Upregulation of lncRNA SSTR5-AS1 promotes osteoblast differentiation and reduces apoptosis.

Abstract

Osteoporotic fractures (OPF) and delayed fracture healing (DFH) pose major health challenges for the elderly. The lncRNA SSTR5-AS1 shows abnormal expression in people with low BMD. Understanding how SSTR5-AS1 regulates fracture healing could help address DFH. This study detected the expression levels of SSTR5-AS1, miR-193b-3p, osteogenic markers (RUNX2, ALP, BSP, OCN, OPN) mRNA, and apoptosis-related genes (Bcl-2, Bax, Bad) in osteoblasts and serum samples from all participants using RT-qPCR. Logistic regression was used to identify the independent factors influencing fracture healing. Cell proliferation and apoptosis were assessed using CCK-8 assays and flow cytometry, respectively. The binding relationship between SSTR5-AS1 and miR-193b-3p was validated through dual-luciferase reporter assays. SSTR5-AS1 is significantly downregulated in patients with OPF and DFH and negatively regulates the expression level of miR-193b-3p. SSTR5-AS1 is a protective factor for fracture healing. Elevating SSTR5-AS1 levels significantly reduces miR-193b-3p expression, thereby decreasing osteoblast apoptosis, increasing Bcl-2 expression, and decreasing Bax and Bad levels. Furthermore, enhancing SSTR5-AS1 promotes osteoblast proliferation, upregulates RUNX2, ALP, BSP, OCN, and OPN expression, and facilitates osteoblast differentiation. SSTR5-AS1 demonstrates significant diagnostic value for OPF and DFH, making it a promising biomarker for these conditions. When overexpressed, SSTR5-AS1 reduces miR-193b-3p levels, promoting osteoblast proliferation and differentiation. This may accelerate fracture healing.