Effect of LncRNA BLACAT1 on the Proliferation and Apoptosis of Osteoblasts in Ankylosing Spondylitis Through Regulating RANKL/OPG Signaling Pathway

Abstract

Ankylosing spondylitis (AS) is an autoimmune disorder. LncRNA BLACAT1 involves in several diseases such as inflammation and immune diseases, but the expression and role of LncRNA BLACAT1 in AS remains unclear. AS patients and controls were selected. LcRNA BLACAT1 expression in peripheral blood was analyzed by Real time PCR, and its correlation with CRP, ESR and AS activity was analyzed. Osteoblast hFOB 1.19 was cultured and transfected with LncRNA BLACAT1 plasmid and si-LncRNA BLACAT1, respectively followed by analysis of cell proliferation by MTT assay, apoptosis by Caspase 3, ADAMTS-4 and Runx2 mRNA expression by Real time PCR, IFN-γ and TNF-α secretion by ELISA, and as RANKL, OPG, and nerve growth factor NGF level by western blot. AS patients presented significantly elevated LcRNA BLACAT1 level than controls (P < 0.05) with higher expression in active AS patients than stable phase (P < 0.05). BLACAT1 was positively associated with CRP and disease activity index (P < 0.05). Overexpression of LncRNA BLACAT1 in osteoblast hFOB 1.19 significantly decreased cell proliferation, elevated Caspase 3 activity, increased ADAMTS-4 mRNA expression, decreased Runx2 mRNA expression, and increased IFN-γ and TNF-α sevretion, and RANKL expression, and decreased OPG and NGF expression (P < 0.05). However, the above changes were reversed by si-LncRNA BLACAT1. LncRNA BLACAT1 expression in AS patients can reflect the degree of disease activity, and its mechanism may be through regulation of RANKL/OPG signaling pathway, which affects the proliferation and apoptosis of osteoblasts in AS.