Key result
Gravitational mechanical unloading significantly decreased the expression of adhesion molecules and pro-inflammatory cytokines while increasing eNOS and caveolin expression in endothelial cells, effects that were reversed by mechanical loading.
Simulated microgravity induces an anti-inflammatory phenotype and alters cytoskeletal organization in endothelial cells, suggesting a role for gravitational forces in vascular function and potential therapies.
These endothelial effects of unloading are hypothesis-generating; leaves open gravitational modulation of vascular inflammation pending human studies.
Mechanical forces including gravity affect endothelial cell (ECs) function, and have been implicated in vascular disease as well as physiologic changes associated with low gravity environments. The goal of this study was to investigate the impact of gravitational mechanical unloading on ECs phenotype as determined by patterns of gene expression. Human umbilical vascular endothelial cells were exposed to 1-gravity environment or mechanical unloading (MU) for 24 hours, with or without periods of mechanical loading (ML). MU led to a significant decrease in gene expression of several adhesion molecules and pro-inflammatory cytokines. On the contrary, eNOS, Caveolin-1 and -2 expression were significantly increased with MU. There was a decrease in the length and width of the cells with MU. Addition of ML during the MU period was sufficient to reverse the changes triggered by MU. Our results suggest that gravitational loading could dramatically affect vascular endothelial cell function.
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Grenon et al. (2013) studied Endothelial cell function in microgravity. Gravitational mechanical unloading (simulated microgravity) vs. 1-gravity environment (ground controls) was evaluated on Gene expression of adhesion molecules, inflammatory cytokines, eNOS, and caveolins (p=<0.05). Gravitational mechanical unloading significantly decreased the expression of adhesion molecules and pro-inflammatory cytokines while increasing eNOS and caveolin expression in endothelial cells, effects that were reversed by mechanical loading.
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