Affiliation: | 1. Department of Orthopedics, Jinling Hospital, Medical School of Nanjing University, Nanjing, China;2. Department of Orthopedics, No. 454 Hospital of PLA, Anhui Medical University, Nanjing, China;3. Department of Emergency, First Affiliated Hospital, Xi’an Medical University, Xi’an, China;4. Department of Orthopedics, No. 454 Hospital of PLA, Anhui Medical University, Nanjing, China Medical Services Section, No. 454 Hospital of PLA, Anhui Medical University, Nanjing, China;5. Department of Pharmacy, No. 454 Hospital of PLA, Anhui Medical University, Nanjing, China;6. Medical Services Section, No. 454 Hospital of PLA, Anhui Medical University, Nanjing, China;7. The Key Laboratory of Aerospace Medicine, Chinese Ministry of Education, Fourth Military Medical University, Xi’an, China |
Abstract: | Calcium homeostasis in osteoblasts plays fundamental roles in the physiology and pathology of bone tissue. Various types of mechanical stimuli promote osteogenesis and increase bone formation elicit increases in intracellular-free calcium concentration in osteoblasts. However, whether microgravity, a condition of mechanical unloading, exerts an influence on intracellular-free calcium concentration in osteoblasts or what mechanisms may underlie such an effect are unclear. Herein, we show that simulated microgravity reduces intracellular-free calcium concentration in primary mouse osteoblasts. In addition, simulated microgravity substantially suppresses the activities of L-type voltage-sensitive calcium channels, which selectively allow calcium to cross the plasma membrane from the extracellular space. Moreover, the functional expression of ryanodine receptors and inositol 1,4,5-trisphosphate receptors, which mediate the release of calcium from intracellular storage, decreased under simulated microgravity conditions. These results suggest that simulated microgravity substantially reduces intracellular-free calcium concentration through inhibition of calcium channels in primary mouse osteoblasts. Our study may provide a novel mechanism for microgravity-induced detrimental effects in osteoblasts, offering a new avenue to further investigate bone loss induced by mechanical unloading. |