Organ culture: a new model for vascular endothelium dysfunction

Abstract Objectives Vascular dementia (VaD), being strongly associated with metabolic conditions is a major health concern around the world. Diabetes is a major risk factor for the development of VaD. This study investigates the efficacy of quercetin and folacin in diabetes induced vascular endothelium dysfunction and related dementia. Methods Single dose streptozotocin (STZ) (50 mg/kg i.p) was administered to albino Wistar rats (male, 200–250 g) by dissolving in citrate buffer. Morris water maze (MWM) and attentional set shifting tests were used to assess the spatial learning, memory, reversal learning, and executive functioning in animals. Body weight, serum glucose, serum nitrite/nitrate, vascular endothelial function, aortic superoxide anion, brains’ oxidative markers (thiobarbituric acid reactive species-TBARS, reduced glutathione-GSH, superoxide dismutase-SOD, and catalase-CAT), mitochondrial enzyme complex (I, II, and IV), inflammatory markers (interleukin-IL-6, IL-10, tumor necrosis factor-TNF-α, and myeloperoxidase-MPO), and acetylcholinesterase activity-AChE were also assessed. Quercetin (30 mg kg−1/60 mg kg−1) and folacin (30 mg kg−1/60 mg kg−1) were used as the treatment drugs. Donepezil (0.5 mg kg−1) was used as a positive control. Results STZ administered rats showed reduction in learning, memory, reversal learning, executive functioning, impairment in endothelial function, increase in brains’ oxidative stress; inflammation; AChE activity, and decrease in mitochondrial complex (I, II, and IV) activity. Administration of quercetin and folacin in two different doses, significantly attenuated the STZ induced diabetes induced impairments in the behavioral, endothelial, and biochemical parameters. Conclusions STZ administration caused diabetes and VaD which was attenuated by the administration of quercetin and folacin. Therefore, these agents may be studied further for the assessment of their full potential in diabetes induced VaD conditions.

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Plasma phospholipid transfer protein prevents vascular endothelium dysfunction by delivering α‐tocopherol to endothelial cells

The FASEB Journal ◽

10.1096/fasebj.13.8.883 ◽

1999 ◽

Vol 13 (8) ◽

pp. 883-892 ◽

Cited By ~ 69

Author(s):

Catherine Desrumaux ◽

Valérie Deckert ◽

Anne Athias ◽

David Masson ◽

Gérard Lizard ◽

...

Keyword(s):

Endothelial Cells ◽

Vascular Endothelium ◽

Plasma Phospholipid ◽

Phospholipid Transfer Protein ◽

Endothelium Dysfunction ◽

Transfer Protein ◽

Phospholipid Transfer

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Endothelial progenitor cells in pathogenesis of new coronaviral infection

Medical Council ◽

10.21518/2079-701x-2021-4-199-204 ◽

2021 ◽

pp. 199-204

Author(s):

N. A. Kuzubova ◽

O. N. Titova ◽

E. S. Lebedeva ◽

E. V. Volchkova

Keyword(s):

Progenitor Cells ◽

Endothelial Progenitor Cells ◽

Vascular Endothelium ◽

Clinical Manifestations ◽

Endothelial Progenitor ◽

Hematopoietic Stem ◽

Damage Area ◽

Endothelium Dysfunction ◽

Pathogenic Factors ◽

And Migration

Pulmonary vascular endothelium dysfunction is one of the main pathogenic factors responsible for many clinical manifestations of the severe course of COVID-19. Circulating endothelial progenitor cells (EPCs) are the endogenous regenerative reserve that maintains the integrity of the vascular endothelium and its restoration in case of damage by pathogenic factors. A decrease in the circulating EPCs is regarded as a predictor of morbidity and mortality in conditions associated with development of endothelial dysfunction, including COVID-19. The exact phenotype of progenitor cells capable of differentiating into endothelial cells has not been determined. In most laboratories antigens CD133+, CD34+, VEGFR-2+ (CD 309) or combination of these are used to identify EPCs. The process of EPCs mobilization and migration is controlled by molecular signals from immune cells located in the damage area. Stromal cell factor 1 (SDF-1), produced by the bone marrow and many other tissues, is an important chemoattractant for EPCs which express its receptors. The results of studies carried out in 2020 indicate that SARS-Cov-2 infects both hematopoietic stem cells, transforming into EPCs, and directly circulating EPCs, causing inflammatory and procoagulant reactions that complicate the COVID-19 course. There is no consensus on the mechanism of EPCs infection with coronavirus – directly through the expression of angiotensin-converting enzyme (ACE2) receptor or through an ACE2-independent mechanism. Today there is no effective therapy for COVID-19. The use of the EPCs regenerative potential, and the search for ways to enhance the EPCs mobilization from the depot, and increase their functional activity may become a promising approach to the prevention of severe complications and mortality from COVID-19.

