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Spaceflight Modulates the Expression of Key Oxidative Stress and Cell Cycle Related Genes in Heart

Spaceflight causes cardiovascular changes due to microgravity-induced redistribution of body fluids and musculoskeletal unloading. Cardiac deconditioning and atrophy on Earth are associated with altered and oxidative stress-related pathways, but the effects of spaceflight on cardiac changes at the m...

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Bibliographic Details
Published in:International journal of molecular sciences 2021-08, Vol.22 (16), p.9088
Main Authors: Kumar, Akhilesh, Tahimic, Candice G T, Almeida, Eduardo A C, Globus, Ruth K
Format: Article
Language:English
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Summary:Spaceflight causes cardiovascular changes due to microgravity-induced redistribution of body fluids and musculoskeletal unloading. Cardiac deconditioning and atrophy on Earth are associated with altered and oxidative stress-related pathways, but the effects of spaceflight on cardiac changes at the molecular level are less understood. We tested the hypothesis that spaceflight alters the expression of key genes related to stress response pathways, which may contribute to cardiovascular deconditioning during extended spaceflight. Mice were exposed to spaceflight for 15 days or maintained on Earth (ground control). Ventricle tissue was harvested starting ~3 h post-landing. We measured expression of select genes implicated in oxidative stress pathways and signaling by quantitative PCR. Cardiac expression levels of 37 of 168 genes tested were altered after spaceflight. Spaceflight downregulated transcription factor, , upregulated and downregulated , suggesting a persistent increase in oxidative stress-related target genes. Spaceflight also substantially upregulated ( ) and cell cycle/apoptosis-related gene , and downregulated the inflammatory response gene . There were no changes in apoptosis-related genes such as . Spaceflight altered the expression of genes regulating redox balance, cell cycle and senescence in cardiac tissue of mice. Thus, spaceflight may contribute to cardiac dysfunction due to oxidative stress.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms22169088