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Mechanisms and consequences of myeloid adhesome dysfunction in atherogenesis I

ABSTRACT: Mechanisms and consequences of myeloid adhesome dysfunction in atherogenesis I

PROVIDER: PRJNA1071606 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27819600_1.fastq.gz	Fastqsanger.gz
	SRR27819600_2.fastq.gz	Fastqsanger.gz
	SRR27819601_1.fastq.gz	Fastqsanger.gz
	SRR27819601_2.fastq.gz	Fastqsanger.gz
	SRR27819602_1.fastq.gz	Fastqsanger.gz

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Mechanisms and consequences of myeloid adhesome dysfunction in atherogenesis II

Project description:Mechanisms and consequences of myeloid adhesome dysfunction in atherogenesis II

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Mechanisms and consequences of myeloid adhesome dysfunction in atherogenesis II

Project description:Exposure of macrophages to oxLDL in vitro or to oxidized lipids-rich milieu of atherosclerotic lesions induces dysregulation of multiple cellular processes including adhesome-dependent functions. Kindlin3 (K3) is indispensable for integrin activation and is directly involved in all adhesome-dependent cell functions. In the current study, we demonstrated that disturbance of the Kindlin3-integrin axis in myeloid cells leads to proatherogenic phenotype in hyperlipidemic LDLR-/- mice. We also found that lipid accumulation in macrophages in vivo in atherosclerotic plaque and in vitro after exposure to oxLDL was associated with strongly reduced K3 protein, likely contributing to deficient adhesome function of macrophages in lesions. RNA-seq analysis of BMDM isolated from K3 mutant with disrupted Itgβ binding site revealed multiple dysregulated adhesion-related genes and pathways overlapping with ones dysregulated in WT cells after oxLDL treatment. In addition, many dysregulated genes overlapped with genes involved in atherogenesis. These included dramatically increased expression of OLR1, a gene encoding Lectin-like oxidized LDL receptor-1 (LOX1). Disturbed Kindlin3-integrin axis in macrophages leads to dramatically increased level of LOX1 receptor in macrophages, providing a mechanism for increased uptake of oxLDL and foam cell formation. A similar proatherogenic phenotype, increased macrophage LOX1 and foam cell formation, was observed in Itgβ1 deficient mice but not Itgβ2 deficient mice, indicating that lack of Kindlin3/Itgβ1 interaction can be, at least partially, responsible for the observed phenotype.

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Mechanisms and consequences of myeloid adhesome dysfunction in atherogenesis I

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Mitochondrial dysfunction and consequences in calpain-3-deficient muscle

Project description:Mitochondrial dysfunction and consequences in calpain-3-deficient muscle

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Mitochondrial dysfunction and consequences in calpain-3-deficient muscle myoblasts

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Deficiency of myeloid PHD proteins aggravates atherogenesis via macrophage apoptosis and paracrine fibrotic signaling

Project description:Deficiency of myeloid PHD proteins aggravates atherogenesis via macrophage apoptosis and paracrine fibrotic signaling

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Macrophage-KLF6 signaling promotes experimental atherogenesis

Project description:Cardiovascular disease accounts for one in every four deaths in the United States and is the single largest cause of mortality around the world. The most common cause of cardiovascular-related deaths are due to development of occlusive atherosclerotic plaques. A hallmark event in the development of atherosclerotic plaque is the accumulation of lipid-laden macrophages in the subendothelial layers of affected blood vessels. Macrophages are key players in all stages of atherogenesis, including plaque initiation, growth, rupture, as well as healing of ruptured plaques. In this context, macrophages are the principal innate immune cells that modulate atherogenesis by engaging in various processes such as inflammation, extracellular matrix degradation, phagocytosis, and efferocytosis. Here, we report that macrophage Kruppel-like factor 6 (KLF6) deficiency attenuates pro-inflammatory gene expression and experimentally induced atherosclerotic plaque development. Our in vivo studies show that myeloid-KLF6 deficiency on Apoe-null background significantly curtails high-fat/high-cholesterol diet-induced atherosclerotic lesion formation and macrophage abundance in atherosclerotic plaques. Integrated transcriptomics and Gene Set Enrichment Analysis show that KLF6 deficiency significantly attenuates a large number of TNF-induced gene targets, and TNF-induced IFN response, IFN response, and inflammatory response signaling in macrophages. At the molecular level, KLF6 promotes IRF1 signaling to enhance TNF-induced pro-inflammatory gene expression in macrophages. Collectively, our analyses show that KLF6 promotes pro-inflammatory gene expression in macrophages and boosts experimentally induced atherosclerotic plaque formation in vivo.

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Macrophage-KLF6 signaling promotes experimental atherogenesis

Project description:Macrophage-KLF6 signaling promotes experimental atherogenesis

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Mechanisms of Treg cell dysfunction in activated mtDNANZB mice.

Project description:Mechanisms of Treg cell dysfunction in activated mtDNANZB mice.

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Deficiency of myeloid PHD proteins aggravates atherogenesis via macrophage apoptosis and paracrine fibrotic signaling [bulk RNA-seq]

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