LncRNA CTBP1-AS2 is upregulated in osteoarthritis and increases the methylation of miR-130a gene to inhibit chondrocyte proliferation
OBJECTIVES: 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.
METHODS: 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.
RESULTS: 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.
CONCLUSION: 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.
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2020 |
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Erschienen: |
2020 |
Enthalten in: |
Zur Gesamtaufnahme - volume:39 |
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Enthalten in: |
Clinical rheumatology - 39(2020), 11 vom: 09. Nov., Seite 3473-3478 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Zhang, Hongfei [VerfasserIn] |
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Links: |
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Themen: |
CTBP1-AS2 |
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Anmerkungen: |
Date Completed 14.05.2021 Date Revised 31.05.2022 published: Print-Electronic Citation Status MEDLINE |
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doi: |
10.1007/s10067-020-05113-4 |
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funding: |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
NLM309719569 |
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500 | |a Citation Status MEDLINE | ||
520 | |a OBJECTIVES: 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 | ||
520 | |a METHODS: 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 | ||
520 | |a RESULTS: 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 | ||
520 | |a CONCLUSION: 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 | ||
650 | 4 | |a Journal Article | |
650 | 4 | |a CTBP1-AS2 | |
650 | 4 | |a Chondrocyte | |
650 | 4 | |a Osteoarthritis | |
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700 | 1 | |a Shao, Weiguang |e verfasserin |4 aut | |
700 | 1 | |a Shen, Naipeng |e verfasserin |4 aut | |
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