The protective effects of HGF against apoptosis in vascular endothelial cells caused by peripheral vascular injury

Tight Junctions (TJ) are important components of paracellular pathways, and their destruction enhances vascular permeability. Resolvin D1 (RvD1) is a novel lipid mediator that has treatment effects on inflammatory diseases, but its effect on inflammation induced increase in vascular permeability is unclear. To understand whether RvD1 counteracts the lipopolysaccharide (LPS) induced increase in vascular cell permeability, we investigated the effects of RvD1 on endothelial barrier permeability and tight junction reorganization and expression in the presence or absence of LPS stimulation in cultured Human Vascular Endothelial Cells (HUVECs). Our results showed that RvD1 decreased LPS-induced increased in cellular permeability and inhibited the LPS-induced redistribution of zo-1, occludin, and F-actin in HUVECs. Moreover, RvD1 attenuated the expression of IκBαin LPS-induced HUVECs. The NF-κB inhibitor PDTC enhanced the protective effects of RvD1 on restoration of occludin rather than zo-1 expression in LPS-stimulated HUVECs. By contrast, the ERK1/2 inhibitor PD98059 had no effect on LPS-induced alterations in zo-1 and occludin protein expressions in HUVECs. Our data indicate that RvD1 protects against impairment of endothelial barrier function induced by LPS through upregulating the expression of TJ proteins in HUVECs, which involves the IκBαpathway but not the ERK1/2 signaling.

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Sirt1 Inhibits Oxidative Stress in Vascular Endothelial Cells

Oxidative Medicine and Cellular Longevity ◽

10.1155/2017/7543973 ◽

2017 ◽

Vol 2017 ◽

pp. 1-8 ◽

Cited By ~ 51

Author(s):

Weijin Zhang ◽

Qiaobing Huang ◽

Zhenhua Zeng ◽

Jie Wu ◽

Yaoyuan Zhang ◽

...

Keyword(s):

Oxidative Stress ◽

Endothelial Cells ◽

Vascular Endothelial Cells ◽

Protective Role ◽

Vascular Endothelial ◽

Protective Effects ◽

Beneficial Effects ◽

Key Factor ◽

Antioxidative Stress

The vascular endothelium is a layer of cells lining the inner surface of vessels, serving as a barrier that mediates microenvironment homeostasis. Deterioration of either the structure or function of endothelial cells (ECs) results in a variety of cardiovascular diseases. Previous studies have shown that reactive oxygen species (ROS) is a key factor that contributes to the impairment of ECs and the subsequent endothelial dysfunction. The longevity regulator Sirt1 is a NAD+-dependent deacetylase that has a potential antioxidative stress activity in vascular ECs. The mechanisms underlying the protective effects involve Sirt1/FOXOs, Sirt1/NF-κB, Sirt1/NOX, Sirt1/SOD, and Sirt1/eNOs pathways. In this review, we summarize the most recent reports in this field to recapitulate the potent mechanisms involving the protective role of Sirt1 in oxidative stress and to highlight the beneficial effects of Sirt1 on cardiovascular functions.

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Protective Effect of Fenofibrate on Oxidative Stress-Induced Apoptosis in Retinal–Choroidal Vascular Endothelial Cells: Implication for Diabetic Retinopathy Treatment

Antioxidants ◽

10.3390/antiox9080712 ◽

2020 ◽

Vol 9 (8) ◽

pp. 712 ◽

Cited By ~ 1

Author(s):

Ying-Jung Hsu ◽

Chao-Wen Lin ◽

Sheng-Li Cho ◽

Wei-Shiung Yang ◽

Chung-May Yang ◽

...

Keyword(s):

Oxidative Stress ◽

Endothelial Cells ◽

Diabetic Retinopathy ◽

B Cell ◽

Cell Lymphoma ◽

Vascular Endothelial Cells ◽

B Cell Lymphoma ◽

Vascular Endothelial ◽

Protective Effects ◽

Amino Terminal

Diabetic retinopathy (DR) is an important microvascular complication of diabetes and one of the leading causes of blindness in developed countries. Two large clinical studies showed that fenofibrate, a peroxisome proliferator-activated receptor type α (PPAR-α) agonist, reduces DR progression. We evaluated the protective effects of fenofibrate on retinal/choroidal vascular endothelial cells under oxidative stress and investigated the underlying mechanisms using RF/6A cells as the model system and paraquat (PQ) to induce oxidative stress. Pretreatment with fenofibrate suppressed reactive oxygen species (ROS) production, decreased cellular apoptosis, diminished the changes in the mitochondrial membrane potential, increased the mRNA levels of peroxiredoxin (Prx), thioredoxins (Trxs), B-cell lymphoma 2 (Bcl-2), and Bcl-xl, and reduced the level of B-cell lymphoma 2-associated X protein (Bax) in PQ-stimulated RF/6A cells. Western blot analysis revealed that fenofibrate repressed apoptosis through cytosolic and mitochondrial apoptosis signal-regulated kinase-1 (Ask)-Trx-related signaling pathways, including c-Jun amino-terminal kinase (JNK) phosphorylation, cytochrome c release, caspase 3 activation, and poly (ADP-ribose) polymerase-1 (PARP-1) cleavage. These protective effects of fenofibrate on RF/6A cells may be attributable to its anti-oxidative ability. Our research suggests that fenofibrate could serve as an effective adjunct therapy for ocular oxidative stress-related disorders, such as DR.

