Objective: To investigate the effect of long non-coding ribonucleic acid (lncRNA) AK023948 (AK0) on rats with postmenopausal osteoporosis via the phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signaling pathway.
Materials and methods: Firstly, postmenopausal osteoporosis rat models were established to obtain osteoblasts. The phosphorylation level of AKT was analyzed by controlling the expression of AK0 gene in osteoblasts. Finally, XTT was used to analyze the proliferation of osteoblasts and the messenger ribonucleic acid (mRNA) expression level of caspase in AK0 gene knockout (KO) rat model.
Results: In the bone tissue of postmenopausal osteoporosis rats, the levels of phospho-PI3K (p-PI3K), p-Akt, and p-phosphoinositide-dependent kinase-1(PDK1) were significantly decreased (p<0.05). In rat model osteoblasts, the overexpression of AK0 gene upregulated the phosphorylation level of AKT, while the interference with small interfering RNA (siRNA) in AK0 gene decreased that of AKT. Knocking out AK0 gene led to the down-regulation of phosphorylation level of AKT in cells. Moreover, if the AK0 gene was re-expressed in the KO rat model cells, the phosphorylation level of AKT was restored to a certain extent, but still lower than that after the overexpression of AK0 gene. Although the proliferation rate of osteoblasts in estrogen deficiency-related osteoporosis rats was low, the growth rate of osteoblasts with AK0 KO was remarkably lower than that in blank control group (p<0.05). It was also found that there was a certain correlation between AK0 gene and osteoblast apoptosis.
Conclusions: LncRNA AK0 can regulate the phosphorylation level of AKT in osteoblasts of rats with estrogen deficiency-related osteoporosis through the PI3K/AKT signaling pathway, thus regulating the proliferation of osteoblasts. It is speculated that lncRNA AK0 may be an important factor in regulating the PI3K/AKT signaling pathway.