The H19/let-7 feedback loop contributes to developmental dysplasia and dislocation of the hip
Language English Country Czech Republic Media print-electronic
Document type Journal Article
PubMed
30628827
DOI
10.33549/physiolres.933920
PII: 933920
Knihovny.cz E-resources
- MeSH
- Chondrocytes physiology MeSH
- Epigenesis, Genetic physiology MeSH
- Rats MeSH
- Cells, Cultured MeSH
- MicroRNAs genetics metabolism MeSH
- Animals, Newborn MeSH
- Rats, Wistar MeSH
- Cell Proliferation physiology MeSH
- RNA, Long Noncoding genetics metabolism MeSH
- Pregnancy MeSH
- Hip Dislocation, Congenital genetics metabolism MeSH
- Feedback, Physiological physiology MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Pregnancy MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- H19 long non-coding RNA MeSH Browser
- MicroRNAs MeSH
- MIRNLET7 microRNA, rat MeSH Browser
- RNA, Long Noncoding 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.
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