Dan Xu,Yu-Bing Guo,Min Zhang,Ye-Qing Sun.[J].Chin J Traumatol,2018,21(4):229-237. 10.1016/j.cjtee.2018.04.004
The subsequent biological effects of simulated microgravity on endothelial cell growth in HUVECs
  
DOI：10.1016/j.cjtee.2018.04.004
KeyWord: Simulated microgravityGrowth inhibitionmiR-22Serum response factorLAMC1mTOR
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Author NameAffiliation
Dan Xu Institute of Environmental Systems Biology, Dalian Maritime University, Dalian 116026, China 
Yu-Bing Guo Institute of Environmental Systems Biology, Dalian Maritime University, Dalian 116026, China 
Min Zhang Institute of Environmental Systems Biology, Dalian Maritime University, Dalian 116026, China
Department of Molecular Physiology and Medical Bioregulation, Yamaguchi University, 1-1-1 Minami-Kogushi, Ube, 755-8505, Japan 
Ye-Qing Sun Institute of Environmental Systems Biology, Dalian Maritime University, Dalian 116026, China 
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Abstract:
      Purpose: Microgravity is known to cause endothelium dysfunction in astronauts returning from spaceflight. We aimed to reveal the regulatory mechanism in alterations of human endothelial cells after simulated microgravity (SMG). Methods: We utilized the rotary cell culture system (RCCS-1) to explore the subsequent effects of SMG on human umbilical vein endothelial cells (HUVECs). Results: SMG-treated HUVECs appeared obvious growth inhibition after return to normal gravity, which might be attributed to a set of responses including alteration of cytoskeleton, decreased cell adhesion capacity and increased apoptosis. Expression levels of mTOR and its downstream Apaf-1 were increased during subsequent culturing after SMG. miR-22 was up-regulated and its target genes SRF and LAMC1 were down-regulated at mRNA levels. LAMC1 siRNAs reduced cell adhesion rate and inhibited stress fiber formation while SRF siRNAs caused apoptosis. Conclusion: SMG has the subsequent biological effects on HUVECs, resulting in growth inhibition through mTOR signaling and miR-22-mediated mechanism.
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