High glucose and interleukin 1β-induced apoptosis in human umbilical vein endothelial cells involves in down-regulation of monocarboxylate transporter 4

Wang, Dong; Wang, Qingjie; Yan, Gaoliang; Ye, Qiao; Zhu, Bingqian; Tang, Chengchun; Gu, Yuchun

doi:10.1016/j.bbrc.2015.09.016

Cited by 15 publications

(14 citation statements)

References 27 publications

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“…In addition, based on the degree of mucosal inflammation, we found that forty-three of 54 patients (79.6%) with lactate increased, but no difference among IBD grades ( Figure 1(b) ), which is attributed to various cells, including inflammatory cell, could produce lactate. In line with a study reported by Wang et al, HG and IL-1b decrease MCT4 and its location on plasma membrane as well as increase lactic acid accumulation and apoptosis in HUVECs [ 22 ], suggesting the critical role of inflammation in regulation of MCT4 expression. However, the expression of MCT4 in inflammatory bowel disease remains poorly understood.…”

Section: Resultssupporting

confidence: 90%

Evaluation of Monocarboxylate Transporter 4 in Inflammatory Bowel Disease and Its Potential Use as a Diagnostic Marker

Wang

Zhang³

et al. 2018

Disease Markers

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Background Monocarboxylate transporter 4 (MCT4), encoded by SLC16A3 gene, is responsible for exporting lactic acid into the extracellular microenvironment, and an acidic microenvironment promotes cytokine production and remodels chronic inflammation, providing a link from glycolysis to inflammatory bowel disease (IBD). Objective The aim of this study is to explore the value of MCT4 as a potential biomarker in IBD. Methods The study group consisted of 39 cases with UC and 15 cases with CD. The centration of lactate level in serum was assessed by blood gas analysis, and MCT4 expression was analyzed by IHC. Results Lactate level was increased in the forty-three of 54 patients (79.6%) with IBD by blood gas analysis compared with normal level (P < 0.001), in line with the result that showed increased MCT4 expression in inflamed colonic mucosa analyzed by immunohistochemistry. Most importantly, abundance of MCT4 expression was significantly associated with mucosal inflammation, which could be a clinical prognosis marker. Conclusion The data suggested that increased lactate level in blood was possibly due to highly expressed MCT4 expression caused by inflammation in intestinal mucosal epithelial tissue, which could be a prognosis indicator of IBD in children.

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Section: Resultssupporting

confidence: 90%

Evaluation of Monocarboxylate Transporter 4 in Inflammatory Bowel Disease and Its Potential Use as a Diagnostic Marker

Wang

Zhang³

et al. 2018

Disease Markers

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“…Aldose reductase inhibitors slightly suppressed Slc16a4 mRNA levels in the absence of TNF-α, and TNF-α stimulation resulted in an additional suppression, which was not affected by aldose reductase inhibitors ( Figure 7H). Consistently, MCT4 levels have been shown to be reduced by IL-1β in endothelial cells (39). TNF-α-induced GLUT1 also was not altered by aldose reductase inhibitors ( Figure 7I).…”

Section: Resultssupporting

confidence: 72%

Smooth muscle glucose metabolism promotes monocyte recruitment and atherosclerosis in a mouse model of metabolic syndrome

