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C1Q+macrophage interacts with activated CD8+ promoting atherosclerosis development

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE245667 | GEO | 2024/05/29

REPOSITORIES: GEO

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C1Q+macrophage interacts with activated CD8+ promoting atherosclerosis development [DC]

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C1Q+macrophage interacts with activated CD8+ promoting atherosclerosis development [T cell]

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C1Q+macrophage interacts with activated CD8+ promoting atherosclerosis development

Project description:C1Q+macrophage interacts with activated CD8+ promoting atherosclerosis development

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C1Q+macrophage interacts with activated CD8+ promoting atherosclerosis development [DC]

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C1Q+macrophage interacts with activated CD8+ promoting atherosclerosis development [T cell]

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Thyrotropin aggravates atherosclerosis by promoting macrophage inflammation in plaques.

Project description:Subclinical hypothyroidism is associated with cardiovascular diseases, yet the underlying mechanism remains largely unknown. Herein, in a common population (n = 1,103), TSH level was found to be independently correlated with both carotid plaque prevalence and intima-media thickness. Consistently, TSH receptor ablation in ApoE -/- mice attenuated atherogenesis, accompanied by decreased vascular inflammation and macrophage burden in atherosclerotic plaques. These results were also observed in myeloid-specific Tshr-deficient ApoE -/- mice, which indicated macrophages to be a critical target of the proinflammatory and atherogenic effects of TSH. In vitro experiments further revealed that TSH activated MAPKs (ERK1/2, p38α, and JNK) and IκB/p65 pathways in macrophages and increased inflammatory cytokine production and their recruitment of monocytes. Thus, the present study has elucidated the new mechanisms by which TSH, as an independent risk factor of atherosclerosis, aggravates vascular inflammation and contributes to atherogenesis.

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LDL delivery of microbial small RNAs drives atherosclerosis through macrophage TLR8

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Analysis of gene expression in CD8+ T cells activated in vitro or in vivo

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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GM-CSF-activated STAT5A regulates macrophage functions and inflammation in atherosclerosis.

Project description:IntroductionInhibition of STAT5 was recently reported to reduce murine atherosclerosis. However, the role of STAT5 isoforms, and more in particular STAT5A in macrophages in the context of human atherosclerosis remains unknown.Methods and resultsHere, we demonstrate reciprocal expression regulation of STAT5A and STAT5B in human atherosclerotic lesions. The former was highly upregulated in ruptured over stable plaque and correlated with macrophage presence, a finding that was corroborated by the high chromosomal accessibility of STAT5A but not B gene in plaque macrophages. Phosphorylated STAT5 correlated with macrophages confirming its activation status. As macrophage STAT5 is activated by GM-CSF, we studied the effects of its silencing in GM-CSF differentiated human macrophages. STAT5A knockdown blunted the immune response, phagocytosis, cholesterol metabolism, and augmented apoptosis terms on transcriptional levels. These changes could partially be confirmed at functional level, with significant increases in apoptosis and decreases in lipid uptake and IL-6, IL-8, and TNFa cytokine secretion after STAT5A knockdown. Finally, inhibition of general and isoform A specific STAT5 significantly reduced the secretion of TNFa, IL-8 and IL-10 in ex vivo tissue slices of advanced human atherosclerotic plaques.DiscussionIn summary, we identify STAT5A as an important determinant of macrophage functions and inflammation in the context of atherosclerosis and show its promise as therapeutic target in human atherosclerotic plaque inflammation.

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