W Li1, H-M Zhu, H-D Xu, B Zhang, S-M Huang. 1. Department of Neuroscience, Institute of Chinese Medicine, Heilongjiang University of Chinese Medicine, Heilongjiang, Harbin, China. huangshuminghljzyy@126.com.
Abstract
OBJECTIVE: Bone loss is the main reason for postmenopausal osteoporosis, caused by estrogen deficiency. ERT (estrogen replacement therapy) has been demonstrated to protect bone loss efficiently. LncRNA (long non-coding RNA) has been proved to be important in different disease progression. We aimed at analyzing whether the lncRNAs influence the activity of osteoclasts and the progression of this disease. PATIENTS AND METHODS: RT-PCR (reverse transcriptase-polymerase chain reaction) was used to detect the expression of lncRNA CRNDE in OH (osteoclast from healthy people) and OP (osteoclast from patients with postmenopausal osteoporosis). MTT (methylthiazolyl tetrazolium) assay was used to detect the viability of the cells. The cell cycle and apoptosis rate in OH and OP were measured by the flow cytometry analysis. Western blot was used to analyze the possible related mechanism that CRNDE regulated the cells proliferation in postmenopausal osteoporosis. RESULTS: We found that the CRNDE was highly expressed in the osteoclast from patients with OP, compared with OH. We also found that overexpressing CRNDE increased the viability in OH whilst reducing CRNDE in OP decreased the viability. The cell cycle was arrested in G0/G1 phase and the apoptosis rate was improved in OP after transfection with siRNA. Moreover, CRNDE could impact the proliferation of osteoclasts by PI3K/Akt signaling pathway and estrogen could inhibit this proliferation. CONCLUSIONS: We found that lncRNA CRNDE was closely related to the postmenopausal osteoporosis with estrogen deficiency. CRNDE may be involved in the development and progression of postmenopausal osteoporosis in the absence of estrogen and become a potential target for treating.
OBJECTIVE:Bone loss is the main reason for postmenopausal osteoporosis, caused by estrogen deficiency. ERT (estrogen replacement therapy) has been demonstrated to protect bone loss efficiently. LncRNA (long non-coding RNA) has been proved to be important in different disease progression. We aimed at analyzing whether the lncRNAs influence the activity of osteoclasts and the progression of this disease. PATIENTS AND METHODS: RT-PCR (reverse transcriptase-polymerase chain reaction) was used to detect the expression of lncRNA CRNDE in OH (osteoclast from healthy people) and OP (osteoclast from patients with postmenopausal osteoporosis). MTT (methylthiazolyl tetrazolium) assay was used to detect the viability of the cells. The cell cycle and apoptosis rate in OH and OP were measured by the flow cytometry analysis. Western blot was used to analyze the possible related mechanism that CRNDE regulated the cells proliferation in postmenopausal osteoporosis. RESULTS: We found that the CRNDE was highly expressed in the osteoclast from patients with OP, compared with OH. We also found that overexpressing CRNDE increased the viability in OH whilst reducing CRNDE in OP decreased the viability. The cell cycle was arrested in G0/G1 phase and the apoptosis rate was improved in OP after transfection with siRNA. Moreover, CRNDE could impact the proliferation of osteoclasts by PI3K/Akt signaling pathway and estrogen could inhibit this proliferation. CONCLUSIONS: We found that lncRNA CRNDE was closely related to the postmenopausal osteoporosis with estrogen deficiency. CRNDE may be involved in the development and progression of postmenopausal osteoporosis in the absence of estrogen and become a potential target for treating.