C-reactive protein down-regulates endothelial nitric oxide synthase expression and promotes apoptosis in endothelial progenitor cells through receptor for advanced glycation end-products

Chen, Jianfei; Jin, Jun; Song, Minbao; Dong, Hongmei; Zhao, Gan; Huang, Lan

doi:10.1016/j.gene.2011.12.039

Cited by 33 publications

(21 citation statements)

References 27 publications

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“…NOS3 transcripts are modulated by transcriptional and post-transcriptional modifications (22). We demonstrated that heteronuclear RNA levels (hnRNA), which serve as a surrogate measure of transcription rate were unchanged (Figure 2D).…”

Section: Resultsmentioning

confidence: 99%

IFN-α Negatively Regulates the Expression of Endothelial Nitric Oxide Synthase and Nitric Oxide Production: Implications for Systemic Lupus Erythematosus

Buie

Renaud

Muise‐Helmericks

et al. 2017

The Journal of Immunology

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Systemic lupus erythematosus (SLE) is a known risk factor for endothelial dysfunction. Murine and human lupus studies have implicated a role for IFNα in vascular abnormalities associated with impaired blood vessel dilation. However, the impact of IFNα on mediators that induce vasodilation and modulate inflammation including endothelial nitric oxide synthase (eNOS) and nitric oxide (NO) bioavailability are unknown. The objectives of this study were to determine how IFNα promotes endothelial dysfunction in SLE focusing on its regulation of eNOS and NO production in endothelial cells. We demonstrate that IFNα promotes an endothelial dysfunction signature in human umbilical vein endothelial cells (HUVECs), characterized by transcription suppression and mRNA instability of eNOS complemented by upregulation of MCP1 and VCAM1. These changes are associated with interferon-inducible gene expression. IFNα impairs insulin mediated NO production and Altered gene expression resulted from eNOS instability, possibly due to enhanced miR-155 expression. IFNα significantly impaired NO production in insulin stimulated HUVECs. IFNα treatment also lead to enhanced neutrophil adhesion. Our study introduces a novel pathway whereby IFNα serves as a pro-atherogenic mediator through repression of eNOS dependent pathways. This could promote development of endothelial dysfunction and cardiovascular disease in SLE.

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Section: Resultsmentioning

confidence: 99%

IFN-α Negatively Regulates the Expression of Endothelial Nitric Oxide Synthase and Nitric Oxide Production: Implications for Systemic Lupus Erythematosus

Buie

Renaud

Muise‐Helmericks

et al. 2017

The Journal of Immunology

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“…Diabetes is associated with continuous, low-level inflammation, leading to an increase in the prototype marker of inflammation, hs-CRP levels [41]. Notably, previous in vitro studies have demonstrated that hs-CRP, at concentrations known to predict adverse vascular outcomes, directly impairs EPC levels and function [42,43]. Therefore, it is easy to understand the inverse relationship between hs-CRP and EPC levels in diabetics found in the present study.…”

Section: Black Bars=cd45dimcd34+mentioning

confidence: 57%

Impact of prior chronic statin therapy and high-intensity statin therapy at discharge on circulating endothelial progenitor cell levels in patients with acute myocardial infarction: a prospective observational study

António

Fernandes

Soares

et al. 2014

Eur J Clin Pharmacol

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“…In addition, eNOS also plays a critical role in the angiogenic response. A reduction in eNOS expression is linked with reduced proliferation, migration and adhesion of EPCs and increased apoptosis [45]. In addition, eNOS increases the production of nitric oxide, which can induce angiogenic responses in vivo and is further induced by VEGF expression [46][47][48].…”

Section: Discussionmentioning

confidence: 99%

Impaired recovery of hind limb muscle perfusion following ischemic injury in rodents receiving B vitamin supplementation

Lee¹,

Desjardins²,

Sorokin³

et al. 2017

Blood Heart Circ

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C-reactive protein down-regulates endothelial nitric oxide synthase expression and promotes apoptosis in endothelial progenitor cells through receptor for advanced glycation end-products

Cited by 33 publications

References 27 publications

IFN-α Negatively Regulates the Expression of Endothelial Nitric Oxide Synthase and Nitric Oxide Production: Implications for Systemic Lupus Erythematosus

IFN-α Negatively Regulates the Expression of Endothelial Nitric Oxide Synthase and Nitric Oxide Production: Implications for Systemic Lupus Erythematosus

Impact of prior chronic statin therapy and high-intensity statin therapy at discharge on circulating endothelial progenitor cell levels in patients with acute myocardial infarction: a prospective observational study

Impaired recovery of hind limb muscle perfusion following ischemic injury in rodents receiving B vitamin supplementation

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