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Increased endothelial expression of Toll-like receptor 2 at sites of disturbed blood flow exacerbates early atherogenic events. | LitMetric

AI Article Synopsis

  • - Toll-like receptors (TLRs) are important for the innate immune response and can worsen chronic inflammatory diseases like atherosclerosis through inflammatory pathways.
  • - Research using laser scanning confocal microscopy showed that TLR2 is mainly found in damaged areas of blood vessels in atherosclerosis-prone mice, particularly in regions with disturbed blood flow, and its expression increases with a high-fat diet.
  • - A study with genetically modified mice indicated that the absence of TLR2 leads to less damage and inflammation in the aorta, suggesting that TLR2 in endothelial cells plays a significant role in the development of atherosclerosis in these vulnerable regions.

Article Abstract

Toll-like receptors (TLRs) are pattern recognition receptors of innate immunity. TLRs initiate inflammatory pathways that may exacerbate chronic inflammatory diseases like atherosclerosis. En face laser scanning confocal microscopy (LSCM) of isolated aortic segments revealed the distribution of intimal TLR2 expression and the atheroprotective outcomes resulting from a TLR2 deficiency. TLR2 expression was restricted to endothelial cells in regions of disturbed blood flow, such as the lesser curvature region, in atherosclerosis-prone, low-density lipoprotein receptor-deficient (LDLr(-/-)) mice. Diet-induced hyperlipidemia in LDLr(-/-) mice increased this regional endothelial TLR2 expression. Bone marrow (BM) reconstitution of LDLr(-/-) and LDLr(-/-)TLR2(-/-) mice created chimeric mice with green fluorescent protein (GFP) expression in BM-derived cells (BMGFP(+)). Lesser curvature BMGFP(+) leukocyte accumulation, lipid accumulation, foam cell generation and endothelial cell injury were all increased by hyperlipidemia, whereas hyperlipidemic double mutant BMGFP(+)LDLr(-/-)TLR2(-/-) mice had reduced BMGFP(+) leukocyte accumulation, lipid accumulation, foam cells, and endothelial cell injury. This is the first report of in vivo site-specific expression of endothelial cell TLR2. Expression of this receptor on endothelial cells contributed to early atherosclerotic processes in lesion-prone areas of the mouse aorta.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2271019PMC
http://dx.doi.org/10.1084/jem.20071096DOI Listing

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