ArticleJournal of lipid research2005
Apolipoprotein E inhibition of vascular hyperplasia and neointima formation requires inducible nitric oxide synthase.
Article in Journal of lipid research, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- Review
- Regulation of cardiovascular health and disease by visceral adipose tissue-derived metabolic hormones.The Journal of physiology · 2023Article
- Apolipoprotein E in Cardiometabolic and Neurological Health and Diseases.International journal of molecular sciences · 2022Review
- Transplanted perivascular adipose tissue accelerates injury-induced neointimal hyperplasia: role of monocyte chemoattractant protein-1.Arteriosclerosis, thrombosis, and vascular biology · 2014Article
- apoE3[K146N/R147W] acts as a dominant negative apoE form that prevents remnant clearance and inhibits the biogenesis of HDL.Journal of lipid research · 2014Article
- Kalirin promotes neointimal hyperplasia by activating Rac in smooth muscle cells.Arteriosclerosis, thrombosis, and vascular biology · 2013Article
- Apolipoprotein E4 impairs macrophage efferocytosis and potentiates apoptosis by accelerating endoplasmic reticulum stress.The Journal of biological chemistry · 2012Article
- Changing topographic Hox expression in blood vessels results in regionally distinct vessel wall remodeling.Biology open · 2012Article
- Apolipoprotein E inhibits toll-like receptor (TLR)-3- and TLR-4-mediated macrophage activation through distinct mechanisms.The Biochemical journal · 2010Article
- Up-regulation of apolipoprotein E by leptin in the hypothalamus of mice and rats.Physiology & behavior · 2009Article
- Article
- Regulation of smooth muscle by inducible nitric oxide synthase and NADPH oxidase in vascular proliferative diseases.Free radical biology & medicine · 2008Review
- Intimal hyperplasia in murine models.Current drug targets · 2008Review
- High glucose oxidizes SERCA cysteine-674 and prevents inhibition by nitric oxide of smooth muscle cell migration.Journal of molecular and cellular cardiology · 2008Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Previous studies have shown apolipoprotein E (apoE) recruitment to medial layers of carotid arteries after vascular injury in vivo and apoE activation of inducible nitric oxide synthase (iNOS) in smooth muscle cells in vitro. This investigation explored the relationship between medial apoE recruitment and iNOS activation in protection against neointimal hyperplasia. ApoE was present in both neointimal-resistant C57BL/6 mice and neointimal-susceptible FVB/N mice 24 h after carotid denudation, but iNOS expression was observed only in the neointimal-resistant C57BL/6 mice. However, iNOS was not observed in apoE-defective C57BL/6 mice. In contrast, overexpression of apoE in FVB/N mice activated iNOS expression in the injured vessels, resulting in protection against neointimal hyperplasia. ApoE and iNOS were colocalized in the medial layer of neointimal-resistant mouse strains. Endothelial denudation of carotid arteries in the iNOS-deficient NOS2(-/-) mice did not increase neointimal hyperplasia but significantly increased medial thickness and area. The iNOS-specific inhibitor also abrogated the apoE protective effects on vascular response to injury in apoE-overexpressing FVB/N mice. Thus, injury-induced activation of iNOS requires apoE recruitment. Moreover, both apoE and iNOS are necessary for the suppression of cell proliferation, and apoE recruitment without iNOS expression resulted in medial hyperplasia without cell migration to the intima.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.