LncRNA CRNDE ameliorates bone fracture by regulating cell viability and apoptosis of osteoblasts.

Abstract

Delayed healing is a common postoperative complication among fractured patients, imposing an additional financial burden. This research examined the clinical relationship between CRNDE and delayed fracture healing (DFH) and the potential regulatory mechanisms underlying fracture improvement. qRT-PCR was utilized to assess the expression of CRNDE and miR-29a-3p in serum and cellular samples, and to evaluate the expression of genes associated with osteogenic differentiation. The diagnostic and predictive significance of serum CRNDE was analyzed using ROC analysis and logistic regression. Additionally, an hFOB 1.19 osteogenic differentiation model was established. The CCK-8 assay and flow cytometry techniques were used to investigate the effects of silencing CRNDE, as well as the concurrent inhibition of both CRNDE and miR-29a-3p, on the proliferation and apoptosis of hFOB 1.19 cells. CRNDE was down-regulated, while miR-29a-3p was up-regulated in DFH patients. The serum CRNDE could effectively identify DFH patients and predict the DFH occurrence. In the hFOB 1.19 osteogenic differentiation model, silencing CRNDE led to a significant decrease in the expression of osteogenic differentiation markers, a reduction in the proliferation activity of hFOB 1.19 cells, and an increase in apoptosis. There was a negative regulatory interaction between CRNDE and miR-29a-3p. Concurrently inhibiting the expression of both CRNDE and miR-29a-3p could effectively restore the functional activity of hFOB 1.19 cells. Serum CRNDE holds potential as a biomarker for the diagnosis and prediction of DFH. The sponging effect of CRNDE on miR-29a-3p could ameliorate fracture healing.