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In vitro cytotoxicity of IgG antibodies on vascular endothelial cells from patients with endemic peripheral vascular disease in Taiwan

Atherosclerosis ◽

10.1016/s0021-9150(97)00272-4 ◽

1998 ◽

Vol 137 (1) ◽

pp. 141-147 ◽

Cited By ~ 10

Author(s):

H Yu

Keyword(s):

Endothelial Cells ◽

Vascular Disease ◽

Peripheral Vascular Disease ◽

Vascular Endothelial Cells ◽

In Vitro Cytotoxicity ◽

Vascular Endothelial ◽

Igg Antibodies ◽

Peripheral Vascular

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IL-17 produced by Th17 cells alleviates the severity of fungal keratitis by suppressing CX43 expression in corneal peripheral vascular endothelial cells

Cell Cycle ◽

10.1080/15384101.2018.1556059 ◽

2019 ◽

Vol 18 (3) ◽

pp. 274-287 ◽

Cited By ~ 6

Author(s):

Xiu-Hong Qin ◽

Xiang Ma ◽

Shi-Feng Fang ◽

Zhen-Zhen Zhang ◽

Jian-Min Lu

Keyword(s):

Endothelial Cells ◽

Th17 Cells ◽

Vascular Endothelial Cells ◽

Fungal Keratitis ◽

Vascular Endothelial ◽

Peripheral Vascular ◽

Cx43 Expression

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Bone Marrow–Derived MicroRNA‐223 Works as an Endocrine Genetic Signal in Vascular Endothelial Cells and Participates in Vascular Injury From Kawasaki Disease

Journal of the American Heart Association ◽

10.1161/jaha.116.004878 ◽

2017 ◽

Vol 6 (2) ◽

Cited By ~ 16

Author(s):

Maoping Chu ◽

Rongzhou Wu ◽

Shanshan Qin ◽

Wenfeng Hua ◽

Zhen Shan ◽

...

Keyword(s):

Bone Marrow ◽

Endothelial Cells ◽

Kawasaki Disease ◽

Vascular Injury ◽

Vascular Endothelial Cells ◽

Vascular Endothelial ◽

Genetic Signal

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Protective effects of Histidine-rich glycoprotein on human vascular endothelial cells

Proceedings for Annual Meeting of The Japanese Pharmacological Society ◽

10.1254/jpssuppl.wcp2018.0_po3-3-52 ◽

2018 ◽

Vol WCP2018 (0) ◽

pp. PO3-3-52

Author(s):

Yuan Gao ◽

Hidenori Wake ◽

Keyue Liu ◽

Kiyoshi Teshigawara ◽

Shuji Mori ◽

...

Keyword(s):

Endothelial Cells ◽

Vascular Endothelial Cells ◽

Vascular Endothelial ◽

Protective Effects

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Cordycepin Attenuates Palmitic Acid-Induced Inflammation and Apoptosis of Vascular Endothelial Cells through Mediating PI3K/Akt/eNOS Signaling Pathway

The American Journal of Chinese Medicine ◽

10.1142/s0192415x21500804 ◽

2021 ◽

pp. 1-20

Author(s):

Chang-Wen Ku ◽

Tsung-Jung Ho ◽

Chih-Yang Huang ◽

Pei-Ming Chu ◽

Hsiu-Chung Ou ◽

...

Keyword(s):

Endothelial Cells ◽

Palmitic Acid ◽

Signaling Pathway ◽

Inflammatory Responses ◽

Vascular Endothelial Cells ◽

Cordyceps Sinensis ◽

Ros Generation ◽

Vascular Endothelial ◽

Protective Effects ◽

Anti Inflammatory

A well-known medicinal mushroom in the field of traditional Chinese medicine, Cordyceps sinensis, is a rare natural-occurring entomopathogenic fungus, and it typically grows at high altitudes on the plateau of the Himalayan. Previous studies indicated that cordycepin, the main bioactive chemical of Cordyceps sinensis, has very potent anticancer, anti-oxidant and anti-inflammatory activities. However, its protective effects against atherosclerotic changes in vascular endothelial cells have not been fully elucidated. In this study, we showed that pretreatment with cordycepin significantly attenuated palmitic acid (PA)-induced cytotoxicity, reactive oxygen species (ROS) generation, and inflammatory responses. We found that PA decreased phosphorylation of Akt, eNOS, and bioavailability of nitric oxide (NO), which in turn activated NF-[Formula: see text]B and the downstream inflammatory responses. All these detrimental events were markedly blocked by pretreatment with cordycepin. Moreover, cordycepin ameliorated destabilization of mitochondrial permeability, cytosolic calcium rises, and apoptotic features caused by PA. In addition, all these anti-inflammatory and anti-apoptosis effects of cordycepin were found to be inhibited by the PI3K and eNOS inhibitor, suggesting that its anti-atherosclerotic effects may partially be mediated by the PI3K/Akt/eNOS signaling pathway.

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