scholarly journals Protective Effect of Atorvastatin on Radiation-induced Vascular Endothelial Cell Injury In Vitro

2010 ◽  
Vol 51 (5) ◽  
pp. 527-533 ◽  
Author(s):  
Xin-Ze RAN ◽  
Xi RAN ◽  
Zhao-Wen ZONG ◽  
Deng-Qun LIU ◽  
Gui-Ming XIANG ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Protective Effect ◽  
Cell Injury ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Endothelial Cell Injury ◽  
Radiation Induced

scholarly journals LncRNA NORAD Promotes Vascular Endothelial Cell Injury and Atherosclerosis Through Suppressing VEGF Gene Transcription via Enhancing H3K9 Deacetylation by Recruiting HDAC6

2021 ◽  
Vol 9 ◽  
Author(s):  
Huihua Kai ◽  
Qiyong Wu ◽  
Ruohan Yin ◽  
Xiaoqiang Tang ◽  
Haifeng Shi ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Thoracic Aorta ◽  
Gene Transcription ◽  
Cell Injury ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Endothelial Cell Injury ◽  
Atherosclerosis Development

Coronary artery disease (CAD) is a major atherosclerotic cardiovascular disease and the leading cause of mortality globally. Long non-coding RNAs (lncRNAs) play crucial roles in CAD development. To date, the effect of lncRNA non-coding RNA activated by DNA damage (NORAD) on atherosclerosis in CAD remains unclear. The primary aim of this study was to investigate the effect of lncRNA NORAD on vascular endothelial cell injury and atherosclerosis. Here, ox-LDL-treated human umbilical vein endothelial cells (HUVECs) and high-fat-diet (HFD)-fed ApoE–/– mice were utilized as in vitro and in vivo models. The present study found that lncRNA NORAD expression was increased in ox-LDL-treated HUVECs and thoracic aorta of atherosclerotic mice, and knockdown of lncRNA NORAD alleviated vascular endothelial cell injury and atherosclerosis development in vitro and in vivo. Knockdown of lncRNA NORAD aggravated ox-LDL-reduced or atherosclerosis-decreased vascular endothelial growth factor (VEGF) expression in HUVECs and thoracic aorta of mice to ameliorate vascular endothelial cell injury and atherosclerosis development. Moreover, nucleus lncRNA NORAD suppressed VEGF gene transcription through enhancing H3K9 deacetylation via recruiting HDAC6 to the VEGF gene promoter in ox-LDL-treated HUVECs. In addition, VEGF reduced FUS (FUS RNA binding protein) expression by a negative feedback regulation in HUVECs. In summary, lncRNA NORAD enhanced vascular endothelial cell injury and atherosclerosis through suppressing VEGF gene transcription via enhancing H3K9 deacetylation by recruiting HDAC6. The findings could facilitate discovering novel diagnostic markers and therapeutic targets for CAD.

Multi-omics analysis reveals size-dependent toxicity and vascular endothelial cell injury induced by microplastic exposure in vivo and in vitro

2022 ◽  
Author(s):  
min zhang ◽  
jun shi ◽  
qiong huang ◽  
yi xie ◽  
ruihao wu ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Injury ◽  
Vascular System ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Endothelial Cell Injury ◽  
Size Dependent ◽  
Exposure In Vivo

Microplastics (MPs) pollution has gained increasing attention recently. Fewer studies have examined the effects of these small items on the vascular system. The aim of this work was to precisely...

Abstract 1563: Alpha1-adrenoceptor Autoantibody from Sera of Patients with Primary Hypertension Induced Vascular Endothelial Cell Injury

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Li Yan ◽  
Yanwu Xu ◽  
Xiangdong Wu ◽  
Guangzhao Yang ◽  
Jingyi Liu ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Caspase 3 ◽  
Cell Injury ◽  
Vascular Endothelial Cell ◽  
Primary Hypertension ◽  
Control Group ◽  
Vascular Endothelial ◽  
Endothelial Cell Injury ◽  
Apoptosis Index

