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Loss of PRMT2 in myeloid cells in normoglycemic mice phenocopies impaired regression of atherosclerosis in diabetic mice

ABSTRACT: Loss of PRMT2 in myeloid cells in normoglycemic mice phenocopies impaired regression of atherosclerosis in diabetic mice

PROVIDER: PRJNA841190 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19347018_1.fastq.gz	Fastqsanger.gz
	SRR19347018_2.fastq.gz	Fastqsanger.gz
	SRR19347019_1.fastq.gz	Fastqsanger.gz
	SRR19347019_2.fastq.gz	Fastqsanger.gz
	SRR19347020_1.fastq.gz	Fastqsanger.gz

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Loss of PRMT2 in myeloid cells in normoglycemic mice phenocopies impaired regression of atherosclerosis in diabetic mice

Project description:The goal of this study is to determine whether PRMT2 plays a causal role in the impairment of atherosclerosis regression in diabetes. We examined the consequence of deleting PRMT2 in myeloid cells during the regression of atherosclerosis in normal and diabetic mice. We found significant impairment of atherosclerosis regression under normoglycemic conditions in mice lacking PRMT2 (Prmt2-/-) in myeloid cells that mimic the decrease in regression of atherosclerosis in WT mice under diabetic conditions. This was associated with increased plaque macrophage retention. PRMT2-deficient plaque CD68+ cells under normoglycemic conditions showed increased expression of genes involved in cytokine signaling and inflammation compared to WT cells by RNA seq. Thus, the loss of PRMT2 is causally linked to impaired atherosclerosis regression.

2022-07-20 | GSE203523 | GEO

Loss of PRMT2 in myeloid cells in normoglycemic mice phenocopies impaired regression of atherosclerosis in diabetic mice.

Project description:The regression, or resolution, of inflammation in atherosclerotic plaques is impaired in diabetes. However, the factors mediating this effect remain incomplete. We identified protein arginine methyltransferase 2 (PRMT2) as a protein whose expression in macrophages is reduced in hyperglycemia and diabetes. PRMT2 catalyzes arginine methylation to target proteins to modulate gene expression. Because PRMT2 expression is reduced in cells in hyperglycemia, we wanted to determine whether PRMT2 plays a causal role in the impairment of atherosclerosis regression in diabetes. We, therefore, examined the consequence of deleting PRMT2 in myeloid cells during the regression of atherosclerosis in normal and diabetic mice. Remarkably, we found significant impairment of atherosclerosis regression under normoglycemic conditions in mice lacking PRMT2 (Prmt2-/-) in myeloid cells that mimic the decrease in regression of atherosclerosis in WT mice under diabetic conditions. This was associated with increased plaque macrophage retention, as well as increased apoptosis and necrosis. PRMT2-deficient plaque CD68+ cells under normoglycemic conditions showed increased expression of genes involved in cytokine signaling and inflammation compared to WT cells. Consistently, Prmt2-/- bone marrow-derived macrophages (BMDMs) showed an increased response of proinflammatory genes to LPS and a decreased response of inflammation resolving genes to IL-4. This increased response to LPS in Prmt2-/- BMDMs occurs via enhanced NF-kappa B activity. Thus, the loss of PRMT2 is causally linked to impaired atherosclerosis regression via a heightened inflammatory response in macrophages. That PRMT2 expression was lower in myeloid cells in plaques from human subjects with diabetes supports the relevance of our findings to human atherosclerosis.

| S-EPMC9283439 | biostudies-literature

Genomic profiling of type-1 adult diabetic and aged normoglycemic mice liver

Project description:Here we characterized and compared differential gene expression from diabetic and normoglycemic NOD mice and from aged and young-adults Balb/c mice. Total RNA from NOD diabetic (3 weeks with glicemia over 500mg/dl) and normoglycemic NOD mice from the same age was used. To compare the effects of aging in genomic expression, total RNA from young-adult Balb/c (9 weeks old) and middle-aged Balb/c (47 weeks old) were used.

