LncRNA NORAD promotes bone marrow stem cell differentiation and proliferation by targeting miR-26a-5p in steroid-induced osteonecrosis of the femoral head

• Published in: Stem cell research & therapy Vol. 12; no. 1; p. 18
• Main Authors: Fu, Dapeng, Yang, Sheng, Lu, Jianmin, Lian, Haoyi, Qin, Kairong
• Format: Journal Article
• Language: English
• Published: England BioMed Central Ltd 07-01-2021; BioMed Central; BMC
• Subjects: Apoptosis; Binding sites; Bone marrow; Bone surgery; Bones; Cbfa-1 protein; Cell differentiation; Cell growth; Cell proliferation; Cholecystokinin; Dexamethasone; Femur; Flow cytometry; Fractures; Gene expression; LncRNA NORAD; Medical research; Medicine, Experimental; Mesenchyme; miR-26a-5p; Necrosis; OPG/RANK/ RANKL pathway; Orthopedics; Osteonecrosis; Osteoprotegerin; Pathogenesis; Proliferation; Proteins; Quality of life; Rankings; Reporter gene; RNA; siRNA; Statistical analysis; Stem cells; Steroid-induced osteonecrosis of the femoral head; Surgery; TRANCE protein; United States > US; China; LncRNA NORAD; Steroid-induced osteonecrosis of the femoral head; Proliferation; OPG/RANK/ RANKL pathway; miR-26a-5p
• ISSN: 1757-6512; 1757-6512
• DOI: 10.1186/s13287-020-02075-x

Steroid-induced osteonecrosis of the femoral head (SONFH) is a devastating orthopedic disease, which seriously affects the quality of life of patients. The study aims to investigate the effects of LncRNA NORAD on SONFH.
Human bone marrow-derived mesenchymal stem cells (hBMSCs) were isolated from the proximal femur of patients during routine orthopedic surgery and then cultured with dexamethasone (Dex) and transfected with NORAD overexpression vector, siRNA-NORAD and miR-26a-5p mimics. The mRNA expression of NORAD, miR-26a-5p, OPG, RANK, and RANKL was detected by RT-qPCR. Cell proliferation and apoptosis was measured by CCK-8 assay and flow cytometry, respectively. The protein expression of RUNX2, OPG, RANK, and RANKL was detected by western blot. The dual-luciferase reporter gene assay was performed to confirm the binding between NORAD and miR-26a-5p.
NORAD expression was downregulated in SONFH tissues, while miR-26a-5p expression was upregulated. Overexpression of NORAD improved DEX-induced inhibition of proliferation and differentiation, and promotion of apoptosis in hBMSCs, while knockdown of NORAD led to the opposite results. Moreover, NORAD improved DEX-induced inhibition of proliferation and differentiation, and promotion of apoptosis by regulation of miR-26a-5p in hBMSCs.
NORAD expression was downregulated in SONFH tissues, while miR-26a-5p expression was upregulated. NORAD improved DEX-induced inhibition of proliferation and differentiation, and promotion of apoptosis by regulation of miR-26a-5p in hBMSCs.