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Effect of MKP5 deletion in bone-marrow-derived macrophages on gene expression during oxidized-LDL stimulation

ABSTRACT: Effect of MKP5 deletion in bone-marrow-derived macrophages on gene expression during oxidized-LDL stimulation

PROVIDER: PRJNA1054983 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27295022_1.fastq.gz	Fastqsanger.gz
	SRR27295022_2.fastq.gz	Fastqsanger.gz
	SRR27295023_1.fastq.gz	Fastqsanger.gz
	SRR27295023_2.fastq.gz	Fastqsanger.gz
	SRR27295024_1.fastq.gz	Fastqsanger.gz

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Effect of MKP5 deletion in bone-marrow-derived macrophages on gene expression during oxidized-LDL stimulation

Project description:MKP-5 is a MAP kinase phosphatase that is responsible for the dephosphorylation of MAP kinases p-38 MAPK, JNK, and sometimes ERK. MKP-5 has been implicated in many diseases and its deletion results in increased inflammation. However, MKP-5 expression and regulation have not been studied in atherosclerosis, and our project aims to identify MKP-5 as a relevant gene in this disease. Specifically, we aim to identify the role of MKP-5 in the regulation of plaque stability. In atherosclerotic diseased states, oxidized LDL particles promote inflammatory mechanisms and form macrophage foam cells. We show that comparing wild-type and MKP-5-/- bone-marrow-derived macrophages stimulated with oxidized-LDL, results in the identification of significant gene expressions and major up- and down-regulated targeted pathways via bulk-RNA sequencing. Taken together, our data provides an unbiased way to test the mechanistic role of MKP-5 in an atherogenic environment. Furthermore, our data confirms and contributes to the current knowledge of gene expression influenced by MKP-5, as well as the influence of MKP-5 deletion on pathways critical to plaque stability including inflammation and collagen synthesis and deposition.

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Lectin-type oxidized LDL receptor 1 defines population of polymorphonuclear myeloid-derived suppressor cells in cancer patients

Project description:Polymorphonuclear myeloid-derived suppressor cells (PMN-MDSC) are important regulators of immune responses and promoters of tumor progression in cancer1,2. The heterogeneity of these cells as well as their distinction from neutrophils hampers the progress in understanding of the biology and clinical significance of these cells. PMN-MDSC had a distinct gene signature from neutrophils isolated from the same patients with most prominent changes in genes associated with endoplasmic reticulum (ER) stress response. Surprisingly, low-density lipoprotein (LDL) was one of the most enriched gene regulators and oxidized LDL receptor 1 (OLR1) was one of the most overexpressed genes in PMN-MDSC. Lectin-type oxidized LDL receptor 1 (LOX-1) encoded by OLR1 was expressed in only 0.7% of neutrophils in peripheral blood of healthy donors, whereas 5-15% of neutrophils in cancer patients and 15-50% of neutrophils in tumor tissues were LOX-1+. In contrast to their LOX-1- counterparts, LOX-1+ neutrophils had gene signature, biochemical and functional characteristics of PMN-MDSC. Induction of ER stress in neutrophils from healthy donors up-regulated LOX-1 expression and converted these cells to suppressive PMN-MDSC. Thus, PMN-MDSC have distinct gene signature and LOX-1 can define this population of cells, which may provide new insight to the biology and clinical evaluation of these cells. Examination of LOX1+/LOX1- and PMN/MDSC cells in cancer patient samples

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Expression data of human vascular smooth muscle cells (hVSMC) in response to n-LDL and ox-LDL.

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Expression data of human vascular smooth muscle cells (hVSMC) in response to n-LDL and ox-LDL.

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Transcription profiling of macrophages from Familial Hypercholesterolemia(FH) patients with tendon xanthomas (TX+) and without tendon xanthomas (TX-) to evaluate the gene expression profile in presence and absence of oxidized LDL

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