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Published in: BMC Musculoskeletal Disorders 1/2020

01-12-2020 | Osteoarthrosis | Research article

LncRNA SNHG9 is downregulated in osteoarthritis and inhibits chondrocyte apoptosis by downregulating miR-34a through methylation

Authors: Hongfei Zhang, Jinglian Li, Weiguang Shao, Naipeng Shen

Published in: BMC Musculoskeletal Disorders | Issue 1/2020

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Abstract

Background

Our preliminary RNA-Seq data revealed altered expression of small nucleolar RNA host gene 9 (SNHG9) in osteoarthritis (OA) and its reverse correlation with miR-34a, which can regulate chondrocyte apoptosis in rat OA model. This study was therefore carried out to investigate the potential interaction between SNHG9 and miR-34a in OA.

Methods

A total of 60 healthy volunteers (Control group) as well as 60 OA patients (OA group) were enrolled in this study. Transfections, RT-qPCR, methylation-specific PCR (MSP) and cell apoptosis assay were performed.

Results

We found that SNHG9 was downregulated in OA and its expression was reversely correlated with the expression of miR-34a only across OA samples but not healthy control samples. In chondrocytes from OA patients, overexpression of SNHG9 led to downregulation of miR-34a and increased methylation of miR-34a gene. In contrast, in chondrocytes from healthy controls, overexpression of SNHG9 did not affect the expression of miR-34a and the methylation of miR-34a gene. Cell apoptosis analysis showed that overexpression of SNHG9 led to decreased apoptotic rate of chondrocytes from OA patients but not chondrocytes from the healthy controls through miR-34a.

Conclusion

In conclusion, SNHG9 is downregulated in OA and inhibits chondrocyte apoptosis by downregulating miR-34a through methylation.
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Metadata
Title
LncRNA SNHG9 is downregulated in osteoarthritis and inhibits chondrocyte apoptosis by downregulating miR-34a through methylation
Authors
Hongfei Zhang
Jinglian Li
Weiguang Shao
Naipeng Shen
Publication date
01-12-2020
Publisher
BioMed Central
Published in
BMC Musculoskeletal Disorders / Issue 1/2020
Electronic ISSN: 1471-2474
DOI
https://doi.org/10.1186/s12891-020-03497-7

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