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The H19/let-7 feedback loop contributes to developmental dysplasia and dislocation of the hip
B. Ning, R. Jin, D. Wang, J. Sun
Jazyk angličtina Země Česko
Typ dokumentu časopisecké články
NLK
Directory of Open Access Journals
od 1991
Free Medical Journals
od 1998
ProQuest Central
od 2005-01-01
Medline Complete (EBSCOhost)
od 2006-01-01
Nursing & Allied Health Database (ProQuest)
od 2005-01-01
Health & Medicine (ProQuest)
od 2005-01-01
ROAD: Directory of Open Access Scholarly Resources
od 1998
- MeSH
- chondrocyty fyziologie MeSH
- epigeneze genetická fyziologie MeSH
- krysa rodu rattus MeSH
- kultivované buňky MeSH
- mikro RNA genetika metabolismus MeSH
- novorozená zvířata MeSH
- potkani Wistar MeSH
- proliferace buněk fyziologie MeSH
- RNA dlouhá nekódující genetika metabolismus MeSH
- těhotenství MeSH
- vývojová kyčelní dysplazie genetika metabolismus MeSH
- zpětná vazba fyziologická fyziologie MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- těhotenství MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
Developmental dysplasia and dislocation of the hip (DDH) is the most common type of lower limb deformity in pediatric orthopedics. The mechanism of the signaling pathway has been studied in depth. However, the role of epigenetic regulation, such as lncRNA, is still far from clear. In this study, we successfully established a rat model of DDH and demonstrated that H19 was down-regulated in the development of DDH. Further, we constructed H19 knockdown (KD) and overexpression chondrocytes. H19 KD suppressed the proliferation of normal chondrocytes, while overexpression of H19 promoted cell proliferation of DDH chondrocytes. Finally, we revealed that H19 bound to let-7 and inhibited its function, acting as a competing endogenous RNA. Down-regulation of H19 is closely associated with DDH progression and H19 is an important epigenetic factor that regulates the proliferation of chondrocytes. H19 may thus be a potential clinical marker for DDH diagnosis and treatment.
Citace poskytuje Crossref.org
Literatura
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