جستجوی مقالات مرتبط با کلیدواژه "endothelial cell" در نشریات گروه "پزشکی"

Endothelial cells (ECs) that line the inner surface of blood vessels play a crucial role in maintaining healthy blood vessels and regulating consistent blood flow. EC dysfunction (ECD) is the improper functioning of ECs as a result of any modification or damage. Numerous health issues such as cardiovascular disease, hypertension, lightheadedness, exhaustion, diabetes, and the like could result from this. Both extrinsic and intrinsic factors may cause ECD. Many virus-induced hemorrhagic fevers, including dengue fever, Ebola, and Lassa fever, exhibit ECD. ECs maintain barrier functions by regulating immune cell interactions, homeostasis, and capillary permeability, and in viral infections, viral interaction alters these factors. These pathogens destroy ECs, leading to a loss of integrity in the blood vessels and increased permeability. Hemorrhagic fever can cause a wide range of symptoms such as fever, headache, muscle pain, weakness, exhaustion, bruises, bleeding, shock, and occasionally even the emergence of additional issues such as organ failure. Hemorrhagic fevers can be life-threatening if not treated promptly and correctly. Considering that ECD can be a silent condition, consultation with physicians about individuals’ risk factors and regular screenings to detect and prevent this condition is highly important. There is no specific antiviral treatment for most hemorrhagic fevers, but research is ongoing to develop effective treatments. This review will discuss the ECD due to viral interactions to cause hemorrhagic fevers, available treatments, and challenges associated with such viral hemorrhagic fevers (VHFs).

Cardiovascular disease is the principal cause of mortality and morbidity in developed countries, leading to the formation of atherosclerosis plaques and thrombosis. Apoptosis of endothelial cells is one of the primary factors in vascular thrombosis. Lipids, when oxidized by endothelial cells, result in an increased thickness of the arterial wall. Iron is also recognized as an atherogenic element that induces atherosclerosis. There remains uncertainty about the antioxidative role of vitamin E in the formation of atherosclerosis. In this study, the authors evaluated the effect of iron and vitamin E on the apoptosis of endothelial cells in the carotid arteries of hypercholesterolemic male rabbits.

Thirty white male rabbits were randomly divided into five groups and fed the following diet for six weeks: Group 1: control, Group 2: cholesterol (1%), Group 3: cholesterol (1%) + vitamin E (50 mg/kg), Group 4: cholesterol (1%) + Iron (50 mg/kg), and Group 5: cholesterol (1%) + vitamin E (50 mg/kg) + Iron (50 mg/kg). Serum cholesterol, TG, HDL, and LDL levels were assessed after six weeks. Finally, the animals were sacrificed with ketamine, and carotid arteries were removed. The samples were fixed in 10% formalin, and TUNEL staining was used after the tissue processing. Cell counts were carried out under a light microscope.

Vitamin E decreased Serum cholesterol and apoptotic endothelial cells in the hypercholesterolemic + vitamin E diet (P< 0.05). However, they increased significantly in the interference groups compared to the control group (P< 0.05).

According to our findings, vitamin E showed to have a beneficial effect on preventing cardiovascular diseases and may play a positive role in the prevention of atherosclerosis.

Magnetic field is one of the effective and non-invasive modalities on biology and angiogenesis. Studies on the effects of magnetic fields on angiogenesis showed that the shape of the magnetic field could potentially affect angiogenesis. Therefore, this study aimed to control the frequency, intensity, and duration of exposure of magnetic field while investigating the effect of the shape of the magnetic field on the viability of Human Umbilical Vein Endothelial Cells (HUVECs).

The HUVECs were exposed to various shapes of 50 and 60 Hz magnetic fields with intensities of 0.5 and 1 mT in acute and chronic exposure regimes. The viability of HUVECs was assessed via MTT assay.

Results showed that the sin type 50 and 60 Hz magnetic fields are more effective in decreasing the viability. The rectified 100 and 120 Hz with 1 and 0.5 mT could increase and decrease the viability compared with 50 and 60 Hz, respectively.

It can be concluded that the shape of the magnetic field can be an effective factor in biology and must be controlled to have a reliable response.

To compare anterior segment parameters in patients with Fuchs endothelial dystrophy (FED) who underwent Descemet stripping automated endothelial keratoplasty (DSAEK) in one eye and no corneal surgery in the fellow eye.

This prospective study was conducted on 28 eyes of 14 patients with FED who underwent DSAEK in one eye at least one year prior (DSAEK group) and no corneal surgery in the fellow eye (control group). Each eye was analyzed with the anterior segment optical coherence tomography, specular microscopy, and Scheimpflug imaging systems. Data were compared between the two groups.

