Semaphorin-3A protects against neointimal hyperplasia after vascular injury

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Gliotoxin inhibits neointimal hyperplasia after vascular injury in rats.

Neointima formation participates in the pathophysiology of atherosclerosis and restenosis. Proliferation and migration of vascular smooth muscle cells (VSMC) are initial responses to vascular injury. The aim of the present study was to assess the effect of gliotoxin, an inhibitor of nuclear factor (NF)-kappaB, on migration and proliferation of cultured rat VSMC and neointimal formation in injur...

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BACKGROUND In animal models, heparin delivered as a continuous intravenous infusion or via frequent (BID) subcutaneous dosing inhibits neointimal hyperplasia after balloon injury or stent implantation. However, human trials of subcutaneous heparin after percutaneous intervention have proven ineffective against restenosis. It may be that these failures are due to unfavorable heparin pharmacokine...

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Endothelial-like cells differentiated from mesenchymal stem cells attenuate neointimal hyperplasia after vascular injury

The present study investigated the contribution of bone marrow-derived mesenchymal stem cells (BM‑MSCs) to neointimal formation, and whether endothelial‑like cells (ELCs) differentiated from BM‑MSCs could attenuate intimal hyperplasia following vascular injury. BM‑MSCs were isolated from rat femurs and tibias and expanded ex vivo. Differentiation into ELCs was induced by cultivation in the pres...

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Absence of p53 leads to accelerated neointimal hyperplasia after vascular injury.

OBJECTIVE It has been suggested that deregulated expression of the tumor suppressor protein p53 may play a role in the pathogenesis of occlusive vascular remodeling. However, the role of p53 in cell proliferation and apoptosis in vascular lesions has been controversial. METHODS AND RESULTS We tested the potential involvement of p53-mediated molecular signaling in lesion formation using a mous...

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ژورنال

عنوان ژورنال: EBioMedicine

سال: 2019

ISSN: 2352-3964

DOI: 10.1016/j.ebiom.2018.12.023