scholarly journals Natural Antioxidants Improve the Vulnerability of Cardiomyocytes and Vascular Endothelial Cells under Stress Conditions: A Focus on Mitochondrial Quality Control

2021 ◽  
Vol 2021 ◽  
pp. 1-27
Author(s):  
Xing Chang ◽  
Zhenyu Zhao ◽  
Wenjin Zhang ◽  
Dong Liu ◽  
Chunxia Ma ◽  
...  
Keyword(s):  
Quality Control ◽  
Endothelial Cells ◽  
Cardiovascular Diseases ◽  
Vascular Endothelial Cells ◽  
Vascular Complications ◽  
Natural Antioxidants ◽  
Mitochondrial Morphology ◽  
Vascular Endothelial ◽  
Mitochondrial Quality Control ◽  
Main Site

Cardiovascular disease has become one of the main causes of human death. In addition, many cardiovascular diseases are accompanied by a series of irreversible damages that lead to organ and vascular complications. In recent years, the potential therapeutic strategy of natural antioxidants in the treatment of cardiovascular diseases through mitochondrial quality control has received extensive attention. Mitochondria are the main site of energy metabolism in eukaryotic cells, including myocardial and vascular endothelial cells. Mitochondrial quality control processes ensure normal activities of mitochondria and cells by maintaining stable mitochondrial quantity and quality, thus protecting myocardial and endothelial cells against stress. Various stresses can affect mitochondrial morphology and function. Natural antioxidants extracted from plants and natural medicines are becoming increasingly common in the clinical treatment of diseases, especially in the treatment of cardiovascular diseases. Natural antioxidants can effectively protect myocardial and endothelial cells from stress-induced injury by regulating mitochondrial quality control, and their safety and effectiveness have been preliminarily verified. This review summarises the damage mechanisms of various stresses in cardiomyocytes and vascular endothelial cells and the mechanisms of natural antioxidants in improving the vulnerability of these cell types to stress by regulating mitochondrial quality control. This review is aimed at paving the way for novel treatments for cardiovascular diseases and the development of natural antioxidant drugs.

PGI2 Production In Human Endothelial Cells Cultured In Diabetic And Nondiabetic Serum

1981 ◽  
Author(s):  
R C Paton ◽  
R Guillot ◽  
Ph Passa
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Vascular Complications ◽  
Proliferative Retinopathy ◽  
Vascular Endothelial ◽  
Human Endothelial Cells ◽  
Bovine Thrombin ◽  
Control Serum ◽  
Umbilical Cords ◽  
Cells Cultured

Reduced levels of prostaglandin I2 (PGI2) may contribute to the platelet hyper-reactivity and vascular complications found in diabetes mellitus. This study compared PGI2 production (PGI2-like activity and 6-keto-PGF1α levels) by vascular endothelial cells cultured in the presence of serum from 15 diabetics with proliferative retinopathy (5 treated by surgical hypophysectomy) and 15 sex-matched nondiabetic controls. Endothelial cells from human umbilical veins were cultured in M199 with either 20 % diabetic or control serum. At confluence, cultures were washed and stimulated with 0.1 NIH u/ml bovine thrombin. After 2 min incubation, the supernatant was tested for i)PGI2-like activity on ADP- induced platelet aggregation, results expressed as % inhibition and ii) 6-keto-PGF1α by radioimmunoassay, results expressed as nmol/ml. There was a significant correlation between PGI2-like activity and 6-keto-PGF-1α levels (r 0.78, p<0.001). The liberation of PGI2 from endothelial cells from different umbilical cords varied, but both PGI2-like activity (mean± SEM 21.9± 4.8 vs 28.3± 5.1 p<0.05) and 6-keto-PGF-1α (3.15± 0.68 vs 3.95 ±0.91 nmol/ml, p <0.05)were significantly lower in superantant from cells cultured in the presence of diabetic compared to control serum. PGI2 production was not significantly different in cells cultured with serum from hypophysectomised and nonhypophysectomised diabetics.These results suggest that serum from diabetics with proliferative retinopathy contains factors which impair the release or production of PGI2 by endothelial cells and that this effect is not mediated by the pituitary.

scholarly journals Effect of Hyperglycemia on Epcs Function and Regenerative Ability

2020 ◽  
Author(s):  
Hadeel Khalil Hendawi ◽  
Dina Nehad Awartani ◽  
Aya Ghoul ◽  
Isra Marei
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Barrier Function ◽  
Vascular Endothelial Cells ◽  
Vascular Dysfunction ◽  
Vascular Complications ◽  
Cardiovascular Complications ◽  
Diabetic Patients ◽  
Vascular Endothelial ◽  
Cell Functions

