• YAKHAK HOEJI
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• v.56 no.3
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• pp.180-185
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• 2012

The aim of present study was to investigate the possible influence and related mechanism of alcohol on the arterial contraction. Vascular contraction involves the activation of thick or thin filament pathway. However, there are no reports addressing the question whether this pathway is involved in alcohol-induced regulation. We hypothesized that alcohol plays a role in vascular contraction evoked by a vasoconstrictor in rat aortae regardless of endothelial function. Denuded arterial rings from male rats were used and isometric contractions were recorded using a computerized data acquisition system. Interestingly, alcohol at a low concentration (3% v/v) inhibited thromboxane $A_2$ or phorbol ester-induced contraction with endothelial function but at a high concentration (10%) didn't inhibit and rather increased the contraction in the denuded muscle. Therefore, alcohol at a low concentration decreases the contraction and alcohol at a high concentration increases the contraction suggesting that additional pathways different from endothelial nitric oxide synthesis might be involved in the regulation of contractility. In conclusion, alcohol has some effect on the regulation of contractility regardless of endothelial function.

• Korean Journal of Exercise Nutrition
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• v.23 no.2
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• pp.7-12
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• 2019

[Purpose] Eccentric exercise induces a decrease in vascular endothelial function. Curcumin, a major component of turmeric, has potent antioxidant and anti-inflammatory properties that are associated with vascular protective effects. The present study examined the effect of acute supplementation of curcumin on eccentric exercise-induced endothelial dysfunction in healthy young men. [Methods] Fourteen healthy sedentary young men (range, 21-29 years) were assigned to either the curcumin (n = 6) or placebo (n = 8) group. All subjects consumed either curcumin or placebo before exercise, and eccentric exercise of the elbow flexors was performed with their nondominant arm. Before and 60 min after exercise, brachial artery flow-mediated dilation (FMD), as an indicator of endothelial function, was measured in the non-exercised arm. [Results] Brachial artery FMD significantly decreased following eccentric exercise (p < 0.05) in the placebo group, but acute supplementation with curcumin before exercise nullified this change. The change in FMD before and after eccentric exercise between the placebo and curcumin groups was significantly different (p < 0.05). [Conclusion] The present study found that acute curcumin supplementation could attenuate the decrease in endothelial function, as measured by FMD, following eccentric exercise in healthy young men.

• The Korean Journal of Physiology and Pharmacology
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• v.18 no.2
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• pp.177-182
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• 2014

This study was to determine the correlation between endothelial function and neuro-endocrine-immune (NEI) network through observing the changes of NEI network under the different endothelial dysfunction models. Three endothelial dysfunction models were established in male Wistar rats after exposure to homocysteine (Hcy), high fat diet (HFD) and Hcy+HFD. The results showed that there was endothelial dysfunction in all three models with varying degrees. However, the expression of NEI network was totally different. Interestingly, treatment with simvastatin was able to improve vascular endothelial function and restored the imbalance of the NEI network, observed in the Hcy+HFD group. The results indicated that NEI network may have a strong association with endothelial function, and this relationship can be used to distinguish different risk factors and evaluate drug effects.

• The Journal of Korean Medicine
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• v.21 no.4
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• pp.193-203
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• 2000

Objectives : Hindered barrier function of vascular endothelium has been implicated in the initiation and progression of degenerative vascular diseases such as atherosclerosis. In this study, the effect of Sunghyangchungisan(SHCS) as a protectant against oxidant-induced destruction of endothelial barrier function was assessed. Methods : Toward this end, endothelial cells derived from the human umbilical vein were cultured as monolayers on permeable membrane filters. Endothelial permeability was monitored by measuring transendothelial electrical resistance and movement of low density lipoprotein (LDL) across the endothelial monolayer. Results : Along with increased movement of LDL, $H_2O_2$-induced increase in endothelial permeability was paralleled by a decrease in transendotheliaI electrical resistance. The effect of $H_2O_2$ was mimicked by phorbol 12-myristate 13-acetate (PMA), a potent activator of proteinkinase C. Calphostin-C, a protein kinase C inhibitor, effectively blocked the increase in endothelial permeability induced by $H_2O_2$ or PMA, indicating that activation of protein kinase C is associated with the $H_2O_2-induced$ permeability change. SHCS effectively protected the endothelial monolayer against $H_2O_2-induced$ increase in permeability, whereas, it did not affect PMA-induced change. Forskolin, a potent activator of adenylyl cyclase, antagonized $H_2O_2$ to increase endothelial permeability. In addition, in ${H_2O_2}-treated$ cens, intracenular cAMP concentration was significantly decreased, indicating that impaired cAMP production as well as activation of proteinkinase C is a mechanism underlying ${H_2O_2}>-induced$$H_2O_2$ with regard to its effect on intracellular cAMP content. However, SHCS itself did not affect resting cAMP concentration in endothelial cells. Conclusions : These results suggest that SHCS might operate as an effective protectant against oxidant-induced destruction of endothelial barrier function. The mechanism does not appear to involve direct interaction with protein kinase C- or cAMP-associated signaling mechanism.

