Shuai Xiang1, Zeng Li1, Xisheng Weng1. 1. Department of Orthopaedic Surgery, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China.
Abstract
BACKGROUND: Bone marrow stem cells (BMSCs) are involved in steroid-induced osteonecrosis of the femoral head (ONFH). Long noncoding RNAs (lncRNAs) have been demonstrated to regulate functions of BMSCs, especially their differentiation, and have been reported to be implicated in diverse bone disorders. However, the roles of lncRNAs in the progression of steroid-induced ONFH remain unknown. METHODS: BMSCs were isolated from healthy controls or patients with steroid-induced ONFH. RNA-sequencing was used to identify differentially expressed (DE) coding and noncoding transcripts and a lncRNA-messenger RNA coexpression network were created. The function of lncRNA RP11-154D6 in the proliferation, apoptosis, and differentiation of BMSCs was identified by overexpressing or silencing its expression. RESULTS: Altogether, 3114 DE messenger RNAs and 572 DE lncRNAs were identified and the expression of lncRNA RP11-154D6 was significantly decreased in BMSCs of patients with ONFH. Although no effects on proliferation and apoptosis were identified, we proved lncRNA RP11-154D6 promoted osteogenic differentiation while inhibiting adipogenic differentiation in BMSCs. Aberrant expression of lncRNA was identified in BMSCs of steroid-induced patients with ONFH. CONCLUSIONS: Our results demonstrated that lncRNA RP11-154D6 might contribute to the progression of steroid-induced ONFH through regulating the behavior of BMSCs and might provide new insights into the pathogenesis as well as treatment for steroid-induced ONFH.
BACKGROUND: Bone marrow stem cells (BMSCs) are involved in steroid-induced osteonecrosis of the femoral head (ONFH). Long noncoding RNAs (lncRNAs) have been demonstrated to regulate functions of BMSCs, especially their differentiation, and have been reported to be implicated in diverse bone disorders. However, the roles of lncRNAs in the progression of steroid-induced ONFH remain unknown. METHODS: BMSCs were isolated from healthy controls or patients with steroid-induced ONFH. RNA-sequencing was used to identify differentially expressed (DE) coding and noncoding transcripts and a lncRNA-messenger RNA coexpression network were created. The function of lncRNA RP11-154D6 in the proliferation, apoptosis, and differentiation of BMSCs was identified by overexpressing or silencing its expression. RESULTS: Altogether, 3114 DE messenger RNAs and 572 DE lncRNAs were identified and the expression of lncRNA RP11-154D6 was significantly decreased in BMSCs of patients with ONFH. Although no effects on proliferation and apoptosis were identified, we proved lncRNA RP11-154D6 promoted osteogenic differentiation while inhibiting adipogenic differentiation in BMSCs. Aberrant expression of lncRNA was identified in BMSCs of steroid-induced patients with ONFH. CONCLUSIONS: Our results demonstrated that lncRNA RP11-154D6 might contribute to the progression of steroid-induced ONFH through regulating the behavior of BMSCs and might provide new insights into the pathogenesis as well as treatment for steroid-induced ONFH.