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Implication of protein tyrosine phophatase in vascular endothelium dysfunction

Atherosclerosis ◽

10.1016/j.atherosclerosis.2017.06.425 ◽

2017 ◽

Vol 263 ◽

pp. e133

Author(s):

Saurabh Sharma ◽

Manjeet Singh ◽

Pyare Lal Sharma

Keyword(s):

Vascular Endothelium ◽

Protein Tyrosine ◽

Endothelium Dysfunction

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Prevention of LDL α-tocopherol consumption, cholesterol oxidation, and vascular endothelium dysfunction by polyphenolic compounds from red wine

Atherosclerosis ◽

10.1016/s0021-9150(02)00189-2 ◽

2002 ◽

Vol 165 (1) ◽

pp. 41-50 ◽

Cited By ~ 20

Author(s):

Valérie Deckert ◽

Catherine Desrumaux ◽

Anne Athias ◽

Linda Duverneuil ◽

Viviane Palleau ◽

...

Keyword(s):

Vascular Endothelium ◽

Red Wine ◽

Polyphenolic Compounds ◽

Cholesterol Oxidation ◽

Endothelium Dysfunction

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Specific Features of Vascular Endothelium in Patients with Severe Forms of Inflammatory Bowel Diseases

Russian Journal of Gastroenterology Hepatology Coloproctology ◽

10.22416/1382-4376-2018-28-5-98-104 ◽

2018 ◽

Vol 28 (5) ◽

pp. 98-104

Author(s):

O. V. Khlynova ◽

E. A. Stepina

Keyword(s):

Endothelial Dysfunction ◽

Systemic Inflammation ◽

Vascular Endothelium ◽

Inflammatory Bowel Diseases ◽

Serum Markers ◽

Pathological Process ◽

Vascular Endothelial ◽

Endothelium Dysfunction ◽

Bowel Diseases ◽

Inflammatory Bowel

Aim.In this work, we set out to assess the specific features of vascular endothelium in patients suffering from severe (pan-ulcerative) and complicated forms of ulcerative colitis (UC) and Crohn’s disease (CD).Materials and methods.The research sample consisted in 65 patients with UC (n = 45) and CD (n = 20), who were either in the acute phase or had been diagnosed with such conditions for the first time. For assessing endothelial dysfunction (ED), we used such markers as levels of vascular endothelial growth factor (VEGF) in the blood serum and the number of plasma desquamated endotheliocytes (DEC).Results.The indicators of vascular endothelial dysfunction are shown to be significantly higher in patients with severe, pan-ulcerative forms of inflammatory bowel diseases (IBD). A statistically significant relationship has been established between ED indicators and the severity and localisation of the pathological process, the extra-intestinal manifestations and complications of the disease. A dependence of the endothelial dysfunction indicators on the UC endoscopic activity has been determined. A positive correlation between the levels of VEGF and DEC and the markers of systemic inflammation (ESR, CRP and fibrinogen) has been revealed.Conclusion. It is determined that, in IBD patients, endothelium dysfunction is manifested in an increase in the VEGF and DEC levels. The indicators of endothelial dysfunction are shown to be directly correlated with the serum markers of systemic inflammation. Therefore, VEGF and DEC values can be used not only as criteria for assessing the intensity of IBD, but also as predictors of a complicated disease course.

