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Core regulatory RNA molecules identified in articular cartilage stem/progenitor cells during osteoarthritis progression.
Epigenomics 2019 Februrary 19
AIM: To assess cartilage-derived-stem/progenitor cells (CSPCs) in osteoarthritis (OA) by employing mRNA-miRNA-circRNA-lncRNA network biology approach.
METHODS: Differentially expressed (DE) RNAs in CSPCs from 2-/4-/8-month-old STR/Ort and CBA mice were identified to construct networks via RNA sequencing.
RESULTS: Compared with age-matched CBA mice, 4-/8-month-old STR/Ort mice had cartilage lesions and their CSPCs exhibited lower proliferative and differentiation capacity (decreased CD44 and CD90), and identified 7082 DE RNAs in STR/Ort mice were associated with strain differences or OA progression. OA-related core RNAs were identified via the networks constructed with the predominant DE RNAs, which were involved in the signaling pathways (NF-κB/MAPK/Hippo/Wnt/TGF-β/cytoskeleton organization). The core RNAs (miR-322-5p/miR-493-5p/miR-378c/CPNE1/Cdh2/PRDM16/CTGF/NCAM1) were validated in CSPCs from OA patients.
CONCLUSION: RNA-based networks identifying core RNAs and signaling pathways contribute to CSPC-dependent OA mechanisms.
METHODS: Differentially expressed (DE) RNAs in CSPCs from 2-/4-/8-month-old STR/Ort and CBA mice were identified to construct networks via RNA sequencing.
RESULTS: Compared with age-matched CBA mice, 4-/8-month-old STR/Ort mice had cartilage lesions and their CSPCs exhibited lower proliferative and differentiation capacity (decreased CD44 and CD90), and identified 7082 DE RNAs in STR/Ort mice were associated with strain differences or OA progression. OA-related core RNAs were identified via the networks constructed with the predominant DE RNAs, which were involved in the signaling pathways (NF-κB/MAPK/Hippo/Wnt/TGF-β/cytoskeleton organization). The core RNAs (miR-322-5p/miR-493-5p/miR-378c/CPNE1/Cdh2/PRDM16/CTGF/NCAM1) were validated in CSPCs from OA patients.
CONCLUSION: RNA-based networks identifying core RNAs and signaling pathways contribute to CSPC-dependent OA mechanisms.
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