ZNF185 prevents stress fiber formation through the inhibition of RhoA in endothelial cells.

ABSTRACT: Signaling through cAMP/protein kinase A (PKA) promotes endothelial barrier function to prevent plasma leakage induced by inflammatory mediators. The discovery of PKA substrates in endothelial cells increases our understanding of the molecular mechanisms involved in vessel maturation. In this study, we evaluate a cAMP inducer, forskolin, and a phospho-PKA substrate antibody to identify ZNF185 as a PKA substrate. ZNF185 interacts with PKA and colocalizes with F-actin in endothelial cells. Both ZNF185 and F-actin accumulate in the plasma membrane region in response to forskolin to stabilize the cortical actin structure. By contrast, ZNF185 knockdown disrupts actin filaments and promotes stress fiber formation without inflammatory mediators. Constitutive activation of RhoA is induced by ZNF185

SUBMITTER: Suzuki S 

PROVIDER: S-EPMC9834212 | biostudies-literature | 2023 Jan

REPOSITORIES: biostudies-literature