Cargando…
MicroRNA-33 suppresses CCL2 expression in chondrocytes
CCL2-mediated macrophage infiltration in articular tissues plays a pivotal role in the development of the osteoarthritis (OA). miRNAs regulate the onset and progression of diseases via controlling the expression of a series of genes. How the CCL2 gene was regulated by miRNAs was still not fully eluc...
Autores principales: | , , , , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Portland Press Ltd.
2016
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4859085/ https://www.ncbi.nlm.nih.gov/pubmed/27129293 http://dx.doi.org/10.1042/BSR20160068 |
_version_ | 1782430907879129088 |
---|---|
author | Wei, Meng Xie, Qingyun Zhu, Jun Wang, Tao Zhang, Fan Cheng, Yue Guo, Dongyang Wang, Ying Mo, Liweng Wang, Shuai |
author_facet | Wei, Meng Xie, Qingyun Zhu, Jun Wang, Tao Zhang, Fan Cheng, Yue Guo, Dongyang Wang, Ying Mo, Liweng Wang, Shuai |
author_sort | Wei, Meng |
collection | PubMed |
description | CCL2-mediated macrophage infiltration in articular tissues plays a pivotal role in the development of the osteoarthritis (OA). miRNAs regulate the onset and progression of diseases via controlling the expression of a series of genes. How the CCL2 gene was regulated by miRNAs was still not fully elucidated. In the present study, we demonstrated that the binding sites of miR-33 in the 3′UTR of CCL2 gene were conserved in human, mouse and rat species. By performing gain- or loss-of-function studies, we verified that miR-33 suppressed CCL2 expression in the mRNA and protein levels. We also found that miR-33 suppressed the CCL2 levels in the supernatant of cultured primary mouse chondrocytes. With reporter gene assay, we demonstrated that miR-33 targeted at AAUGCA in the 3′UTR of CCL2 gene. In transwell migration assays, we demonstrated that the conditional medium (CM) from miR-33 deficient chondrocytes potentiated the monocyte chemotaxis in a CCL2 dependent manner. Finally, we demonstrated that the level of miR-33 was decreased, whereas the CCL2 level was increased in the articular cartilage from the OA patients compared with the control group. In summary, we identified miR-33 as a novel suppressor of CCL2 in chondrocytes. The miR-33/CCL2 axis in chondrocytes regulates monocyte chemotaxis, providing a potential mechanism of macrophage infiltration in OA. |
format | Online Article Text |
id | pubmed-4859085 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Portland Press Ltd. |
record_format | MEDLINE/PubMed |
spelling | pubmed-48590852016-06-01 MicroRNA-33 suppresses CCL2 expression in chondrocytes Wei, Meng Xie, Qingyun Zhu, Jun Wang, Tao Zhang, Fan Cheng, Yue Guo, Dongyang Wang, Ying Mo, Liweng Wang, Shuai Biosci Rep Original Papers CCL2-mediated macrophage infiltration in articular tissues plays a pivotal role in the development of the osteoarthritis (OA). miRNAs regulate the onset and progression of diseases via controlling the expression of a series of genes. How the CCL2 gene was regulated by miRNAs was still not fully elucidated. In the present study, we demonstrated that the binding sites of miR-33 in the 3′UTR of CCL2 gene were conserved in human, mouse and rat species. By performing gain- or loss-of-function studies, we verified that miR-33 suppressed CCL2 expression in the mRNA and protein levels. We also found that miR-33 suppressed the CCL2 levels in the supernatant of cultured primary mouse chondrocytes. With reporter gene assay, we demonstrated that miR-33 targeted at AAUGCA in the 3′UTR of CCL2 gene. In transwell migration assays, we demonstrated that the conditional medium (CM) from miR-33 deficient chondrocytes potentiated the monocyte chemotaxis in a CCL2 dependent manner. Finally, we demonstrated that the level of miR-33 was decreased, whereas the CCL2 level was increased in the articular cartilage from the OA patients compared with the control group. In summary, we identified miR-33 as a novel suppressor of CCL2 in chondrocytes. The miR-33/CCL2 axis in chondrocytes regulates monocyte chemotaxis, providing a potential mechanism of macrophage infiltration in OA. Portland Press Ltd. 2016-05-06 /pmc/articles/PMC4859085/ /pubmed/27129293 http://dx.doi.org/10.1042/BSR20160068 Text en © 2016 The Author(s) http://creativecommons.org/licenses/by/4.0/ This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution Licence 4.0 (CC BY) (http://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Original Papers Wei, Meng Xie, Qingyun Zhu, Jun Wang, Tao Zhang, Fan Cheng, Yue Guo, Dongyang Wang, Ying Mo, Liweng Wang, Shuai MicroRNA-33 suppresses CCL2 expression in chondrocytes |
title | MicroRNA-33 suppresses CCL2 expression in chondrocytes |
title_full | MicroRNA-33 suppresses CCL2 expression in chondrocytes |
title_fullStr | MicroRNA-33 suppresses CCL2 expression in chondrocytes |
title_full_unstemmed | MicroRNA-33 suppresses CCL2 expression in chondrocytes |
title_short | MicroRNA-33 suppresses CCL2 expression in chondrocytes |
title_sort | microrna-33 suppresses ccl2 expression in chondrocytes |
topic | Original Papers |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4859085/ https://www.ncbi.nlm.nih.gov/pubmed/27129293 http://dx.doi.org/10.1042/BSR20160068 |
work_keys_str_mv | AT weimeng microrna33suppressesccl2expressioninchondrocytes AT xieqingyun microrna33suppressesccl2expressioninchondrocytes AT zhujun microrna33suppressesccl2expressioninchondrocytes AT wangtao microrna33suppressesccl2expressioninchondrocytes AT zhangfan microrna33suppressesccl2expressioninchondrocytes AT chengyue microrna33suppressesccl2expressioninchondrocytes AT guodongyang microrna33suppressesccl2expressioninchondrocytes AT wangying microrna33suppressesccl2expressioninchondrocytes AT moliweng microrna33suppressesccl2expressioninchondrocytes AT wangshuai microrna33suppressesccl2expressioninchondrocytes |