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.