scholarly journals Study on Damage Mechanism and Repair of Vascular Endothelial Cells Based on Ultrasound Technology

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Shuhao Deng ◽  
Quan Jiang ◽  
Xin Lu ◽  
Yuan Zhang
Keyword(s):  
Endothelial Cells ◽  
Endothelial Function ◽  
Relaxation Function ◽  
Vascular Endothelial Cells ◽  
Early Stage ◽  
Gradient Centrifugation ◽  
Control Group ◽  
Dependent Manner ◽  
Vascular Endothelial ◽  
Vascular Endothelial Function

Objective. To detect the endothelial function of external iliac artery in rats with different stages of atherosclerosis by high-resolution ultrasound, so as to provide experimental methodological basis for evaluating the function of vascular endothelial cells by ultrasound. Methods. The animals were randomly divided into the control group ( n = 6 ) and the atherosclerosis model group ( n = 15 ). The atherosclerosis group was further divided into 4-week group, 8-week group, and 12-week group, with 5 animals in each group. After separating and grinding rat spleen, the obtained cells were cultured by density gradient centrifugation. After the cells adhered, the morphology of the cells was observed under a microscope and identified by DiI-Ac-LDL and FITC-UEA-I double staining. The activities of LDH and SOD, the contents of MDA and GSH, and the contents of NO in plasma were detected by biochemical methods. Results. The protective effect of rosanilin on brain injury in rats with acute hypobaric hypoxia and its regulation on the expression of pAkt protein; ox-LDL inhibited the proliferation activity of EPCs in a concentration-dependent manner. The expression of KLF2 and S1PR1 in HAEC can be knocked down by small interfering RNA, and knocking down KLF2 can not only downregulate the expression of S1PR1 but also downregulate HAVEN. With the development of atherosclerosis, the endothelium-dependent relaxation function and endothelium-independent relaxation function of the control group and the atherosclerosis model at 4, 8, and 12 weeks were damaged in different degrees and gradually aggravated. Conclusion. Atherosclerosis is a disease with both morphological and functional damage, and vascular endothelial function is damaged in the early stage with corresponding pathological changes. Ultrasound is an effective method to evaluate vascular endothelial function.

scholarly journals Vascular Endothelial Estrogen Receptor α Is Modulated by Estrogen Status and Related to Endothelial Function and Endothelial Nitric Oxide Synthase in Healthy Women

2009 ◽  
Vol 30 (5) ◽  
pp. 542-542
Author(s):  
Kathleen M. Gavin ◽  
Douglas R. Seals ◽  
Annemarie E. Silver ◽  
Kerrie L. Moreau
Keyword(s):  
Endothelial Cells ◽  
Menstrual Cycle ◽  
Endothelial Function ◽  
Postmenopausal Women ◽  
Vascular Endothelial Cells ◽  
Premenopausal Women ◽  
Estrogen Receptor Α ◽  
Vascular Endothelial ◽  
Vascular Endothelial Function ◽  
Endothelial Nitric Oxide

ABSTRACT Context and Objective Estrogen receptor α (ERα), a potent transcription factor expressed in vascular endothelial cells, plays a key role in regulating vascular function and health. We determined whether vascular endothelial cell expression of ERα is influenced by estrogen status and is related to vascular endothelial function in healthy women. Methods ERα protein expression was measured (quantitative immunofluorescence) in endothelial cells from peripheral veins of 16 healthy, premenopausal women during the early follicular (EF) and late follicular (LF) phases of the menstrual cycle and 17 estrogen-deficient postmenopausal women. Endothelial-dependent dilation (EDD; brachial artery flow-mediated dilation) and endothelial nitric oxide synthase (eNOS) expression and activation were also measured in a subgroup of women. Results In premenopausal women (n = 10), ERα expression was 30% lower (P < 0.001) during the EF (low estrogen) compared with the LF (high estrogen) phase of the menstrual cycle. In postmenopausal women, ERα expression was 33% lower (P < 0.001) compared with the LF phase of the menstrual cycle in premenopausal women. ERα expression was strongly related (r = 0.67; P < 0.001) to EDD, which was reduced in postmenopausal women. ERα abundance was positively related to expression of eNOS (r = 0.54; P = 0.009; n = 21) and ser1177 phosphorylated eNOS (r = 0.59; P = 0.006; n = 20). Conclusions These results provide the first evidence that expression of ERα in vascular endothelial cells is modulated by estrogen status and may be a key determinant of vascular endothelial function in healthy pre- and postmenopausal women. ERα expression may influence vascular endothelial function in women by affecting protein levels and activation of eNOS.

