Role of vascular peroxidase 1 in senescence of endothelial cells in diabetes rats

Liu, Siyu; Yuan, Qiong; Li, Xiaohui; Hu, Chong; Hu, Rong; Zhang, Guogang; Li, Dai; Li, Yuan‐Jian

doi:10.1016/j.ijcard.2015.06.098

Cited by 16 publications

(14 citation statements)

References 35 publications

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“…Through the coordination between NOX and VPO1, the oxidative stress is markedly enhanced. Thus, the NOX/VPO1 pathway-mediated oxidative stress is reported to be involved in smooth muscle cell proliferation [34], cardiomyocyte or endothelial cell apoptosis, or senescence [18,35]. As expectedly, in the present study, with the upregulation of NOX2 and NOX4 in the RV of hypoxic PAH rats or hypoxia-treated H9c2 cells, VPO1 was also upregulated concomitant with an elevation in H 2 O 2 and HOCl production, indicating that the NOX/ VPO1 pathway-mediated oxidative stress contributes to the RV remodeling in PAH rats.…”

Section: Discussionmentioning

confidence: 99%

Magnesium Lithospermate B Derived from Salvia miltiorrhiza Ameliorates Right Ventricle Remodeling in Pulmonary Hypertensive Rats via Inhibition of NOX/VPO1 Pathway

Peng

Wang

et al. 2019

Planta Med

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Right ventricle (RV) remodeling is a major pathological feature in pulmonary arterial hypertension (PAH). Magnesium lithospermate B (MLB) is a compound isolated from the roots of Salvia miltiorrhiza and it possesses multiple pharmacological activities such as anti-inflammation and antioxidation. This study aims to investigate whether MLB is able to prevent RV remodeling in PAH and the underlying mechanisms. In vivo, SD rats were exposed to 10% O2 for 21 d to induce RV remodeling, which showed hypertrophic features (increases in the ratio of RV weight to tibia length, cellular size, and hypertrophic marker expression), accompanied by upregulation in expression of NADPH oxidases (NOX2 and NOX4) and vascular peroxidase 1 (VPO1), increases in hydrogen peroxide (H2O2) and hypochlorous acid (HOCl) production and elevation in phosphorylation levels of ERK; these changes were attenuated by treating rats with MLB. In vitro, the cultured H9c2 cells were exposed to 3% O2 for 24 h to induce hypertrophy, which showed hypertrophic features (increases in cellular size and hypertrophic marker expression). Administration of MLB or VAS2870 (a positive control for NOX inhibitor) could prevent cardiomyocyte hypertrophy concomitant with decreases in NOX (NOX2 and NOX4) and VPO1 expression, H2O2 and HOCl production, and ERK phosphorylation. Based on these observations, we conclude that MLB is able to prevent RV remodeling in hypoxic PAH rats through a mechanism involving a suppression of NOX/VPO1 pathway as well as ERK signaling pathway. MLB may possess the potential clinical value for PAH therapy.

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Section: Discussionmentioning

confidence: 99%

Magnesium Lithospermate B Derived from Salvia miltiorrhiza Ameliorates Right Ventricle Remodeling in Pulmonary Hypertensive Rats via Inhibition of NOX/VPO1 Pathway

Peng

Wang

et al. 2019

Planta Med

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“…High glucose concentration is important in the senescence of endothelial cells or endothelial dysfunction in T2DM rats because it can regulate miRNA activity. For example, high glucose concentration reduced EZH2 binding to the miRNA (miR‐101) locus, whereas EZH2‐β overexpression inhibited miR‐101 promoter activity in human foetal endothelial cells of the umbilical cord vein .…”

Section: Discussionmentioning

confidence: 99%

High glucose concentration induces endothelial cell proliferation by regulating cyclin‐D2‐related miR‐98

Liu

et al. 2016

J Cellular Molecular Medi

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Cyclin D2 is involved in the pathology of vascular complications of type 2 diabetes mellitus (T2DM). This study investigated the role of cyclin‐D2‐regulated miRNAs in endothelial cell proliferation of T2DM. Results showed that higher glucose concentration (4.5 g/l) significantly promoted the proliferation of rat aortic endothelial cells (RAOECs), and significantly increased the expression of cyclin D2 and phosphorylation of retinoblastoma 1 (p‐RB1) in RAOECs compared with those under low glucose concentration. The cyclin D2‐3′ untranslated region is targeted by miR‐98, as demonstrated by miRNA analysis software. Western blot also confirmed that cyclin D2 and p‐RB1 expression was regulated by miR‐98. The results indicated that miR‐98 treatment can induce RAOEC apoptosis. The suppression of RAOEC growth by miR‐98 might be related to regulation of Bcl‐2, Bax and Caspase 9 expression. Furthermore, the expression levels of miR‐98 decreased in 4.5 g/l glucose‐treated cells compared with those treated by low glucose concentration. Similarly, the expression of miR‐98 significantly decreased in aortas of established streptozotocin (STZ)‐induced diabetic rat model compared with that in control rats; but cyclin D2 and p‐RB1 levels remarkably increased in aortas of STZ‐induced diabetic rats compared with those in healthy control rats. In conclusion, this study demonstrated that high glucose concentration induces cyclin D2 up‐regulation and miR‐98 down‐regulation in the RAOECs. By regulating cyclin D2, miR‐98 can inhibit human endothelial cell growth, thereby providing novel therapeutic targets for vascular complication of T2DM.