The mean age of the patients was 76.9 ± 7.0 years. There were no statistically significant differences in the mean central corneal thickness (CCT), central anterior chamber depth, anterior chamber angle parameters, cylinder and keratometry values between two groups (all P-values > 0.05). The paracentral corneal thickness, corneal volume, endothelial cell density, and hexagonal cell ratio measurements were statistically significantly higher in the DSAEK group than the control (all P-values < 0.05), and anterior chamber volume in the DSAEK group was significantly less than the control (P = 0.046). While posterior and total corneal densitometry values in the DSAEK group were statistically significantly lower than the control (P < 0.001 and P = 0.011, respectively), there were no statistically significant differences in the anterior or middle corneal densities (P = 0.108 and P = 0.134, respectively).

We found that total corneal densitometry value decreased in DSAEK group. Although DSAEK surgery did not affect the anterior chamber angle parameters, it reduced the anterior chamber volume and increased the corneal volume and paracentral corneal thickness due to the addition of the DSAEK graft.

Endothelial cell (EC) apoptosis plays a critical role in the physiological and pathological vascular regression, remodeling, and angiogenesis. There are several therapeutic agents such as glucocorticoids (GCs), which could influence EC apoptosis, causing coagulation events. Due to the paradoxical effects of GCs on cellular apoptosis, the aim of the current study was to investigate the dose and time in which GCs could initiate and terminate in vitro cellular apoptosis.

Dexamethasone (DEXA) was serially diluted 10-folds for 8 serial concentrations (from 1 mM to 0.1 nM) added to cultured human umbilical vein endothelial cells (HUVECs). The cytotoxic effects of DEXA on HUVEC were tested with a rapid colorimetric test using 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide assay. Apoptotic assays based on quantitative polymerase chain reaction was performed for Bax and Bcl-2 genes and terminal deoxynucleotidyl transferase dUTP nick end labeling assay.

DEXA at the concentration of 1 µM showed significant cytotoxic effects, more intense anti-apoptotic effects in lower concentrations (1 nM to 100 nM), and anti-apoptotic effects with less intensity in higher concentrations (10 µM to 1 mM). Six hours of treatment by 1 µM of DEXA was estimated as the initial time of DEXA that could remarkably induce HUVECs apoptosis. The maximum significant increase of apoptosis was detected 24 hours after treatment with DEXA.

Our findings suggested that GCs can influence cellular apoptosis in a dose- and time-dependent manner.

The aim of this study was to investigate the relationship between serum endothelial cellspecific molecule-1 endocan levels and coronary artery ectasia (CAE). This cross-sectional study was conducted on 99 patients. According to angiographic data, the patients were divided into 3 groups: 1) patients with isolated CAE (n = 33), 2) patients with documented coronary artery diseases without CAE (n = 33), and 3) those with normal coronary arteries (n = 33). The endocan concentration was measured via the ELISA technique. patients with isolated CAE had significantly lower levels of endocan than did the controls (261.30 ± 61.34 vs 564.58 ± 81.69; P < 0.05). There was no significant correlation between endocan levels and the severity of CAE according to the Markis classification (P > 0.05). The patients who used opium had a significantly higher prevalence rate of CAE (65.6% vs 35.3%; P = 0.012). Moreover, in the group with ectasia, by comparison with the non-ectatic group, significantly high levels of serum triglyceride, cholesterol, and LDL levels, as well as low HDL levels, were detected. Among our study population, a decrease in endocan levels was a sensitive and accurate indicator for predicting the presence of CAE, although the level of this marker was not very effective in determining the severity of ectasia. In addition to a drop in endocan expression levels, the use of opium and also an abnormal lipid profile were the other predictors of CAE.

Vascular endothelial growth factor-A (VEGF-A), an endothelial cell-specific mitogen produced by various cell types, plays important roles in cell differentiation and proliferation. In this study we investigated the effect of recombinant VEGF-A on differentiation of mesenchymal stem cells (MSCs) to endothelial cells (ECs).
VEGF-A was expressed in E. coli BL21 (DE3) and BL21 pLysS competent cells with the pET32a expression vector. Recombinant VEGF-A protein expression was verified by SDS-PAGE and western blotting. Mesenchymal stem cell differentiation to ECs in the presence of VEGF-A was evaluated by flow cytometry and fluorescence microscopy.
Recombinant VEGF-A was produced in E. coli BL21 (DE3) cells at 0.8 mg/mL concentration. Expression of CD31 and CD 144 was significantly greater, while expression of CD90, CD73, and CD44 was significantly less, in MSCs treated with our recombinant VEGF-A than in those treated with the commercial protein (p Recombinant VEGF-A expressed in a prokaryotic system can induce MSCs differentiation to ECs and can be used in research and likely therapeutic applications.

