LncRNA CTBP1-AS2 is upregulated in osteoarthritis and increases the methylation of miR-130a gene to inhibit chondrocyte proliferation.


Journal

Clinical rheumatology
ISSN: 1434-9949
Titre abrégé: Clin Rheumatol
Pays: Germany
ID NLM: 8211469

Informations de publication

Date de publication:
Nov 2020
Historique:
received: 06 11 2019
accepted: 16 04 2020
revised: 24 03 2020
pubmed: 11 5 2020
medline: 15 5 2021
entrez: 11 5 2020
Statut: ppublish

Résumé

LncRNA CTBP1-AS2 has been reported to be involved in type 2 diabetes and cardiomyocyte hypertrophy, while its roles in other human diseases are unknown. Our preliminary deep sequencing analysis showed altered expression of CTBP1-AS2 in osteoarthritis (OA). In addition, CTBP1-AS2 was inversely correlated with miR-130a. This study was therefore carried out to investigate the interactions between CTBP1-AS2 and miR-130a in OA. Synovial fluid was collected from 62 OA patients and 62 healthy controls. RT-qPCR was performed to determine the expression levels of CTBP1-AS2 and miR-130a in synovial fluid. Cell transfections were performed to investigate the interactions between CTBP1-AS2 and miR-130a. Methylation-specific PCR (MSP) was performed to assess the effects of CTBP1-AS2 on the methylation of miR-130a. Cell counting Kit-8 (CCK-8) assay was performed to evaluate the roles of CTBP1-AS2 and miR-130a in regulating proliferation of chondrocytes. The results showed that CTBP1-AS2 was upregulated in OA and inversely correlated with miR-130a. In chondrocytes of OA patients, overexpression of CTBP1-AS2 led to increased methylation of miR-130a gene and downregulated expression of miR-130a, while overexpression of miR-130a did not affect the expression of CTBP1-AS2. In contrast, no interaction between CTBP1-AS2 and miR-130a was observed in chondrocytes from healthy adults. Analysis of chondrocyte proliferation showed that overexpression of miR-130a led to increased proliferation rate of chondrocytes extracted from OA patients. Overexpression of CTBP1-AS2 led to decreased proliferation rate of chondrocytes and reversed the effects of overexpressing miR-130a. Therefore, CTBP1-AS2 is upregulated in OA and may increase the methylation of miR-130a gene to inhibit chondrocyte proliferation. Key Points • CTBP1-AS2 is overexpressed in OA and may downregulate miR-130a through methylation to suppress the proliferation of chondrocytes. • The interaction between CTBP1-AS2 and miR-130a is indirect and mediated by certain pathological mediators.

Identifiants

pubmed: 32388751
doi: 10.1007/s10067-020-05113-4
pii: 10.1007/s10067-020-05113-4
doi:

Substances chimiques

MIRN130 microRNA, human 0
MicroRNAs 0
RNA, Long Noncoding 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

3473-3478

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Auteurs

Hongfei Zhang (H)

Department of Arthritis, Affiliated Hospital of Weifang Medical University, No. 2428, Yuhe Road, Kuiwen District, Weifang City, 261031, Shandong Province, China.

Jinglian Li (J)

Weifang Medical University, NO.4948 Shengli East Street, Weifang City,, 261042, Shandong Province, China.

Weiguang Shao (W)

Department of Arthritis, Affiliated Hospital of Weifang Medical University, No. 2428, Yuhe Road, Kuiwen District, Weifang City, 261031, Shandong Province, China. ic3884@163.com.

Naipeng Shen (N)

Department of Arthritis, Affiliated Hospital of Weifang Medical University, No. 2428, Yuhe Road, Kuiwen District, Weifang City, 261031, Shandong Province, China. kgibovvgbk4@163.com.

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