• IMMUNE NETWORK
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• v.8 no.3
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• pp.75-81
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• 2008

Background: Platelets take part in repairing the lesions of endothelial damage. To understand the molecular mechanism of this process, we tested the hypothesis that CD154 expressed on activated platelets stimulates proliferation of human endothelial cells. Methods: The expression levels of CD154 and CD40 on platelets and endothelial cells, respectively, were measured by flow cytometry and confocal microscopy. Function-blocking monoclonal antibody against CD154 was developed after immunization with CD154-transfected L cells. Results: An anti-CD40 agonist antibody and soluble CD154 both induced significant proliferation of endothelial cells. In addition, a function-blocking anti-CD154 antibody inhibited the platelet-induced proliferation of endothelial cells, indicating that the CD154-CD40 pathway is involved in these cellular interactions. An anti-VEGF antibody failed to inhibit the proliferation. This, in addition to the fact that very small amounts of VEGF are released from platelets or endothelial cells, suggests that VEGF does not play an important role in the platelet-stimulated proliferation of endothelial cells. Conclusion: Our results indicate that platelets induce proliferation of endothelial cells by CD154-CD40 interactions independently of VEGF.

• Journal of Biomedical Engineering Research
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• v.17 no.2
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• pp.255-262
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• 1996

Antithrombogenic surFace is one of the most important things to the artificial vascular prostheses. This problem will be solved if the surface of prosthesis is covered with endothelial cells. The attachment and the growth of endothelial cells onto vascular prosthesis are very difficult. So many studies have been concentrated on the attachement of endothelial cell. But no good performance of the in uiwo experiments has been shown until now. In this study, we used the whole extracellular matrix (ECM) excreted from fibroblasts as an underlying matrix, and the endothelial cells were seeded to obtain the long term patency of vascular graft(i.e., for the patent 8 week implanted wafts in the animal model of rat). In order to study the antithrombogenic functions of cultured endothelial cells, prostaglandin(PGF 1 a) synthesis and platelet adhesion were assayed. The concentration of PGF a of stimulated group was sisnificantly higher than that of control group(21.97 $\pm$ 3.45 vs 4.93 $\pm$0.71 pg/1000 cells). The platelet adhesion of the polyurethane sheet covered with endothelial cells was lower than that of polyurethane sheet or sheet covered with ECM(1.04$\pm$0.28, 2.87$\pm$0.77, 2.89$\pm$0.70, % radioactivities, respectively). Endothelial cells grew well on polyurethane coated with ECM, synthesized the prostacyclin and functioned well as antithrombogenic. Therefore the endothelialization onto the ECM excreted from fibroblasts may be a good method for the vfudig prosthesis.

• Advances in nano research
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• v.12 no.5
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• pp.501-514
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• 2022

