Plasma Prolylcarboxypeptidase (Angiotensinase C) Is Increased in Obesity and Diabetes Mellitus and Related to Cardiovascular Dysfunction

Xu, Shaoyuan; Lind, Lars; Zhao, Liyan; Lindahl, Bertil

doi:10.1373/clinchem.2011.179291

Cited by 36 publications

(47 citation statements)

References 23 publications

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“…Of these Ehd2, Kctd15 and Prcp have previously been associated with obesity. 17,18,21 The gene encoding the transcription factor, IRF8, which is necessary for production of IgG2a and mounting a type 1 immune response 32 was hypomethylated and exhibited upregulated expression in obesity. This is in line with the finding that visceral adipose tissue inflammation and insulin resistance is dominated by a type 1 response.…”

Section: Discussionmentioning

confidence: 99%

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Obesity is associated with depot-specific alterations in adipocyte DNA methylation and gene expression

et al. 2017

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The present study aimed to identify genes exhibiting concomitant obesity-dependent changes in DNA methylation and gene expression in adipose tissues in the mouse using diet-induced obese (DIO) C57BL/6J and genetically obese ob/ob mice as models. Mature adipocytes were isolated from epididymal and inguinal adipose tissues of ob/ob and DIO C57BL/6J mice. DNA methylation was analyzed by MeDIP-sequencing and gene expression by microarray analysis. The majority of differentially methylated regions (DMRs) were hypomethylated in obese mice. Global methylation of long interspersed elements indicated that hypomethylation did not reflect methyl donor deficiency. In both DIO and ob/ob mice, we observed more obesity-associated methylation changes in epididymal than in inguinal adipocytes. Assignment of DMRs to promoter, exon, intron and intergenic regions demonstrated that DIO-induced changes in DNA methylation in C57BL/6J mice occurred primarily in exons, whereas inguinal adipocytes of ob/ob mice exhibited a higher enrichment of DMRs in promoter regions than in other regions of the genome, suggesting an influence of leptin on DNA methylation in inguinal adipocytes. We observed altered methylation and expression of 9 genes in epididymal adipocytes, including the known obesity-associated genes, Ehd2 and Kctd15, and a novel candidate gene, Irf8, possibly involved in immune type 1/type2 balance. The use of 2 obesity models enabled us to dissociate changes associated with high fat feeding from those associated with obesity per se. This information will be of value in future studies on the mechanisms governing the development of obesity and changes in adipocyte function associated with obesity.

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Section: Discussionmentioning

confidence: 99%

“…20 In line with this, elevated levels of serum PRCP have been described in obese subjects. 21 DNA methylation changes in diet-induced obesity associate with expression of genes involved in adipogenesis…”

Section: Obesity Is Associated With Hypomethylationmentioning

confidence: 99%

Obesity is associated with depot-specific alterations in adipocyte DNA methylation and gene expression

et al. 2017

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“…mononuclear / macrophages) via inducing vascular endothelial growth factor (VEGF) production and RAGE-NF-κB pathway activation (Heier et al, 2015;Yamagishi et al, 2009). Therefore, pro-inflammatory cytokines and chemokines may recruit neutrophil subsets in the vascular wall and promote microvascular inflammation through forming neutrophil extracellular traps (NETs) (a process termed NETosis) (Xu et al, 2012). However, the exact molecular mechanisms contributed in diabetes-induced vasculopathy via NETs are still not clear.…”

Section: Introductionmentioning

confidence: 99%

Is the neutrophil extracellular trap-driven microvascular inflammation essential for diabetes vasculopathy?

Berezin

2016

Biomed Res Ther

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Abstract-The neutrophil extracellular traps (NETs) are defined as an extensive web consisting decondensed chromatin, which is released from activated neutrophils, as well as cytotoxic proteins, histones and microbicidal proteases that cause tissue damage. NETs contribute to endothelial damage, inflammation, thrombosis, platelet aggregation, ischemia, that are essential players in the pathobiology of diabetic complications. The objective of the review is to highlight the possible role of NETosis in early diabetes-related vasculopathy beyond cardiovascular complications. Although the clinical significance of NETosis in diabetes beyond early atherosclerosis and cardiovascular complications is not still clear, there is limited data with respect to useful to use biological markers of NETosis aimed early stratification of the diabetics at risk of disease progression. Furthermore, several inductors of NETosis might be a target for novel pharmacological approaches to delay advance in diabetes and prevent diabetes-related vasculopathy.

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“…The interaction of AGEs with their receptor RAGE directly elicits proliferative, inflammatory, thrombotic and fibrotic reactions in variety of cells (i.e., mononuclears/macrophages) via inducing vascular endothelial growth factor (VEGF) production and RAGE-NF-κB pathway activation [6,7]. Therefore, pro-inflammatory cytokines and chemokines may recruit neutrophil subsets in the vasculature wall and promote microvascular inflammation through forming neutrophil extracellular traps (NETs) [8]. However, the exact molecular mechanisms contributed in diabetes-induced vasculopathy via neutrophil extracellular traps are still not clear.…”

Section: Introductionmentioning

confidence: 99%

The Neutrophil Extracellular Traps: The Missed Link between Microvascular Inflammation and Diabetes?

Berezin¹

2016

Metabolomics

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Microvascular inflammation is considered as a trigger for vasculopathy and early atherosclerosis development in diabetes mellitus. However, activated mononuclears/macrophages/neutrophils play a pivotal role in pathogenesis of vascular complications among individuals with diabetes mellitus. The neutrophil extracellular traps (NETs) have been known as a component of innate immune system for the last few decades. NETosis is induced by pathogens as well as other stimuli such as activated platelets, metabolic triggers, and oxidative stress components. In diabetes, neutrophils are primed to release NETs and die by NETosis. The objective of the mini review is to highlight the possible role of NETosis in early diabetes-related vasculopathy beyond cardiovascular complications.

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Plasma Prolylcarboxypeptidase (Angiotensinase C) Is Increased in Obesity and Diabetes Mellitus and Related to Cardiovascular Dysfunction

Cited by 36 publications

References 23 publications

Obesity is associated with depot-specific alterations in adipocyte DNA methylation and gene expression

Obesity is associated with depot-specific alterations in adipocyte DNA methylation and gene expression

Is the neutrophil extracellular trap-driven microvascular inflammation essential for diabetes vasculopathy?

The Neutrophil Extracellular Traps: The Missed Link between Microvascular Inflammation and Diabetes?

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