What question did this study set out to answer?

To determine the requirement of endothelial RhoA GTPase in endothelial cell behaviors, embryonic development, and retinal angiogenesis, and to examine potential in vivo compensatory mechanisms.

August 12, 2019Scientific ReportsOpen Access

Endothelial RhoA GTPase is essential for in vitro endothelial functions but dispensable for physiological in vivo angiogenesis

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To determine the requirement of endothelial RhoA GTPase in endothelial cell behaviors, embryonic development, and retinal angiogenesis, and to examine potential in vivo compensatory mechanisms.
Assessed in vitro endothelial cell proliferation, migration, and capillary tube formation in response to vascular endothelial growth factor (VEGF) and sphingosine-1 phosphate (S1P).
Generated constitutive and inducible endothelial RhoA-deficient mouse models to analyze embryonic survival and postnatal retinal vascular development.
RhoA is required in vitro for VEGF- and S1P-induced endothelial cell proliferation, migration, and tube formation.
Constitutive endothelial RhoA deficiency reduced overall survival but did not prevent embryonic development in vivo.
Inducible endothelial RhoA deficiency produced only mild vascular defects during retinal angiogenesis, indicating redundant physiological signaling in vivo.

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Implication

Experimental study demonstrates the dispensable role of endothelial RhoA in mice, suggesting in vivo compensatory signaling mechanisms.

Cite This Study

Zahra et al. (2019) studied this question.

synapsesocial.com/papers/6a6f9552c92390ac2d07a38d https://doi.org/10.1038/s41598-019-48053-z

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Endothelial RhoA GTPase is essential for in vitro endothelial functions but dispensable for physiological in vivo angiogenesis

Key Points

Discussion

Implication

Cite This Study

Endothelial RhoA GTPase is essential for in vitro endothelial functions but dispensable for physiological in vivo angiogenesis

Key Points

Discussion

Implication

Cite This Study

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