This study aimed to investigate the effects and potential mechanisms of Chikusetsusaponin V (CsV) on endothelial nitric oxide synthase (eNOS) and vascular endothelial cell functions. Different concentrations of CsV were added to animal models, bovine aorta endothelial cells (BAECs) and human umbilical vein endothelial cells (HUVECs) cultured in vitro. qPCR, Western blotting (WB), and B ultrasound were performed to explore the effects of CsV on mouse endothelial cell functions, vascular stiffness and cellular eNOS mRNA, protein expression and NO release. Bioinformatics analysis, network pharmacology, molecular docking and protein mass spectrometry analysis were conducted to jointly predict the upstream transcription factors of eNOS. Furthermore, pulldown and ChIP and dual luciferase assays were employed for subsequent verification. At the presence or absence of CsV stimulation, either overexpression or knockdown of purine rich element binding protein A (PURA) was conducted, and PCR assay was employed to detect PURA and eNOS mRNA expressions, Western blot was used to detect PURA and eNOS protein expressions, cell NO release and serum NO levels. Tube formation experiment was conducted to detect the tube forming capability of HUVECs cells. The animal vasodilation function test detected the vasodilation functions. Ultrasonic detection was performed to determine the mouse aortic arch pulse wave velocity to identify aortic stiffness. CsV stimulus on bovine aortic cells revealed that CsV could upregulate eNOS protein levels in vascular endothelial cells in a concentration and time dependent manner. The expression levels of eNOS mRNA and phosphorylation sites Ser1177, Ser633 and Thr495 increased significantly after CsV stimulation. Meanwhile, CsV could also enhance the tube forming capability of HUVECs cells. Following the mice were gavaged using CsV, the eNOS protein level of mouse aortic endothelial cells was upregulated in a concentration- and time-dependent manner, and serum NO release and vasodilation ability were simultaneously elevated whereas arterial stiffness was alleviated. The pulldown, ChIP and dual luciferase assays demonstrated that PURA could bind to the eNOS promoter and facilitate the transcription of eNOS. Under the conditions of presence or absence of CsV stimulation, overexpression or knockdown of PURA indicated that the effect of CsV on vascular endothelial function and eNOS was weakened following PURA gene silence, whereas overexpression of PURA gene could enhance the effect of CsV upregulating eNOS expression. CsV could promote NO release from endothelial cells by upregulating the expression of PURA/eNOS pathway, improve endothelial cell functions, enhance vasodilation capability, and alleviate vessel stiffness. The present study plays a role in offering a theoretical basis for the development and application of CsV in vascular function improvement, and it also provides a more comprehensive understanding of the pharmacodynamics of CsV.

• Transactions of the Korean Society of Mechanical Engineers B
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• v.22 no.11
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• pp.1521-1529
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• 1998

The objective of this study is to investigate the effects of the hemodynamics on the morphological changes of the human endothelial cells due to the blood flow by in vitro experiment and computer simulation. The morphological changes of the endothelial cells due to the t10w shear stress were observed in the laminar t10w chamber as a function of the exposure time. The observed shapes of the endothelial cells are used to the model shapes of the endothelial cells for numerical study and the pressure and the wall shear stress variations around the endothelial cells are calculated from the numerical results. The endothelial cells elongate along the t10w direction and lessen their heights in the flow field to reduce the pressure and the wall shear stress on the surface.

• IMMUNE NETWORK
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• v.13 no.3
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• pp.102-106
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• 2013

Emerging evidence suggests that gap formation and opening of the endothelial junctions during leukocyte extravasation is actively controlled to maintain the integrity of the vascular barrier. While the role for endothelial cells to this process has been well defined, it is not clear whether leukocytes are also actively contributing to endothelial barrier function. We have recently showed that extravasating leukocytes deposit microparticles on the subendothelium during the late stages of extravasation, which is LFA-1 dependent. Using multiphotonintravital microscopy (MP-IVM) of mouse cremaster muscle vessels in the current work, we show that microparticle formation and deposition maintains the integrity of the microvascular barrier during leukocyte extravasation. Inhibition of neutrophil-derived microparticle formation resulted in dramatically increased vascular leakage. These findings suggest that deposition of microparticles during neutrophil extravasation is essential for maintaining endothelial barrier function and may result in temporal difference between neutrophil extravasation and an increase in vascular leakage.

• Biomedical Science Letters
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• v.12 no.2
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• pp.127-130
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• 2006

It is important to coordinated interaction among neurons, astrocytes and endothelial cells to maintain the function of brain. To study their regulatory mechanisms in vitro system, the co-culture system among the isolated cells from brain may be needed. However, the method for purifying brain microvascular endothelial cells (BMEC) far culture have not established yet. In this study, the proper culture methods of mice cells using two different strains, CD1 and C57BL6, to obtain the pure and plentiful endothelial cells were described. The flatted-round forms of CD1 endothelial cells grew on the collagen-IV coating plates, while the purified cells from C57 mice preferred type collagen-I dishes for their growth. Both cells displayed anti-PECAM-1 (CD31) and von Willebrand Factor immune-reactivity. These results indicated that different coating materials not only improve attachment of isolated cells but also promoting growth of cells, suggesting that this method of purifying murine Brain microvascular endothelial cells (BMEC) provides a suitable model to investigate blood-brain-barrier (BBB) properties within neurovascular unit in vitro.