Wall¹,

Barnhart²,

Kanter³

et al. 2018

JCI Insight

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Metabolic syndrome contributes to cardiovascular disease partly through systemic risk factors. However, local processes in the artery wall are becoming increasingly recognized to exacerbate atherosclerosis both in mice and humans. We show that arterial smooth muscle cell (SMC) glucose metabolism markedly synergizes with metabolic syndrome in accelerating atherosclerosis progression, using a low-density lipoprotein receptor-deficient mouse model. SMCs in proximity to atherosclerotic lesions express increased levels of the glucose transporter GLUT1. Cytokines, such as TNF-α produced by lesioned arteries, promote GLUT1 expression in SMCs, which in turn increases expression of the chemokine CCL2 through increased glycolysis and the polyol pathway. Furthermore, overexpression of GLUT1 in SMCs, but not in myeloid cells, accelerates development of larger, more advanced lesions in a mouse model of metabolic syndrome, which also exhibits elevated levels of circulating Ly6Chi monocytes expressing the CCL2 receptor CCR2. Accordingly, monocyte tracing experiments demonstrate that targeted SMC GLUT1 overexpression promotes Ly6Chi monocyte recruitment to lesions. Strikingly, SMC-targeted GLUT1 overexpression fails to accelerate atherosclerosis in mice that do not exhibit the metabolic syndrome phenotype or monocytosis. These results reveal a potentially novel mechanism whereby arterial smooth muscle glucose metabolism synergizes with metabolic syndrome to accelerate monocyte recruitment and atherosclerosis progression.

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“…Hyperglycemia plays a central role in the pathogenesis of diabetic vascular complications [2,3], which are the leading cause of morbidity and mortality in patients with diabetes. At cellular level, high glucose can induce apoptotic response in endothelial cells and lead to endothelial damage [4]. Compelling evidence indicates a link between high glucose-induced apoptosis of endothelial cells and reactive oxygen species (ROS) production [5].…”

Section: Introductionmentioning

confidence: 99%

Upregulation of Periostin Prevents High Glucose-Induced Mitochondrial Apoptosis in Human Umbilical Vein Endothelial Cells via Activation of Nrf2/HO-1 Signaling

Zhong

Tang

2016

Cell Physiol Biochem

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Background/Aims: High glucose-induced oxidative damage to endothelial cells plays a central role in the pathogenesis of diabetic vascular complications. This study was undertaken to explore the role of periostin in high glucose-induced endothelial cell apoptosis and associated molecular mechanisms. Methods: Human umbilical vein endothelial cells (HUVECs) were exposed to high glucose (33.3 mmol/L) and examined for the expression of periostin. The effects of periostin upregulation on high glucose-induced apoptosis, mitochondrial dysfunction, and reactive oxygen species (ROS) production were determined. The activation of nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) by periostin was checked. HO-1 knockdown experiments were done to confirm its role in the action of periostin in high glucose-exposed HUVECs. Results: High glucose significantly upregulated the expression of periostin in HUVECs. Enforced expression of periostin attenuated high glucose-induced apoptosis in HUVECs, as determined by TUNEL staining and caspase-3 activity assay. Periostin overexpression prevented loss of Δψm, release of mitochondrial cytochrome c, and dysregulation of Bcl-2 and Bax in high glucose-exposed HUVECs. Periostin upregulation suppressed high glucose-induced ROS generation and activated the Nrf2/HO-1 signaling. HO-1 silencing restored high glucose-induced ROS generation and apoptotic response in periostin-overexpressing HUVECs. Conclusion: Periostin mitigates high glucose-induced mitochondrial apoptosis in endothelial cells, via activation of Nrf2/HO-1 signaling and reduction of ROS formation. Further studies are warranted to explore the therapeutic potential of periostin in diabetic vascular complications.

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High glucose and interleukin 1β-induced apoptosis in human umbilical vein endothelial cells involves in down-regulation of monocarboxylate transporter 4

Cited by 15 publications

References 27 publications

Evaluation of Monocarboxylate Transporter 4 in Inflammatory Bowel Disease and Its Potential Use as a Diagnostic Marker

Evaluation of Monocarboxylate Transporter 4 in Inflammatory Bowel Disease and Its Potential Use as a Diagnostic Marker

Smooth muscle glucose metabolism promotes monocyte recruitment and atherosclerosis in a mouse model of metabolic syndrome

Upregulation of Periostin Prevents High Glucose-Induced Mitochondrial Apoptosis in Human Umbilical Vein Endothelial Cells via Activation of Nrf2/HO-1 Signaling

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