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We began analyzing https://link.springer.com/article/10.1007/s00395-012-0269-1, but it redirected us to https://link.springer.com/article/10.1007/s00395-012-0269-1. The analysis below is for the second page.

Title[redir]:
Toll-like receptor 7 stimulation by imiquimod induces macrophage autophagy and inflammation in atherosclerotic plaques | Basic Research in Cardiology
Description:
Atherosclerotic plaques tend to rupture as a consequence of a weakened fibrous cap, particularly in the shoulder regions where most macrophages reside. Macrophages express Toll-like receptors to recognize pathogens and eliminate intracellular pathogens by inducing autophagy. Because Toll-like receptor 7 (TLR7) is thought to be expressed in macrophages but not in smooth muscle cells (SMCs), we investigated whether induction of macrophage autophagic death by TLR7 ligand imiquimod can affect the composition of atherosclerotic plaques in favor of their stability. Immunohistochemical staining of human carotid plaques as well as Western blotting of cultured macrophages and SMCs confirmed that TLR7 was expressed in macrophages, but not in SMCs. In vitro experiments showed that only TLR7 expressing cells underwent imiquimod-induced cell death, which was characterized by autophagosome formation. Imiquimod-treated macrophages activated nuclear factor-κB (NF-κB) and released pro-inflammatory cytokines and chemokines. This effect was inhibited by the glucocorticoid dexamethasone. Imiquimod-induced cytokine release was significantly decreased in autophagy-deficient macrophages because these cells died by necrosis at an accelerated pace. Local in vivo administration of imiquimod to established atherosclerotic lesions in rabbit carotid arteries induced macrophage autophagy without induction of cell death, and triggered cytokine production, upregulation of vascular adhesion molecule-1, infiltration of T-lymphocytes, accumulation of macrophages and enlargement of plaque area. Treatment with dexamethasone suppressed these pro-inflammatory effects in vivo. SMCs and endothelial cells in imiquimod-treated plaques were not affected. In conclusion, imiquimod induces macrophage autophagy in atherosclerotic plaques, but stimulates plaque progression through cytokine release and enhanced infiltration of inflammatory cells.

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Keywords {🔍}

article, pubmed, google, scholar, cas, autophagy, van, atherosclerotic, meyer, cell, macrophages, plaque, basic, plaques, cells, res, tolllike, macrophage, cardiol, martinet, gry, bult, death, vascular, access, herman, content, research, receptor, imiquimod, inflammation, tlr, mice, atherosclerosis, biol, antwerp, privacy, cookies, april, human, carotid, dois, thromb, coronary, publish, search, induces, schrijvers, timmermans, receptors,

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autophagy-mediated anti-tumoral activity month download article/chapter macrophage autophagic death collar-induced intimal thickening jean-pierre timmermans high-grade carotid stenosis multi-slice computed tomography hmg-coa reductase inhibitors anne-elise van hoydonck imiquimod-induced cytokine release immune response modifiers—mode released pro-inflammatory cytokines smooth muscle cells article basic research rupture-prone plaque phenotype full article pdf van der pg van der veken imiquimod-treated plaques tlr7 ligand imiquimod human carotid plaques de meyer gry vascular adhesion molecule-1 transgenic mice expressing necrotic cell death privacy choices/manage cookies related subjects human atherosclerotic lesions van de ven sala-newby gb concomitant immune response macrophage-specific loss macrophage-specific initiation van de rm atherosclerotic vascular disease autophagy-deficient macrophages cuffed carotid artery atg7-deficient mice apoe-deficient mice burke ap chantal de groote gimbrone ma jr advanced atherosclerotic plaques rabbit atherosclerotic plaques myocardial ischemia/reperfusion foam cell phenotypes check access instant access acute coronary syndromes established atherosclerotic lesions

Questions {❓}

Kockx MM, Herman AG (2000) Apoptosis in atherosclerosis: beneficial or detrimental?

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