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Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
Three regulatory proteins control their activity:
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Rac1 GTPase silencing counteracts microgravity-induced effects on osteoblastic cells.

Alain Guignandon1, Céline Faure2, Thibaut Neutelings3

  • 1Institute National de la Santé et de la Recherche Médicale (INSERM), Unité 1059, Laboratoire de Biologie Intégrée du Tissu Osseux, Université de Lyon, St-Etienne, France; alain.guignandon@univ-st-etienne.fr.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
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Summary
This summary is machine-generated.

Spaceflight alters bone cells by affecting cytoskeleton and focal adhesions. Rac1 and Cdc42 (Ras homology family GTPases) modulation can counteract these microgravity-induced changes, particularly concerning focal contacts and vascular endothelial growth factor (VEGF) levels.

Keywords:
Cdc42MG-63RhoAVEGFspaceflight

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Area of Science:

  • Cell Biology
  • Space Biology
  • Biotechnology

Background:

  • Microgravity affects bone cells, altering critical mechanosensitive structures like the cytoskeleton and focal adhesions.
  • These cellular structures are regulated by small GTPases of the Ras homology (Rho) family, including RhoA, Rac1, and Cdc42.

Purpose of the Study:

  • To investigate the impact of modulating RhoA, Rac1, and Cdc42 on osteoblastic cells under microgravity conditions.
  • To identify potential therapeutic targets for mitigating the adverse effects of spaceflight on bone cells.

Main Methods:

  • Human MG-63 osteoblast-like cells with silenced RhoGTPases were cultured in a spaceflight bioreactor and compared to ground controls.
  • Postflight analysis included assessing focal contacts, F-actin polymerization, vascular endothelial growth factor (VEGF) expression, and matrix interactions.

Main Results:

  • RhoA silencing did not alter microgravity sensitivity.
  • Abrogation of Rac1, and to a lesser extent Cdc42, effectively counteracted spaceflight-induced reductions in focal contacts, F-actin fibers, and matrix-bound VEGF.
  • SiRac1 cells showed only a -15% reduction in focal contacts compared to -50% in controls.

Conclusions:

  • The VEGF/Rho GTPase axis plays a crucial role in cellular mechanosensing.
  • Rac1-mediated signaling pathways are validated as promising targets for developing countermeasures against microgravity's detrimental effects on bone cells.