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PeerJ. 2019 Sep 2;7:e7491. doi: 10.7717/peerj.7491. eCollection 2019.

lnc-SAMD14-4 can regulate expression of the COL1A1 and COL1A2 in human chondrocytes.

Author information

1
Department of Orthopedics, The NO.921 Hospital of the People's Liberation Army Joint Support Force, The Second Affiliated Hospital of Hunan Normal University, Changsha, Hunan, China.
2
Department of Pharmaceutical Sciences, Hunan Normal University, changsha, Hunan, China.
3
Department of Orthopedics, Changsha central hospital, Changsha, Hunan, China.
4
Department of Traumatology, Shanxi Fenyang Hospital, The Fenyang Hospital of Shanxi Medical University, Fenyang, Shanxi, China.
5
Department of Orthopedics, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
6
Department of Orthopedics, People's Hospital of Xiangxi Autonomous Prefecture, Jishou, Hunan, China.

Abstract

Osteoarthritis (OA) is the most common motor system disease in aging people, characterized by matrix degradation, chondrocyte death, and osteophyte formation. OA etiology is unclear, but long noncoding RNAs (lncRNAs) that participate in numerous pathological and physiological processes may be key regulators in the onset and development of OA. Because profiling of lncRNAs and their biological function in OA is not understood, we measured lncRNA and mRNA expression profiles using high-throughput microarray to study human knee OA. We identified 2,042 lncRNAs and 2,011 mRNAs that were significantly differentially expressed in OA compared to non-OA tissue (>2.0- or < - 2.0-fold change; p < 0.5), including 1,137 lncRNAs that were upregulated and 905 lncRNAs that were downregulated. Also, 1,386 mRNA were upregulated and 625 mRNAs were downregulated. QPCR was used to validate chip results. Gene Ontology analysis and the Kyoto Encyclopedia of Genes and Genomes was used to study the biological function enrichment of differentially expressed mRNA. Additionally, coding-non-coding gene co-expression (CNC) network construction was performed to explore the relevance of dysregulated lncRNAs and mRNAs. Finally, the gain/loss of function experiments of lnc-SAMD14-4 was implemented in IL-1β-treated human chondrocytes. In general, this study provides a preliminary database for further exploring lncRNA-related mechnisms in OA.

KEYWORDS:

Expression profile; Long-coding ribonucleicacids; Microarray; Osteoarthritis

Conflict of interest statement

The authors declare there are no competing interests.

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