Pericyte contraction generates angiostatic effect via cell force-dependent activation of TGFβ.

R-Ras–mediated contractility in pericytes activates TGFβ via integrin-dependent, actomyosin-generated traction force, and this drives EC quiescence through ALK5–Smad2/3 signaling.

• Why it matters: The mechanistic link between pericyte contraction and vascular stability is unclear, despite TGFβ’s context-dependent pro- and antiangiogenic roles.
• What they did: The study used pericyte contraction signaling to show TGFβ activation depends on integrins and actomyosin traction, then tested EC responses via ALK5–Smad2/3 versus Smad1/5.
• The result: Pericyte-targeted Rras deletion in mice reduced pericyte contractility and EC Smad2/3 phosphorylation, with increased tumor angiogenesis and vessel deformation in skeletal muscle.

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