Delivery of small interfering RNA for inhibition of endothelial cell apoptosis by hypoxia and serum deprivation

Background/Aims: Atherosclerosis is a multifactorial chronic disease and is the main cause of death and impairment in the world. Endothelial injury and apoptosis play a crucial role in the onset and development of atherosclerosis. MicroRNAs (miRNAs) have been proven to be involved in the pathogenesis of atherosclerosis. However, studies of the functional role of apoptosis-related miRNAs in the endothelium during atherogenesis are limited. Methods: Cell injury and apoptosis were measured in five types of cells transfected with miR-1185 or co-transfected with miR-1185 and its inhibitor. Bioinformatics analysis and a luciferase reporter assay were used to confirm the targets of miR-1185. The effects of the targets of miR-1185 on endothelial apoptosis were determined using small-interfering RNA. Results: In this study, we first report that miR-1185 significantly promoted apoptosis in endothelial cells but not in vascular smooth muscle cells and macrophages. A mechanistic analysis showed that ultraviolet irradiation resistance-associated gene (UVRAG) and krev1 interaction trapped gene 1 (KRIT1), targets of miR-1185, mediated miR-1185-induced endothelial cell apoptosis. Conclusion: The results revealed the impact of miR-1185 on endothelial apoptosis, suggesting that miR-1185 may be a potential target for the prevention and treatment of atherosclerosis.

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A miRNA-101-3p/Bim axis as a determinant of serum deprivation-induced endothelial cell apoptosis

Cell Death and Disease ◽

10.1038/cddis.2017.219 ◽

2017 ◽

Vol 8 (5) ◽

pp. e2808-e2808 ◽

Cited By ~ 16

Author(s):

Ji-Hee Kim ◽

Dong-Keon Lee ◽

Joohwan Kim ◽

Seunghwan Choi ◽

Wonjin Park ◽

...

Keyword(s):

Endothelial Cell ◽

Cell Apoptosis ◽

Serum Deprivation ◽

Endothelial Cell Apoptosis

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Faculty Opinions recommendation of Tumor response to radiotherapy regulated by endothelial cell apoptosis.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1002261.195174 ◽

2003 ◽

Author(s):

Guy Laurent

Keyword(s):

Endothelial Cell ◽

Cell Apoptosis ◽

Tumor Response ◽

Endothelial Cell Apoptosis

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Faculty Opinions recommendation of Anthrax lethal toxin induces human endothelial cell apoptosis.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1018157.206656 ◽

2004 ◽

Author(s):

Charles Czuprynski

Keyword(s):

Endothelial Cell ◽

Cell Apoptosis ◽

Lethal Toxin ◽

Human Endothelial Cell ◽

Endothelial Cell Apoptosis ◽

Anthrax Lethal Toxin

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Uric acid promotes oxidative stress and enhances vascular endothelial cell apoptosis in rats with middle cerebral artery occlusion

Bioscience Reports ◽

10.1042/bsr20170939 ◽

2018 ◽

Vol 38 (3) ◽

Cited By ~ 12

Author(s):

Chengfu Song ◽

Xiangdong Zhao

Keyword(s):

Oxidative Stress ◽

Uric Acid ◽

Endothelial Cell ◽

Cell Apoptosis ◽

Vascular Endothelial Cell ◽

Artery Occlusion ◽

Vascular Endothelial ◽

Endothelial Cell Apoptosis ◽

Related Factors ◽

Cerebral Artery Occlusion

In patients with cerebral infarction (CI), elevated serum uric acid (UA) level may exacerbate the occurrence and development of carotid atherosclerosis (AS). Our study intended to explore the underlying mechanism. We enrolled 86 patients with CI, and divided them into four groups: Non-AS, AS-mild, AS-moderate, and AS-severe groups; the levels of UA and oxidative stress-related factors in serum were detected. The middle cerebral artery occlusion (MCAO) model was used to stimulate CI in rats, and different doses of UA were administrated. The levels of oxidative stress-related factors in serum were detected. Hematoxylin & eosin (H&E) staining was used to observe the morphological alterations, and the apoptotic cell death detection kit was used to detect apoptotic cells. Increased UA concentration and enhanced oxidative stress were found in AS patients. H&E staining results showed that UA treatment exacerbated morphological damage in rats with MCAO, promoted oxidative stress, and enhanced vascular endothelial cell apoptosis in rats with MCAO.

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Maternal Anti-HPA-1a Antibodies Increase Endothelial Cell Apoptosis and Permeability

Journal of Vascular Research ◽

10.1159/000515703 ◽

2021 ◽

pp. 1-9

Author(s):

Rima Dardik ◽

Ophira Salomon

Keyword(s):

Endothelial Cells ◽

Endothelial Cell ◽

Intracranial Hemorrhage ◽

Cell Apoptosis ◽

Endothelial Damage ◽

Αvβ3 Integrin ◽

Endothelial Cell Apoptosis ◽

Vascular Beds ◽

Alloimmune Thrombocytopenia

Intracranial hemorrhage (ICH) associated with fetal/neonatal alloimmune thrombocytopenia (FNAIT) is attributed mainly to endothelial damage caused by binding of maternal anti-HPA-1a antibodies to the αvβ3 integrin on endothelial cells (ECs). We examined the effect of anti-HPA-1a antibodies on EC function using 2 EC lines from different vascular beds, HMVEC of dermal origin and hCMEC/D3 of cerebral origin. Anti-HPA-1a sera significantly increased apoptosis in both HMVEC and hCMEC/D3 cells and permeability in hCMEC/D3 cells only. This increase in both apoptosis and permeability was significantly inhibited by a monoclonal anti-β3 antibody (SZ21) binding to the HPA-1a epitope. Our results indicate that (1) maternal anti-HPA-1a antibodies impair EC function by increasing apoptosis and permeability and (2) ECs from different vascular beds vary in their susceptibility to pathological effects elicited by maternal anti-HPA-1a antibodies on EC permeability. Examination of maternal anti-HPA-1a antibodies for their effect on EC permeability may predict potential ICH associated with FNAIT.

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