Domain I-IV of β2-glycoprotein I inhibits advanced glycation end product-induced angiogenesis by down-regulating vascular endothelial growth factor 2 signaling

Wang, Qianqian; Zhou, Saijun; Meng, Zhenxing; Wang, Jie; Chen, Rui; Lin, Liang‐Chuan; Li, Chun‐Jun; Yu, Di; Yu, Pei

doi:10.3892/mmr.2014.2970

Cited by 6 publications

(2 citation statements)

References 24 publications

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“…The phosphorylated Akt could increase the production of NO [ 21 ]. However, NO is significantly reduced in high glucose treated glomerular mesangial cells, indicating the fact that high-glucose treatment caused glomerular mesangial cells VEGF-NO axis uncoupled, which coincides with previous research [ 20 , 22 ].…”

Section: Discussionsupporting

confidence: 92%

Reduced β2GPI Inhibiting Glomerular Mesangial Cells VEGF-NO Axis Uncoupling Induced by High Glucose

Zhou

Wang

et al. 2018

BioMed Research International

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VEGF-NO axis uncoupling is an important pathogenesis for DN. Reduced β2GPI could play a part in VEGF signaling pathway and has a protective effect on diabetic vascular disease. This study investigates the effect of reduced β2GPI on glomerular mesangial cells VEGF-NO axis uncoupling induced by high glucose. Compared to control group, glomerular mesangial cell line HBZY-1 cells treated with high glucose expressed higher levels of VEGF mRNA and protein and produced more ROS but less NO. The related proteins related to VEGF-NO axis were assayed. High glucose could significantly increase the expression of the level of VEGFR2 and obviously increase phosphorylation of Akt and eNOS but significantly decrease the expression of GTP cyclohydrolase 1 (GCH-1), reducing the production of eNOS dimer. Both β2GPI and reduced β2GPI partly reverse these effects caused by high glucose. Reduced β2GPI had stronger effect than β2GPI. GCH-1 is the speed limit of tetrahydrobiopterin (BH4) synthesis enzyme. As the key part of eNOS cofactors, BH4 could partly restore eNOS dimer induced by high glucose. Our results indicated that high glucose could interfere with eNOS dimer formation. β2GPI and reduced β2GPI can partly reverse the VEGF-NO axis uncoupling by restoring the GCH-1 expression level and then promote eNOS dimer formation.

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Section: Discussionsupporting

confidence: 92%

Reduced β2GPI Inhibiting Glomerular Mesangial Cells VEGF-NO Axis Uncoupling Induced by High Glucose

Zhou

Wang

et al. 2018

BioMed Research International

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“…Two forms of β2GPI both exist in vivo. Studies have found that β2GPI is involved in atheromatous plaque formation, oxidative stress, apoptosis and many other biological or pathological processes [13][14][15][16][17][18]. However, the role of R-β2GPI in cardiovascular diseases remains unknown.…”

Section: Introductionmentioning

confidence: 99%

Reduced β2-glycoproteinI Alleviated Rat Myocardial Ischemia/Reperfusion Injury via Mitochondrial Protection and Inhibition of Apoptosis

Zhou¹,

Meng²,

Xiao³

et al. 2020

Preprint

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BackgroundMyocardial ischemia/reperfusion (I/R) injury is one of the most important reasons for death of coronary heart disease after vascular recanalization. New evidences have shown that β2-glycoprotein I (β2GPI) plays a protective role in cardiovascular diseases. This study aims to evaluate the effects of reduced β2GPI (R-β2GPI), one form of β2GPI, on myocardial I/R injury, and to explore related mechanisms. MethodsThe in vivo myocardial I/R models of Sprague Dawley rats and in vitro hypoxia/reoxygenation(H/R) models of H9c2 cells were established. The myocardial infarction and morphological changes in SD rats were measured by the TTC staining and HE staining. Creatine kinase-MB (CK-MB) and cardiac troponin I (cTnI) levels in plasma were detected by ELISA Assay kit. Terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL) method and caspase-3 colorimetric assay kit were used to determine myocardial apoptosis. Intracellular reactive oxygen species (ROS) generation and mitochondrial membrane potential of H9c2 cells were measured by fluorescent probe DCFH-DA and JC-1 fluorescent staining respectively. To evaluate cell damage, cell viability was assessed by determining the release of lactate dehydrogenase (LDH). The ratio of Bcl-2/Bax at mRNA level was detected by reverse transcription-polymerase chain reaction (RT-PCR). Western blot analysis was used to detect the expression levels of total Akt and phosphorylated Akt as well as the expression levels of total GSK-3βand phosphorylated GSK-3β in H9c2 cells. ResultsOur results suggested that R-β2GPI improved I/R model rats’ heart function, decreased infarct size, reduced serum CK-MB, cTnI levels, cell apoptosis and caspase3 activity. In vitro, R-β2GPI decreased LDH leakage, reduced ROS generation, maintained mitochondrial membrane potential and increased bcl-2/bax mRNA ratio; increased phosphorylation of Akt and GSK-3β in H9c2 cells following Hypoxia/Reoxygenation (H/R) jnjury. ConclusionR-β2GPI alleviated myocardial I/R (or H/R) injury by reducing oxidative stress and inhibiting mitochondrial apoptotic pathway via increasing the phosphorylation of Akt/GSK-3β.

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In vitro glycation of an endothelialized and innervated tissue-engineered skin to screen anti-AGE molecules

Cadau¹,

Leoty-Okombi²,

Pain³

et al. 2015

Biomaterials

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Domain I-IV of β2-glycoprotein I inhibits advanced glycation end product-induced angiogenesis by down-regulating vascular endothelial growth factor 2 signaling

Cited by 6 publications

References 24 publications

Reduced β2GPI Inhibiting Glomerular Mesangial Cells VEGF-NO Axis Uncoupling Induced by High Glucose

Reduced β2GPI Inhibiting Glomerular Mesangial Cells VEGF-NO Axis Uncoupling Induced by High Glucose

Reduced β2-glycoproteinI Alleviated Rat Myocardial Ischemia/Reperfusion Injury via Mitochondrial Protection and Inhibition of Apoptosis

In vitro glycation of an endothelialized and innervated tissue-engineered skin to screen anti-AGE molecules

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