The regulation and mechanism of a dual PI3K/mTOR signaling inhibitor in hemangioma vascular endothelial cells in vitro

2020 ◽  
Author(s):  
wangshu liu ◽  
Yang Yu ◽  
Juan Li ◽  
Hui Huang ◽  
Hao Liu ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Signaling Pathway ◽  
Vascular Endothelial Cells ◽  
Mtor Signaling ◽  
Control Group ◽  
Dependent Manner ◽  
Vascular Endothelial ◽  
Mtor Signaling Pathway ◽  
Protein Levels

Abstract Objective To observe the influence of the dual PI3K/mTOR inhibitor NVP-BEZ235 on proliferation and apoptosis of hemangioma cells in vitro and key molecules of the PI3K/Akt/mTOR signaling pathway.Methods Hemangioma-derived endothelial cells (HeECs) were obtained by surgical resection and cultured after the explants with the trypsin-digestion method. Fourth generation cells were cultured with serum-free medium for 24 hours. Then, the intervention group cells were added to the culture medium with 0.50 μM or 1.00 μM NVP-BEZ235. Cell proliferation was detected with CCK-8 assays, apoptosis was detected by flow cytometry, and PI3K, Akt, mTOR, and p70s6k protein levels were detected by Western blots. Then, the relationship between the phenotype of hemangioma vascular endothelial cells and the four proteins was analyzed.Results the 0.50 μM and 1.00 μM NVP-BEZ235 groups were significantly lower (0.88±0.03 and 0.59±0.05, respectively) than the control group (1.10±0.02) (P<0.01). The rate of G0/G1 phase cells in the 0.50 μM and 1.00 μM NVP-BEZ235 group were higher than the control group (P<0.01). The total rates of apoptotic cells in the 0.50 μM and 1.00 μM NVP-BEZ235 groups were higher than the control group (2.77±1.23)% (P<0.01). The PI3K pathway related protein levels in the NVP-BEZ235 group were lower than control group (P<0.01).Conclusion The PI3K/Akt/mTOR signaling pathway participates in hemangioma development. NVP-BEZ235 affected hemangioma vascular endothelial cells in vitro by regulating the PI3K/Akt/mTOR signaling pathway in a dose-dependent manner.

scholarly journals The Use of Fiber-Reinforced Scaffolds Cocultured with Schwann Cells and Vascular Endothelial Cells to Repair Rabbit Sciatic Nerve Defect with Vascularization

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Hongyang Gao ◽  
Yang You ◽  
Guoping Zhang ◽  
Feng Zhao ◽  
Ziyi Sha ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Sciatic Nerve ◽  
Nerve Fiber ◽  
Schwann Cells ◽  
Vascular Endothelial Cells ◽  
Neurological Function ◽  
Control Group ◽  
Vascular Endothelial ◽  
Fiber Reinforced ◽  
3D Scaffolds

To explore the feasibility of biodegradable fiber-reinforced 3D scaffolds with satisfactory mechanical properties for the repair of long-distance sciatic nerve defect in rabbits and effects of vascularized graft in early stage on the recovery of neurological function, Schwann cells and vascular endothelial cells were cocultured in the fiber-reinforced 3D scaffolds. Experiment group which used prevascularized nerve complex for the repair of sciatic nerve defect and control group which only cultured with Schwann cells were set. The animals in both groups underwent electromyography to show the status of the neurological function recovery at 4, 8, and 16 weeks after the surgery. Sciatic nerve regeneration and myelination were observed under the light microscope and electron microscope. Myelin sheath thickness, axonal diameter, and number of myelinated nerve fiber were quantitatively analyzed using image analysis system. The recovery of foot ulcer, the velocity of nerve conduction, the number of regenerating nerve fiber, and the recovery of ultrastructure were increased in the experimental group than those in the control group. Prevascularized tissue engineered fiber-reinforced 3D scaffolds for the repair of sciatic nerve defects in rabbits can effectively promote the recovery of neurological function.

