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Lisette M. Acevedo

Researcher at University of California, San Diego

Publications -  23
Citations -  3418

Lisette M. Acevedo is an academic researcher from University of California, San Diego. The author has contributed to research in topics: Angiogenesis & Endothelial stem cell. The author has an hindex of 16, co-authored 20 publications receiving 3189 citations. Previous affiliations of Lisette M. Acevedo include Sanford-Burnham Institute for Medical Research & Yale University.

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In vivo delivery of the caveolin-1 scaffolding domain inhibits nitric oxide synthesis and reduces inflammation

TL;DR: A chimeric peptide with a cellular internalization sequence fused to the caveolin-1 scaffolding domain was generated and systemic administration of the peptide suppressed acute inflammation and vascular leak to the same extent as a glucocorticoid or an endothelial nitric oxide synthase (eNOS) inhibitor.
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A role for VEGF as a negative regulator of pericyte function and vessel maturation.

TL;DR: A role is defined for VEGF as an inhibitor of neovascularization on the basis of its capacity to disrupt VSMC function and reveals a dichotomous role for V EGF and VEGf-R2 signalling as both a promoter of endothelial cell function and a negative regulator of VSMCs and vessel maturation.
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MicroRNA-132–mediated loss of p120RasGAP activates the endothelium to facilitate pathological angiogenesis

TL;DR: It is concluded that miR-132 acts as an angiogenic switch by suppressing endothelial p120RasGAP expression, leading to Ras activation and the induction of neovascularization, whereas the application of anti–miR- 132 inhibits neov vascularization by maintaining vessels in the resting state.
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VEGF-induced vascular permeability is mediated by FAK

TL;DR: An inducible knockin mouse model is created to study the contribution of the integrin-associated focal adhesion tyrosine kinase (FAK) signaling on vascular function and establishes a role for FAK as an essential signaling switch within ECs regulating adherens junction dynamics.
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A new role for Nogo as a regulator of vascular remodeling.

TL;DR: It is shown that Nogo-B is highly expressed in cultured endothelial and smooth muscle cells, as well as in intact blood vessels, and is a regulator of vascular homeostasis and remodeling.