Diabetes induced hyperglycemia increases the risk of cardiovascular complications as it impacts vascular endothelial cells causing vascular dysfunction. Endothelial progenitor cells (EPCs) have been suggested to participate in the repair of vascular endothelial cells once they are impacted by hyperglycemia in diabetic patients. This research aims to test the EPC subtype blood outgrowth endothelial cells (BOECs) and their ability to survive and function under chronic hyperglycemic conditions. For that, we studied BOECs viability, response to shear stress, angiogenesis ability, and barrier function under normoglycemic (5.5mM) and hyperglycemic (25mM) conditions. The results have shown significant effects of chronic hyperglycemic conditions on cell proliferation (n=3, p<0.05), and migration (n=3, p<0.05) which were decreased when compared to control. Cells responses to shear stress were not affected under these conditions. There was a trend towards an increase in permeability as indicated by barrier function assays. The decrease in those endothelial cell functions might impact the repair mechanisms needed in diabetic patients to protect from vascular complications. Further investigations are required to establish therapeutic targets to improve EPCs repair function.

scholarly journals A GSK3-SRF Axis Mediates Angiotensin II Induced Endothelin Transcription in Vascular Endothelial Cells

2021 ◽  
Vol 9 ◽  
Author(s):  
Yuyu Yang ◽  
Huidi Wang ◽  
Hongwei Zhao ◽  
Xiulian Miao ◽  
Yan Guo ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Angiotensin Ii ◽  
Cardiovascular Diseases ◽  
Serum Response Factor ◽  
Vascular Endothelial Cells ◽  
Glycogen Synthase ◽  
Vascular Endothelial ◽  
Ang Ii ◽  
Over Expression ◽  
H3 Acetylation

Endothelin, encoded by ET1, is a vasoactive substance primarily synthesized in vascular endothelial cells (VECs). Elevation of endothelin levels, due to transcriptional hyperactivation, has been observed in a host of cardiovascular diseases. We have previously shown that serum response factor (SRF) is a regulator of ET1 transcription in VECs. Here we report that angiotensin II (Ang II) induced ET1 transcription paralleled activation of glycogen synthase kinase 3 (GSK3) in cultured VECs. GSK3 knockdown or pharmaceutical inhibition attenuated Ang II induced endothelin expression. Of interest, the effect of GSK3 on endothelin transcription relied on the conserved SRF motif within the ET1 promoter. Further analysis revealed that GSK3 interacted with and phosphorylated SRF at serine 224. Phosphorylation of SRF by GSK3 did not influence its recruitment to the ET1 promoter. Instead, GSK3-mediated SRF phosphorylation potentiated its interaction with MRTF-A, a key co-factor for SRF, which helped recruit the chromatin remodeling protein BRG1 to the ET1 promoter resulting in augmented histone H3 acetylation/H3K4 trimethylation. Consistently, over-expression of a constitutively active GSK enhanced Ang II-induced ET1 transcription and knockdown of either MRTF-A or BRG1 abrogated the enhancement of ET1 transcription. In conclusion, our data highlight a previously unrecognized mechanism that contributes to the transcriptional regulation of endothelin. Targeting this GSK3-SRF axis may yield novel approaches in the intervention of cardiovascular diseases.

Airborne Quinones Caused Cytotoxicity and DNA Damage in Human Vascular Endothelial Cells

2012 ◽  
Vol 610-613 ◽  
pp. 681-685
Author(s):  
Yu Shang ◽  
Ling Zhang ◽  
Lan Lan Fan
Keyword(s):  
Dna Damage ◽  
Endothelial Cells ◽  
Cardiovascular Diseases ◽  
Cell Viability ◽  
Vascular Endothelial Cells ◽  
Umbilical Vein ◽  
Membrane Damage ◽  
Ros Generation ◽  
Vascular Endothelial ◽  
Plasma Membrane Damage

Traffic-related particulate matter (PM) is found to be associated with adverse cardiovascular diseases. Quinones present in the traffic-related PM are hypothesized to contribute to these harmful effects through reactive oxygen species (ROS) generation. However, the impacts of the airborne quinones on the cytotoxic and genotoxic effects in human vascular endothelial cells are less well known. The aim of the present study is to assess whether exposure to three typical airborne quinones, including anthraquinone (AQ), 1,4-naphthroquinone (NQ) and benzoquinone (BQ), can induce cytotoxicity and DNA damage in the human umbilical vein endothelial cells (HUVEC). Cell viability, plasma membrane damage (lactate dehydrogenase leakage), and DNA damage were assessed in HUVEC after exposed to the three airborne quinones. Significant cytotoxicity was caused by the three quinones, indicating by the significant decrease in cell viability and significant increase in LDH activity. AQ and BQ slightly increased the DNA damage in HUVEC without significance. The ROS generation was not observed in HUVEC after exposed to AQ, NQ or BQ, suggesting that the cyototoxicity and the DNA damage caused by these quinones in HUVEC were not generated through the oxidative stress pathway. Our results suggest that AQ, NQ and BQ presented in the traffic-related particles may participate in the development of cardiovascular diseases through causing cytotoxicity and DNA damage in vascular endothelial cells.