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“…Similarly, a study performed in 156 PADpatients detected no correlation between MPO levels and ABI values [28]. Evidence linking VPO1 with atherosclerosis in humans is limited, with shortcomings in control for risk factors such as T2DM; nevertheless a previous study performed by Si-Yu Liu et al has considered VPO1 related to endothelial dysfunction and inflammation in diabetes [11]. However, mentioned investigation reporting upregulated VPO1 expression in cultured endothelial cells pre-treated with high glucose, did not address the reference range of glucose values relevant to clinical scenarios.…”

Section: Discussionmentioning

confidence: 97%

“…Pathophysiologically, VPO1 promotes oxidation of lowdensity lipoprotein (LDL) and mediates formation of foam cells, a hallmark of atherogenesis [10]. Moreover, VPO1 plays a role in endothelial dysfunction present in rats with T2DM [11]. Hypohalous acid-derived modification of renal tissues, specifically collagen IV networks, contributes to functional protein damage in experimental diabetic nephropathy models [12].…”

Section: Introductionmentioning

confidence: 99%

“…While several studies have been performed on the role of VPO1 at the cellular level or in animal models [10,11,13], data on an association of VPO1 with clinical parameters of humans under atherosclerotic conditions are missing. Increased concentrations of VPO1 are consistent among preclinical studies addressing cardiovascular disorders, but it is currently unclear whether an elevated level of circulating VPO1 accompanies severity of commonly available clinical markers of CVRF, in humans.…”

Section: Introductionmentioning

confidence: 99%

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Vascular peroxidase 1 is independently associated with worse kidney function in patients with peripheral artery disease

et al. 2020

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Background Oxidative stress is involved in cardiovascular disease such as peripheral artery disease (PAD). Vascular Peroxidase 1 (VPO1), a novel heme-containing peroxidase mainly expressed in the cardiovascular system, aggravates oxidative stress. Evidence in humans is limited. Current work aims to measure VPO1 in patients suffering from PAD, and to evaluate the association of VPO1 with conventional markers of cardiovascular risk factors (CVRF), including the estimated glomerular filtration rate (eGFR) and albuminuria categories. Methods This study is part of a longitudinal observational study. At baseline, 236 PAD-patients were included. VPO1 plasma levels (ng/mL) were measured by commercially available ELISA kits. A two-sided p level of < 0.05 was considered statistically significant. Results In the cross-sectional analysis (n = 236), VPO1 associated with ageing (p = 0.035) as well as with eGFR and albuminuria category, the markers of chronic kidney disease (CKD)-progression (p = 0.042). The longitudinal 18-months follow-up analysis (n = 152) demonstrated that baseline VPO1 predicts rapid kidney function decline (RKFD) (n = 49), defined as more than − 3 mL/min/1.73m 2 eGFR loss per year, (OR per one SD VPO1 1.60 (1.11-2.30); p = 0.009). This association between VPO1 and kidney function withstood the multivariable adjustment for traditional CVRF including baseline eGFR and urine albumin-to-creatinine ratio (UACR), (adjOR per one SD VPO1 1.73 (1.14-2.61); p = 0.046). Conclusion This study is first to reveal that VPO1 is independently associated with declining kidney function in patients with PAD. VPO1 shows a tighter association to kidney function than to other CVRF. This finding points to VPO1 as a potential target protein to assess CKD-progression.

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Role of vascular peroxidase 1 in senescence of endothelial cells in diabetes rats

Cited by 16 publications

References 35 publications

Magnesium Lithospermate B Derived from Salvia miltiorrhiza Ameliorates Right Ventricle Remodeling in Pulmonary Hypertensive Rats via Inhibition of NOX/VPO1 Pathway

Magnesium Lithospermate B Derived from Salvia miltiorrhiza Ameliorates Right Ventricle Remodeling in Pulmonary Hypertensive Rats via Inhibition of NOX/VPO1 Pathway

High glucose concentration induces endothelial cell proliferation by regulating cyclin‐D2‐related miR‐98

Vascular peroxidase 1 is independently associated with worse kidney function in patients with peripheral artery disease

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