results Upregulation of miR-21-5p had increased COL2A1 expression and decreased MM P13 and ADAMTS5 expression, which were in accord with Western blot data. SA-β-gal activity significantly increased, the viability was decreased in OA chondrocytes, and upregulation of miR-21-5p can decrease the SA-β-gal activity and increase cell viability. Conclusion MiR-21-5p might be a potential disease-modifying compound in OA, as it promotes hyaline cartilage production. These results provided that novel insights into the important function in OA pathological development.
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spelling doaj.art-2f6551836abd4255bd0acd7eab6b1cd32022-12-22T04:23:12ZengBMCJournal of Orthopaedic Surgery and Research1749-799X2019-05-011411910.1186/s13018-019-1160-7miR-21-5p protects IL-1β-induced human chondrocytes from degradationHai Zhu0Xin Yan1Meng Zhang2Feng Ji3Shouguo Wang4Department of Orthopaedics, The Affiliated Huaian No.1 People’s Hospital of Nanjing Medical UniversityDepartment of Orthopaedics, Affiliated Hospital of Nantong UniversityDepartment of Orthopaedics, The Affiliated Huaian No.1 People’s Hospital of Nanjing Medical UniversityDepartment of Orthopaedics, The Affiliated Huaian No.1 People’s Hospital of Nanjing Medical UniversityDepartment of Orthopaedics, The Affiliated Huaian No.1 People’s Hospital of Nanjing Medical UniversityAbstract Objective Osteoarthritis (OA) is a prevalent degenerative disease caused by various factors. MicroRNAs are important regulators in OA. MiR-21-5p expression is decreased in OA cartilage, but the effects of modulating miR-21-5p on cartilage regeneration are unknown. Therefore, our aim was to investigate the effects of miR-21-5p on cartilage metabolism of OA chondrocytes. Design We used IL-1β (10 ng/ml) to mimic OA chondrocytes. OA chondrocytes were transfected with miR-21-5p, the gene expression of COL2A1, MMP13, and ADAMTS5 was detected by qPCR. At the same time, COL2A1, MMP13, and ADAMTS5 were analyzed at the protein level by Western blot. CCK8 measured the cell’s viability and SA-β-gal detected the cell’s senescence. Results Upregulation of miR-21-5p had increased COL2A1 expression and decreased MM P13 and ADAMTS5 expression, which were in accord with Western blot data. SA-β-gal activity significantly increased, the viability was decreased in OA chondrocytes, and upregulation of miR-21-5p can decrease the SA-β-gal activity and increase cell viability. Conclusion MiR-21-5p might be a potential disease-modifying compound in OA, as it promotes hyaline cartilage production. These results provided that novel insights into the important function in OA pathological development.http://link.springer.com/article/10.1186/s13018-019-1160-7OsteoarthritisChondrocytesmiR-21-5pCOL2A1ADAMTS5MMP13
spellingShingle Hai Zhu
Xin Yan
Meng Zhang
Feng Ji
Shouguo Wang
miR-21-5p protects IL-1β-induced human chondrocytes from degradation
Journal of Orthopaedic Surgery and Research
Osteoarthritis
Chondrocytes
miR-21-5p
COL2A1
ADAMTS5
MMP13
title miR-21-5p protects IL-1β-induced human chondrocytes from degradation
title_full miR-21-5p protects IL-1β-induced human chondrocytes from degradation
title_fullStr miR-21-5p protects IL-1β-induced human chondrocytes from degradation
title_full_unstemmed miR-21-5p protects IL-1β-induced human chondrocytes from degradation
title_short miR-21-5p protects IL-1β-induced human chondrocytes from degradation
title_sort mir 21 5p protects il 1β induced human chondrocytes from degradation
topic Osteoarthritis
Chondrocytes
miR-21-5p
COL2A1
ADAMTS5
MMP13
url http://link.springer.com/article/10.1186/s13018-019-1160-7
work_keys_str_mv AT haizhu mir215pprotectsil1binducedhumanchondrocytesfromdegradation
AT xinyan mir215pprotectsil1binducedhumanchondrocytesfromdegradation
AT mengzhang mir215pprotectsil1binducedhumanchondrocytesfromdegradation
AT fengji mir215pprotectsil1binducedhumanchondrocytesfromdegradation
AT shouguowang mir215pprotectsil1binducedhumanchondrocytesfromdegradation