ArticleArteriosclerosis, thrombosis, and vascular biology2010
Genetic regulation of endothelial inflammatory responses in baboons.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Family-based analyses reveal novel genetic overlap between cytokine interleukin-8 and risk for suicide attempt.Brain, behavior, and immunity · 2019Article
- Cholesterol crystals promote endothelial cell and monocyte interactions via HRedox biology · 2019Article
- Diet-induced early-stage atherosclerosis in baboons: Lipoproteins, atherogenesis, and arterial compliance.Journal of medical primatology · 2018Article
- Genetic variation is the major determinant of individual differences in leukocyte endothelial adhesion.PloS one · 2014Article
- Early endothelial damage detected by circulating particles in baboons fed a diet high in simple carbohydrates in conjunction with saturated or unsaturated fat.American journal of cardiovascular disease · 2014Article
- Endothelial reconstitution by CD34+ progenitors derived from baboon embryonic stem cells.Journal of cellular and molecular medicine · 2013Article
- Baboons as a model to study genetics and epigenetics of human disease.ILAR journal · 2013Review
- Protective Effects of Resveratrol on TNF-α-Induced Endothelial Cytotoxicity in Baboon Femoral Arterial Endothelial Cells.Journal of diabetes research · 2013Article
- Use of a special bioreactor for the cultivation of a new flexible polyurethane scaffold for aortic valve tissue engineering.Biomedical engineering online · 2012Article
- Repertoire of endothelial progenitor cells mobilized by femoral artery ligation: a nonhuman primate study.Journal of cellular and molecular medicine · 2012Article
- Animal models of atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2012Review
- Profound influence of LDL oxidative status and monocyte co-cultures on baboon endothelial activation.American journal of cardiovascular disease · 2012Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
objectiveTo investigate the genetic contributions to the expression of cell surface adhesion molecules on endothelial cells (ECs) and to the release by ECs of chemokines, which are responsible for local inflammation. METHODS AND
resultsMonocyte adhesion to ECs and transmigration across the endothelial barrier are the key steps in the formation of atherosclerotic plaques and the rupture of the existing plaques. Biopsy specimens were obtained from the femoral arteries of 131 pedigreed baboons (65 males and 66 females) aged 10.4+/-1.5 years (mean+/-SD); arterial ECs were harvested and cultured up to the second passage and then subjected to in vitro challenge with tumor necrosis factor (TNF) alpha, 10 ng/mL, or vehicle for 4 hours. Endothelial surface adhesion molecules were measured using flow cytometry, and chemokines released by the ECs were measured by immunoassay. In response to TNF-alpha treatment, interleukin 8 and monocyte chemoattractant protein-1 released by ECs were increased 3.4- and 26-fold, respectively (P<0.001). The expressions of E-selectin, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 were increased 12.2-, 41.4-, and 3.5-fold, respectively (P<0.001). The quantitative levels of several traits were heritable after TNF-alpha stimulation: h(2)=0.24 (P=0.02) for interleukin 8 and h(2)=0.28 (P=0.003) for E-selectin in culture medium; h(2)=0.21 (P=0.03) for intercellular adhesion molecule-1; and h(2)=0.37 (P<0.001) for vascular cell adhesion molecule-1 expression on EC surfaces. Furthermore, significant heritability was observed for lysate protein level, which is a measure of cell growth rate, with (h(2)=0.64, P<0.001) or without (h(2)=0.51, P<0.001) TNF-alpha stimulation.
conclusionsThis study reports on the heritability of adhesion molecules in ECs when activated by TNF-alpha. This finding suggests genetic regulation of key arterial wall inflammatory processes that are responsible for the initiation of atherosclerotic lesions and the plaque rupture of existing atheromas.
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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.