2013-09-06 | E-GEOD-50613 | biostudies-arrayexpress

Hypoxia-inducible PRMT2 addiction in cancers

Project description:Hypoxia-inducible transcription factors (HIFs) are crucial transcription factors for cellular response to low oxygen levels, but the key mediators for their downstream transcription activation are not well characterized. We previously found that PRMT2 activates target gene expression through its methyltransferase activity on histone H3R8. Here we find that PRMT2 expression is activated by HIF1 at hypoxic conditions. And PRMT2 activity is widely required for hypoxia-induced transcription activation. Accordingly, PRMT2 inactivation alleviates hypoxia-induced glioblastoma progression and chemotherapeutic resistance. And PRMT2 expression is associated with hypoxia signature

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Genomic profiling of type-1 adult diabetic and aged normoglycemic mice liver

Project description:Here we characterized and compared differential gene expression from diabetic and normoglycemic NOD mice and from aged and young-adults Balb/c mice.

2013-09-06 | GSE50613 | GEO

Effect of depletion of PRMT2 on gene expression in the HL-60 acute myeloid leukemia cell line

Project description:Arginine methylation is catalyzed by protein arginine methyltransferases (PRMTs) and is involved in various cellular processes, including cancer development. PRMT2 expression is increased in several cancer types although its role in acute myeloid leukemia (AML) remains unknown. Here, we investigate the role of PRMT2 in a cohort of patients with AML, PRMT2 knockout AML cell lines as well as a Prmt2 knockout mouse model. In patients, low PRMT2 expressors are enriched for inflammatory signatures, including the NF-κB pathway, and show inferior survival. In keeping with a role for PRMT2 in control of inflammatory signaling, bone marrow-derived macrophages from Prmt2 KO mice display increased pro-inflammatory cytokine signaling upon LPS treatment. In PRMT2-depleted AML cell lines, aberrant inflammatory signaling has been linked to overproduction of IL6, resulting from a deregulation of the NF-κB signaling pathway, therefore leading to hyperactivation of STAT3. Together, these findings identify PRMT2 as a key regulator of inflammation in AML.

2024-05-17 | GSE266252 | GEO

Expression data from the transplanted mouse islets into hyperglycemic and normoglycemic mice at 6 hours post-transplantation

Project description:insulin treatment protects islets from the initial rapid loss that is usually observed after transplantation and positively affects the outcome of islet transplantation in Akita mice. To study the molecular mechanism underlying the improved islet survival, expression profile analyses was performed to analyze the differences between the grafts transplanted into hyperglycemic and normoglycemic mice at 6 hours post-transplantation Cells were harvested at grafts for RNA extraction and hybridization on Affymetrix microarrays. We performed gene expression profiles of the transplanted mouse islets into hyperglycemic and normoglycemic mice at 6 hours post-transplantation

2014-04-18 | E-GEOD-55764 | biostudies-arrayexpress

PRMT2 links histone H3R8 asymmetric dimethylation to oncogenic activation and tumorigenesis of glioblastoma

Project description:Here we show that PRMT2 is highly expressed in GBM, which is correlated with poor prognosis. The silencing of PRMT2 inhibits GBM cell growth and glioblastoma stem cell self-renewal in vitro and suppreses orthotopic tumor growth. Transcriptome analysis demonstrated that PRMT2 depletion leads to significant deregulation of genes mainly associated with cell cycle progression and pathways in cancer. In agreement with previously published results, we show that PRMT2 is responsible for H3R8 asymmetric methylation (H3R8me2a) and that H3R8me2a enrichment at promoters and enhancers is closely correlated with known active histone marks. Furthermore, we show that PRMT2-mediated H3R8me2a is required for the maintenance of target gene expression and that the catalytic activity of PRMT2 is required for its protumorigenic functions. Taken together, this study demonstrates that PRMT2 acts as a transcriptional co-activator for oncogenic gene expression programs in GBM pathogenesis and provides a rationale for PRMT2 targeting in aggressive gliomas.

2018-08-22 | GSE110424 | GEO

Expression data from the transplanted mouse islets into hyperglycemic and normoglycemic mice at 6 hours post-transplantation

2014-04-18 | GSE55764 | GEO

RNA-seq of dendritic cells isolated from normoglycemic and hyperglycemic mice

Project description:RNA-seq of dendritic cells isolated from normoglycemic and hyperglycemic mice

| PRJEB104339 | ENA