Biomechanical interactions of Schistosoma mansoni eggs with vascular endothelial cells facilitate egg extravasation

2021 ◽  
Author(s):  
Yi-Ting Yeh ◽  
Danielle E. Skinner ◽  
Ernesto Criado-Hidalgo ◽  
Natalie Shee Chen ◽  
Antoni Garcia-De Herreros ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Schistosoma Mansoni ◽  
Disease Transmission ◽  
Vascular Endothelial Cells ◽  
Flexible Substrate ◽  
Blood Stream ◽  
The Body ◽  
Dependent Manner ◽  
Vascular Endothelial ◽  
Maturation State

AbstractThe eggs of the parasitic blood fluke, Schistosoma, are the main drivers of the chronic pathologies associated with schistosomiasis, a disease of poverty afflicting approximately 220 million people worldwide. Eggs laid by Schistosoma mansoni in the bloodstream of the host are encapsulated by vascular endothelial cells (VECs), the first step in the migration of the egg from the blood stream into the lumen of the gut and eventual exit from the body. The biomechanics associated with encapsulation and extravasation of the egg are poorly understood. We demonstrate that S. mansoni eggs induce VECs to form two types of membrane extensions during encapsulation; filopodia that probe eggshell surfaces and intercellular nanotubes that presumably facilitate VEC communication. Encapsulation efficiency, the number of filopodia and intercellular nanotubes, and the length of these structures depend on the egg’s vitality and, to a lesser degree, its maturation state. During encapsulation, live eggs induce VEC contractility and membranous structures formation, in a Rho/ROCK pathway-dependent manner. Using elastic hydrogels embedded with fluorescent microbeads as substrates to culture VECs, live eggs induce VECs to exert significantly greater contractile forces during encapsulation than dead eggs, which leads to 3D deformations on both the VEC monolayer and the flexible substrate underneath. These significant mechanical deformations cause the VEC monolayer tension to fluctuate with eventual rupture of VEC junctions, thus facilitating egg transit out of the blood vessel. Overall, our data on the mechanical interplay between host VECs and the schistosome egg improve our understanding of how this parasite manipulates its immediate environment to maintain disease transmission.

scholarly journals Citrus bergamiaRisso Elevates Intracellular Ca2+in Human Vascular Endothelial Cells due to Release of Ca2+from Primary Intracellular Stores

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Purum Kang ◽  
Seung Ho Han ◽  
Hea Kyung Moon ◽  
Jeong-Min Lee ◽  
Hyo-Keun Kim ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Channel Blocker ◽  
Vascular Endothelial Cells ◽  
Umbilical Vein ◽  
Dependent Manner ◽  
Vascular Endothelial ◽  
Concentration Dependent Manner ◽  
Carbonyl Cyanide ◽  
Intracellular Ca ◽  
Umbilical Vein Endothelial Cells

The purpose of the present study is to examine the effects of essential oil ofCitrus bergamiaRisso (bergamot, BEO) on intracellular Ca2+in human umbilical vein endothelial cells. Fura-2 fluorescence was used to examine changes in intracellular Ca2+concentration[Ca2+]i. In the presence of extracellular Ca2+, BEO increased[Ca2+]i, which was partially inhibited by a nonselective Ca2+channel blocker La3+. In Ca2+-free extracellular solutions, BEO increased[Ca2+]iin a concentration-dependent manner, suggesting that BEO mobilizes intracellular Ca2+. BEO-induced[Ca2+]iincrease was partially inhibited by a Ca2+-induced Ca2+release inhibitor dantrolene, a phospholipase C inhibitor U73122, and an inositol 1,4,5-triphosphate (IP3)-gated Ca2+channel blocker, 2-aminoethoxydiphenyl borane (2-APB). BEO also increased[Ca2+]iin the presence of carbonyl cyanide m-chlorophenylhydrazone, an inhibitor of mitochondrial Ca2+uptake. In addition, store-operated Ca2+entry (SOC) was potentiated by BEO. These results suggest that BEO mobilizes Ca2+from primary intracellular stores via Ca2+-induced and IP3-mediated Ca2+release and affect promotion of Ca2+influx, likely via an SOC mechanism.

scholarly journals Effects of combined use of atorvastatin and losartan in treating patients with diabetic nephropathy

2018 ◽  
Vol 16 ◽  
pp. 205873921879670
Author(s):  
Chao Ding ◽  
Xiaohua Hu
Keyword(s):  
Diabetic Nephropathy ◽  
Endothelial Function ◽  
Cardiovascular Events ◽  
Density Lipoprotein ◽  
Blood Lipid ◽  
Inflammatory Factors ◽  
Control Group ◽  
Vascular Endothelial ◽  
Observation Group ◽  
Vascular Endothelial Function