New paradigms in inflammatory signaling in vascular endothelial cells

2014 ◽  
Vol 306 (3) ◽  
pp. H317-H325 ◽  
Author(s):  
Lei Xiao ◽  
Yahan Liu ◽  
Nanping Wang
Keyword(s):  
Endothelial Cells ◽  
Cardiovascular Diseases ◽  
Inflammatory Response ◽  
Vascular Endothelial Cells ◽  
Nuclear Factor Κb ◽  
Membrane Receptors ◽  
Vascular Endothelial ◽  
Intercellular Signaling ◽  
Inflammatory Signaling ◽  
New Class

Inflammation is a basic cellular process in innate and adaptive immunity. Vascular endothelial cells play an important role in the initiation, amplification, and resolution of the inflammatory response. Deregulated inflammatory response is implicated in a variety of cardiovascular diseases such as atherosclerosis, obesity, diabetes, and hypertension. Recent studies have made significant progresses in the understanding of the complex molecular pathways that mediate the pro- and anti-inflammatory signaling in endothelial cells (ECs). Specifically, a number of macromolecular complexes termed as signalosomes have been identified to integrate the proinflammatory signaling from the membrane receptors to key transcription factors such as nuclear factor-κB (NF-κB). Inflammasomes are associated with the pattern-recognition receptors such as Toll-like receptors (TLRs), nucleotide-binding oligomerization-domain (NOD)-like receptors (NLRs) to mediate innate immunity responses. Emerging evidence has also revealed that noncoding microRNAs constitute a new class of intra- and intercellular signaling molecules to modulate inflammation in ECs. Thus this article will briefly summarize these new mechanisms with a special emphasis in the context of cardiovascular diseases.

scholarly journals Protective Effect of Flavonoids from a Deep-Sea-Derived Arthrinium sp. against ox-LDL-Induced Oxidative Injury through Activating the AKT/Nrf2/HO-1 Pathway in Vascular Endothelial Cells

Marine Drugs ◽  
2021 ◽  
Vol 19 (12) ◽  
pp. 712
Author(s):  
Jia-Rong Hou ◽  
Yan-Hong Wang ◽  
Ying-Nan Zhong ◽  
Tong-Tong Che ◽  
Yang Hu ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cardiovascular Diseases ◽  
Deep Sea ◽  
Nuclear Translocation ◽  
Vascular Endothelial Cells ◽  
Umbilical Vein ◽  
Oxidative Injury ◽  
Vascular Endothelial ◽  
Level Increase ◽  
Induced Apoptosis

Oxidized low-density lipoprotein (ox-LDL)-induced oxidative injury in vascular endothelial cells is crucial for the progression of cardiovascular diseases, including atherosclerosis. Several flavonoids have been shown cardiovascular protective effects. Recently, our research group confirmed that the novel flavonoids isolated from the deep-sea-derived fungus Arthrinium sp., 2,3,4,6,8-pentahydroxy-1-methylxanthone (compound 1) and arthone C (compound 2) effectively scavenged ROS in vitro. In this study, we further investigated whether these compounds could protect against ox-LDL-induced oxidative injury in endothelial cells and the underlying mechanisms. Our results showed that compounds 1 and 2 inhibited ox-LDL-induced apoptosis and adhesion factors expression in human umbilical vein vascular endothelial cells (HUVECs). Mechanistic studies showed that these compounds significantly inhibited the ROS level increase and the NF-κB nuclear translocation induced by ox-LDL. Moreover, compounds 1 and 2 activated the Nrf2 to transfer into nuclei and increased the expression of its downstream antioxidant gene HO-1 by inducing the phosphorylation of AKT in HUVECs. Importantly, the AKT inhibitor MK-2206 2HCl or knockdown of Nrf2 by RNA interference attenuated the inhibition effects of these compounds on ox-LDL-induced apoptosis in HUVECs. Meanwhile, knockdown of Nrf2 abolished the effects of the compounds on ox-LDL-induced ROS level increase and the translocation of NF-κB to nuclei. Collectively, the data showed that compounds 1 and 2 protected endothelial cells against ox-LDL-induced oxidative stress through activating the AKT/Nrf2/HO-1 pathway. Our study provides new strategies for the design of lead compounds for related cardiovascular diseases treatment.

The Endothelial Cell and the Factor VIII Bypassing Activity of Prothrombin Complex Concentrate

1988 ◽  
Vol 60 (02) ◽  
pp. 226-229 ◽  
Author(s):  
Jerome M Teitel ◽  
Hong-Yu Ni ◽  
John J Freedman ◽  
M Bernadette Garvey
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Factor Viii ◽  
Prothrombin Complex Concentrate ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Monolayer Cultures ◽  
Coagulant Activity ◽  
Time Courses ◽  
Privileged Site

SummarySome classical hemophiliacs have a paradoxical hemostatic response to prothrombin complex concentrate (PCC). We hypothesized that vascular endothelial cells (EC) may contribute to this “factor VIII bypassing activity”. When PCC were incubated with suspensions or monolayer cultures of EC, they acquired the ability to partially bypass the defect of factor VIII deficient plasma. This factor VIII bypassing activity distributed with EC and not with the supernatant PCC, and was not a general property of intravascular cells. The effect of PCC was even more dramatic on fixed EC monolayers, which became procoagulant after incubation with PCC. The time courses of association and dissociation of the PCC-derived factor VIII bypassing activity of fixed and viable EC monolayers were both rapid. We conclude that EC may provide a privileged site for sequestration of constituents of PCC which express coagulant activity and which bypass the abnormality of factor VIII deficient plasma.

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