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Vascular Endothelium Dysfunction in REM Sleep Deprivation: Prelude to Cardiovascular Disease

International Journal of Cardiology ◽

10.1016/j.ijcard.2019.11.074 ◽

2019 ◽

Vol 297 ◽

pp. 27

Author(s):

W.A.N. Wan Ahmad ◽

L. Noordin ◽

T.F.A. Tengku Adnan ◽

S. Safuan ◽

C.B. Ab Aziz

Keyword(s):

Cardiovascular Disease ◽

Sleep Deprivation ◽

Rem Sleep ◽

Vascular Endothelium ◽

Rem Sleep Deprivation ◽

Endothelium Dysfunction

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1,8-Cineole Ameliorates LPS-Induced Vascular Endothelium Dysfunction in Mice via PPAR-γ Dependent Regulation of NF-κB

Frontiers in Pharmacology ◽

10.3389/fphar.2019.00178 ◽

2019 ◽

Vol 10 ◽

Cited By ~ 9

Author(s):

Ke-Gang Linghu ◽

Guo-Ping Wu ◽

Ling-Yun Fu ◽

Hong Yang ◽

Hai-Zhi Li ◽

...

Keyword(s):

Vascular Endothelium ◽

Endothelium Dysfunction ◽

Ppar Γ

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The impact of antiretroviral drugs in placental vascular endothelium dysfunction

Placenta ◽

10.1016/j.placenta.2017.07.163 ◽

2017 ◽

Vol 57 ◽

pp. 273-274 ◽

Cited By ~ 1

Author(s):

Onankoy Onyangunga ◽

Jagidesa Moodley ◽

Frederick Odun-Ayo ◽

Thajasvarie Naicker

Keyword(s):

Vascular Endothelium ◽

Antiretroviral Drugs ◽

Endothelium Dysfunction ◽

The Impact

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Effect of phosphatidylinositol 3-kinase-γ inhibitor CAY10505 in hypertension, and its associated vascular endothelium dysfunction in rats

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y2012-089 ◽

2012 ◽

Vol 90 (7) ◽

pp. 881-885 ◽

Cited By ~ 5

Author(s):

Sandeep Tyagi ◽

Saurabh Sharma ◽

Ramji Dass Budhiraja

Keyword(s):

Vascular Endothelium ◽

Specific Inhibitor ◽

Phosphatidyl Inositol ◽

Aortic Ring ◽

Vascular Endothelial ◽

Endothelial Lining ◽

Endothelium Dysfunction ◽

Nitrite Level ◽

Arterial Blood ◽

Endothelium Dependent Relaxation

This study has been designed to investigate the role of phosphatidyl-inositol 3-kinase-γ (PI3Kγ) in deoxycorticosterone acetate salt (DOCA) hypertension induced vascular endothelium dysfunction. Wistar rats were uninephrectomised and DOCA (40 mg·(kg body mass)−1, subcutaneous injection) was administered twice weekly for 6 weeks to produce hypertension. Rats with mean arterial blood pressure ≥ 140 mm Hg (1 mm Hg = 133.322 Pa) were selected as hypertensive. Vascular endothelium dysfunction was assessed in terms of attenuation of acetylcholine-induced endothelium-dependent relaxation (isolated aortic ring preparation), decrease in serum nitrate and (or) nitrite level, as well as reduced level of glutathione and disruption of integrity of vascular endothelium (histopathology). Five weeks of DOCA administration were followed by 7 days of daily administration of PI3Kγ inhibitor (5-[[5-(4-fluorophenyl)-2-furanyl]methylene]-2,4-thiazolidinedione (CAY10505), 0.6 mg·kg−1, per os (p.o.)), atorvastatin (30 mg·kg−1, p.o.), and losartan (25 mg·kg−1, p.o.) (positive control of hypertension), which significantly improved acetylcholine-induced endothelium dependent relaxation, serum nitrate and (or) nitrite level, glutathione level, and the vascular endothelial lining in hypertensive rats.Therefore, it may be concluded that CAY10505, a specific inhibitor of PI3Kγ, improves hypertension-associated vascular endothelial dysfunction. Thus, inhibition of PI3Kγ might be a useful approach in the therapeutics of vascular endothelium dysfunction.

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