This study is to investigate the effect of atorvastatin combined with losartan on inflammatory factors, vascular endothelial function, and cardiovascular events in patients with diabetic nephropathy. A total of 128 patients with diabetic nephropathy treated in our hospital from January 2014 to December 2015 were selected as the study subjects, and 64 cases were randomly divided into observation group and 64 cases in the control group. The control group was treated with losartan on the basis of routine treatment, and the observation group was treated with atorvastatin on the basis of the control group. The blood lipid, inflammatory factors, changes in vascular endothelial function and cardiovascular events were compared between the two groups. The levels of total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) were not significantly different between the two groups before treatment ( P > 0.05); after treatment, the levels of TC, TG, and LDL-C in the observation group were significantly lower than those of the control group, and the level of HDL-C was significantly higher than that of the control group ( P < 0.05). The levels of high-sensitivity C-reactive protein (hs-CRP), tumor necrosis factor alpha (TNF-α), and interleukin 6 (IL-6) were not statistically different between the two groups before treatment ( P > 0.05); after treatment, the levels of hs-CRP, TNF-α, and IL-6 in the observation group were significantly lower than those of the control group ( P < 0.05), the level of HDL-C was significantly higher than that of the control group ( P < 0.05). There were no significant differences in the levels of endothelin-1 (ET-1) and nitric oxide (NO) between the two groups before treatment ( P > 0.05). After treatment, the level of ET-1 in the observation group was significantly lower than that of the control group ( P < 0.05), and the level of NO was significantly higher than that of the control group ( P < 0.05). After treatment, all patients were followed up for 2 years, and the incidence of secondary cardiovascular events in the observation group was 12.50% (8/64), which was significantly lower than 29.69% (19/64) of the control group ( P < 0.05). Combination of atorvastatin and losartan can significantly improve the levels of blood lipid, inflammatory factors, and vascular endothelial function in patients with diabetic nephropathy and can effectively reduce the incidence of cardiovascular events.

scholarly journals Effect of Comprehensive Cerebral Protection Program on Cerebral Oxygen Metabolism and Vascular Endothelial Function in Elderly Patients with Acute Cerebral Infarction

2019 ◽  
Author(s):  
Meihong ZHOU ◽  
Zhaojun HUANG
Keyword(s):  
Elderly Patients ◽  
Cerebral Infarction ◽  
Endothelial Function ◽  
Oxygen Metabolism ◽  
Acute Cerebral Infarction ◽  
Control Group ◽  
Cerebral Oxygen ◽  
Vascular Endothelial ◽  
Vascular Endothelial Function ◽  
Cerebral Oxygen Metabolism

Background: We aimed to explore the effect of comprehensive cerebral protection on cerebral oxygen metabolism and vascular endothelial function in elderly patients with acute cerebral infarction. Methods: A total of 168 elderly patients with acute cerebral infarction treated in The First Affiliated Hospital of Nanchang University, China from January 2016 to January 2018 were selected. The patients were divided into a control group and an observation group using random number method, n=84. Patients in the observation group were given comprehensive cerebral protection treatment, and patients in the control group were treated with conventional standardized treatments. The changes of cerebral oxygen metabolism, hemorheology and vascular endothelial function before and after treatment were compared between the two groups. Results: After treatment, oxygen content in arteries and internal jugular veins (Da-vO2), ofoxygen uptake fraction (OEF), Oxygen saturation (SpO2), nitric oxide (NO) were increased in both groups in comparison to before treatment, jugular venous oxygen saturation (SjvO2), brain oxygen uptake rate (ERO2), endothelin (ET), intracranial pressure (ICP), whole blood viscosity, plasma viscosity, reduced viscosity of whole blood, and hematocrit were decreased. However, the changes in the observation group were larger than those in the control group, the difference was statistically significant (P<0.05). Conclusion: The treatment of cerebral infarction in elderly patients with acute cerebral infarction can effectively improve the cerebral oxygen metabolism and vascular endothelial function and improve the blood rheology, which has important clinical value.

scholarly journals Exchange Protein Directly Activated by cAMP Modulates Ebola Virus Uptake into Vascular Endothelial Cells

Viruses ◽  
2018 ◽  
Vol 10 (10) ◽  
pp. 563 ◽  
Author(s):  
Aleksandra Drelich ◽  
Barbara Judy ◽  
Xi He ◽  
Qing Chang ◽  
Shangyi Yu ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Ebola Virus ◽  
Vascular Endothelial Cells ◽  
Ex Vivo ◽  
Marburg Virus ◽  
Dependent Manner ◽  
Vascular Endothelial ◽  
Ultrastructural Studies ◽  
Ebov Infection ◽  
Exchange Protein

