AI Article Synopsis

  • - The study investigates the role of long non-coding RNAs (lncRNAs) in the aging process of the meniscus, identifying 1608 differentially expressed (DE) lncRNAs and 1809 DE mRNAs through microarray analysis and confirming results with qRT-PCR.
  • - Key findings reveal that DE mRNAs are involved in critical signaling pathways (like TGF-beta and Wnt), with specific upregulations of TNFRSF11B and BMP2 in the aging group.
  • - Four lncRNAs (AC124312.5, HCG11, POC1B-AS1, and AP001011.1) were linked to meniscus degradation, with functional analyses suggesting they interact with various

Article Abstract

Little has been known about the role of long non-coding RNA (lncRNA) involves in change of aged meniscus. Microarray analyses were performed to identify lncRNAs and mRNAs expression profiles of meniscus in young and aging adults and apple bioinformatics methods to analyse their potential roles. The differentially expressed (DE) lncRNAs and mRNAs were confirmed by qRT-PCR. A total of 1608 DE lncRNAs and 1809 DE mRNAs were identified. Functional and pathway enrichment analyses of all DE mRNAs showed that DE mRNAs were mainly involved in the TGF-beta, Wnt, Hippo, PI3K-Akt signaling pathway. The expressions of TNFRSF11B and BMP2 were significantly upregulated in aging group. LASSO logistic regression analysis of the DE lncRNAs revealed four lncRNAs (AC124312.5, HCG11, POC1B-AS1, and AP001011.1) that were associated with meniscus degradation. CNC analysis demonstrated that AP001011 inhibited the expression of TNFRSF11B and AC1243125 upregulated the expression of TNFRSF11B. CeRNA analysis suggested that POC1B-AS1 regulates the expression of BMP2 by sponging miR 130a-3p, miR136-5p, miR 18a-3p, and miR 608. Furthermore, subcellular localization and mA modification sites prediction analysis of these four lncRNAs was performed. These data lay a foundation for extensive studies on the role of lncRNAs in change of aged meniscus.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8960627PMC
http://dx.doi.org/10.3389/fcell.2022.844555DOI Listing

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