Background: Vascular endothelial dysfunction is recognized as a characteristic of patients with primary hypertension, and accumulating evidence demonstrated that immunologic factor play an important role in the pathophysiology of hypertension. Previous study has shown that high level of alpha1-adrenoceptor autoantibody (alpha1-AA) existed in the sera of patients with primary hypertension and induced significant vasoconstrictive effects on arteries from important organs. However, whether alpha1-AA involves in vascular endothelial cell injury in hypertension remains unknown. Therefore, the aim of our present study is to explore the role of alpha1-AA in vascular endothelial cell injury in vitro . Methods: Alpha1-AA was purified from sera of patients with primary hypertension, and its purification, concentration and titer were detected by SDS-PAGE, BCA assay and ELISA, respectively. LDH release, Caspase-3, 8, 9 activity, apoptosis index (aridine orange and propidium iodide staining, AO/PI staining) and DNA damage (single cell gel electrophoresis assay, SCGE) in cultured HUVEC were examined after administration of alpha1-AA (1 μM) for 24h, respectively. Results: In alpha1-AA administration group, apoptosis index was significantly higher than that in control group(12.83 ± 1.19 % vs. 2.92 ± 0.57 %, P <0.01), caspase-3(2.67±0.21 nmol/h/mg protein vs. 0.95±0.28 nmol/h/mg protein, P <0.01) and caspase-8 (0.58±0.12 nmol/h/mg protein vs. 0.14±0.06 nmol/h/mg protein, P <0.01) activity were increased consistently, however, no remarkable change in caspase-9 activity; meanwhile, the autoantibody also resulted in more than 2.5-fold increase in LDH release ( P <0.01) and higher tail moment value of SCGE (15.42 ± 1.28 in alpha1-AA group vs. 1.59 ± 0.29 in control group, P <0.01) respectively. Conclusion: Our results indicated that alpha1-AA can induce DNA damage, pro-apoptotic and cytotoxic effect on vascular endothelial cell in vitro , which may contribute to the vascular injury in patients with primary hypertension. The results suggest that production of alpha1-AA is a novel risk factor in hypertensive patients and this auto-antibody may play an important role in the development of hypertension.

scholarly journals Microparticulate Caspase 1 Regulates Gasdermin D and Pulmonary Vascular Endothelial Cell Injury

2018 ◽  
Vol 59 (1) ◽  
pp. 56-64 ◽  
Author(s):  
Srabani Mitra ◽  
Matthew Exline ◽  
Fabien Habyarimana ◽  
Mikhail A. Gavrilin ◽  
Paul J. Baker ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Injury ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Endothelial Cell Injury ◽  
Caspase 1

scholarly journals Blocking the REDD1/TXNIP axis ameliorates LPS-induced vascular endothelial cell injury through repressing oxidative stress and apoptosis

2019 ◽  
Vol 316 (1) ◽  
pp. C104-C110 ◽  
Author(s):  
Xuhui Hou ◽  
Songbai Yang ◽  
Jian Yin
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cell ◽  
Cell Injury ◽  
Umbilical Vein ◽  
Vascular Endothelial Cell ◽  
Reactive Oxygen Species Generation ◽  
Vascular Endothelial ◽  
Interacting Protein ◽  
Endothelial Cell Injury ◽  
Lactate Dehydrogenase Release

The aim of the present study was to investigate the potential role of regulated in development and DNA damage response 1 (REDD1) in LPS-induced vascular endothelial injury by using human umbilical vein endothelial cells (HUVECs). We observed that REDD1 expression was apparently elevated in HUVECs after exposure to LPS. Additionally, elimination of REDD1 strikingly attenuated the secretion of the proinflammatory cytokines TNF-α, IL-6, IL-1β, and monocyte chemotactic protein-1 and the endothelial cell adhesion markers ICAM-1 and VCAM-1 that was induced by LPS stimulation. Subsequently, knockdown of REDD1 augmented cell viability but ameliorated lactate dehydrogenase release in HUVECs stimulated with LPS. Meanwhile, depletion of REDD1 effectively restricted LPS-induced HUVEC apoptosis, as exemplified by reduced DNA fragmentation, and it also elevated antiapoptotic Bcl-2 protein, concomitant with reduced levels of proapoptotic proteins Bax and cleaved caspase-3. Furthermore, repression of REDD1 remarkably alleviated LPS-triggered intracellular reactive oxygen species generation accompanied by decreased malondialdehyde content and increased the activity of the endogenous antioxidant enzymes superoxide dismutase, catalase, and glutathione peroxidase. Most important, depletion of REDD1 protected HUVECs against inflammation-mediated apoptosis and oxidative damage partly through thioredoxin-interacting protein (TXNIP). Collectively, these findings indicate that blocking the REDD1/TXNIP axis repressed the inflammation-mediated vascular injury process, which may be closely related to oxidative stress and apoptosis in HUVECs, implying that the REDD1/TXNIP axis may be a new target for preventing the endothelial cell injury process.

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