Members of the family Filoviridae, including Ebola virus (EBOV) and Marburg virus (MARV), cause severe hemorrhagic fever in humans and nonhuman primates. Given their high lethality, a comprehensive understanding of filoviral pathogenesis is urgently needed. In the present studies, we revealed that the exchange protein directly activated by cAMP 1 (EPAC1) gene deletion protects vasculature in ex vivo explants from EBOV infection. Importantly, pharmacological inhibition of EPAC1 using EPAC-specific inhibitors (ESIs) mimicked the EPAC1 knockout phenotype in the ex vivo model. ESI treatment dramatically decreased EBOV infectivity in both ex vivo vasculature and in vitro vascular endothelial cells (ECs). Furthermore, postexposure protection of ECs against EBOV infection was conferred using ESIs. Protective efficacy of ESIs in ECs was observed also in MARV infection. Additional studies using a vesicular stomatitis virus pseudotype that expresses EBOV glycoprotein (EGP-VSV) confirmed that ESIs reduced infection in ECs. Ultrastructural studies suggested that ESIs blocked EGP-VSV internalization via inhibition of macropinocytosis. The inactivation of EPAC1 affects the early stage of viral entry after viral binding to the cell surface, but before early endosome formation, in a phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)-dependent manner. Our study delineated a new critical role of EPAC1 during EBOV uptake into ECs.

scholarly journals Protective Effects of Oxymatrine on Vascular Endothelial Cells from High-Glucose-Induced Cytotoxicity by Inhibiting the Expression of A2B Receptor

2018 ◽  
Vol 45 (2) ◽  
pp. 558-571 ◽  
Author(s):  
Yun Yi ◽  
Yulin Shen ◽  
Qin Wu ◽  
Jingan Rao ◽  
Shu Guan ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Viability ◽  
Western Blotting ◽  
High Glucose ◽  
Vascular Endothelial Cells ◽  
Control Group ◽  
Vascular Endothelial ◽  
A2b Receptor ◽  
High Glucose Group ◽  
Glucose Group

Background/Aims: Diabetes mellitus (DM) has become an increasingly epidemic metabolic disease. Vascular endothelial cells play a key role in developing the cardiovascular complications of DM. The A2B receptor is expressed in vascular endothelial cells, and may help regulate the function of endothelial cells. The aim of this study was to investigate the protective effects of oxymatrine (OMT) on human umbilical vein endothelial cells (HUVECs) from high glucose-induced cytotoxicity. Methods: Homology modeling and molecular docking analysis were used to detect the binding sites between the adenosine A2B receptor and OMT. HUVECs were cultured with control (5.5 mM) or elevated glucose (22.2 mM) in the presence or absence of 3 µM OMT or A2B siRNA for 3 days. The MTS cell viability assay was used to measure the toxicity of high glucose on HUVECs and the protective effect of OMT or A2B siRNA. The expression of the adenosine A2B receptor and CCL5 in HUVECs was detected with real-time quantitative PCR (qPCR) and Western blotting methods in each group. Levels of IL-1β and TNF-α were measured using an enzyme-linked immunosorbent assay (ELISA) kit, and the concentration of NO was detected with the nitrate reductase method. Monocyte chemotactic activity in each group was detected using Transwell chambers. Furthermore, the phosphorylation of p38 and ERK1/2 in each group was observed through the Western blotting method. Results: Homology modeling and molecular docking analysis showed that OMT contains well-fitted binding sites to the A2B receptor. After chronic culture at high glucose, the rate of cell viability was significantly lower than that of the control group. After co-treatment with OMT or A2B siRNA, cell viability was significantly increased compared with the high-glucose group. The results from real-time quantitative RT-PCR (qRT-PCR) and Western blotting indicated that high glucose could increase the expression of A2B receptors in HUVECs, an effect that was inhibited by OMT. In addition, the results revealed that the expression of CCL5, IL-1β and TNF-α was increased in the high-glucose group, and that the NO produced by HUVECs decreased due to hyperglycemia; however, co-culture with OMT or A2B siRNA abolished these effects. Meanwhile, the chemotaxis activity of monocytes to HUVECs cultured in high-glucose medium was enhanced 2.59-fold compared to the control cells. However, the inflammatory reactions in HUVECs were completely relieved by co-treatment with OMT or A2B siRNA. Moreover, the phosphorylation of p38 and ERK1/2 in HUVECs in the high-glucose group was significantly higher than that of the control group; these effects were reversed after co-treatment with OMT or A2B siRNA. Conclusion: OMT may protect the HUVECs from high glucose-induced cytotoxicity through inhibitting the expression of A2B receptor and inflammatory factors as well as decreasing the phosphorylation of p38 and ERK1/2.

Sign in / Sign up

Export Citation Format

Share Document