Some studies have demonstrated the potential of herbal drugs for the treatment of various diseases associated with impaired vascular nitric oxide (NO). For diagnosis of the mechanism of these herbal plants, it seems necessary to evaluate the herbal extracts on the Endothelium cell. The aim of the study was to investigate the effect of extract of Trigonella foenum-graecum (T.foenum), Nigella sativa (NS), Allium sativum and Cannabis sativa on nitric oxide (NO) production by the endothelial cells 3T3 cell line. ground herbs suspended in water and methanol, were filtered and concentrated under pressure. Remaining contents were dried and obtained powder dissolved in water. The cell line was treated with plant extracts. The clarified supernatant of the culture was used for evaluation of quantitative changes in NO production using Griess test. Among the four extracts, only the group treated with T.foenum extract, significantly increased NO production in comparison with control group. Also, NO concentration in other extract group was lower than T.foenum group. This study suggested that the T.foenum extract can significantly increase NO concentration in cell culture and the increase in nitric oxide production is because of the presence of diosgenin is T.foenum extracted.

Migration, expansion and survival of endothelial cells that are an important cellular component of blood vessels plays an important role in the induction of tumor growth. Kisspeptins (kp), peptides that bind to coupled-G protein receptor (GPR54), inhibit each step of metastatic cascade include invasion, migration and homing, angiogenesis, survival and proliferation. In this study we investigated effects of kisspeptin-10, the most potent member of kisspeptin family, on Migration and proliferation of endothelial cells that are necessary for angiogenesis and tumor metastasis.

We compared migration of Human Umbilical Vein Endothelial Cells (HUVECs) were treated with 10-100 or 500 nM kp-10 for 24 hours and no treated cells using an in vitro trans membrane migration assay and HUVEC proliferation of treated endothelial cells with 10-100 or 500 nM kp-10 for 48 hours and no treated cells was measured by MTT Cell Proliferation Assay Kit. Analysis of data was performed using the Kruskal-Wallis test followed by the Mann-Whitney test.

Migration and proliferation of endothelial cells were increased at lower concentration of kp-10 specially at 100 nM while higher concentration reduced both migration and proliferation.

Our data showed that different concentrations of kp-10 have distinct effects on migration and proliferation of endothelial cells.

Alzheimer''s disease (AD) is a progressive neurodegenerative disease in which endothelial cell (EC) can be affected. In brain, functional changes in ECs contribute to reductions in resting blood flow. Furthermore, angiotensin-converting enzyme inhibitors (ACE-I) have beneficial effects on endothelial dysfunction. This is the first study that presents direct experimental evidence associating endothelial apoptosis as a basis of AD pathogenesis and response to an ACE-I therapy. Human umbilical vein ECs (HUVECs) were treated with sera from AD patients and sera from healthy volunteers (each group, n = 10). Apoptosis was determined by annexin V–propidium iodide staining and cell death detection kit. The effect of 50 µM enalapril on endothelial apoptosis was assessed. Nitrite (NO2−) levels were determined in the culture supernatants. Enalapril suppressed the induction of apoptosis by the serum of patients only when used before treating HUVECs with the sera of AD. Mean ± SD of apoptosis induction in the control group was 6.7 ± 3.69; in the group treated with sera of AD for 24 h was 47.78 ± 0.65; in the group wherein sera from AD was added (pretreatment) after exposure of HUVECs by 50 µM enalapril for 24 h was 26.6 ± 2.63; and in the group wherein HUVECs were exposed in the sera of AD for 24 h and then 50 µM enalapril was added to these cells for another 24 h (post-treatment) was 56.87 ± 5.51. Also, the mean ± SD of NO2− concentration showed significantly greater levels of dissolved NO2/NO3 metabolite in the culture media of untreated HUVECs by enalapril (1.03 ± 0.06) as compared with control (0.26 ± 0.13; p < 0.05), while the rate of nitric oxide (NO) significantly decreased when enalapril was presented in culture both in the pretreatment (0.07 ± 0.003) and in the post-treatment group (0.06 ± 0.005; p < 0.05). It could be concluded that EC treated with sera from AD patients activates apoptosis in HUVECs; this effect was reversed by enalapril pretreatment. This can be proposed as a therapeutic approach for Alzheimer`s patients.

Alzheimer’s disease (AD) is a progressive neurodegenerative disease and nowadays the role of endothelial cell (EC) injury has been proposed in pathological process in AD. Peroxisome proliferator‑activated receptor‑γ (PPAR‑γ) agonist has anti‑inflammatory properties through activation in glial cells and improves vascular function and prevent atherosclerotic disease progression. The aim of this study is evaluation of pioglitazone effects as a drug of PPAR‑γ agonist on endothelial apoptosis induced by sera from AD patients. Human umbilical vein endothelial cells (HUVECs) were treated with sera from AD patients (n = 10) and sera from controls (n = 10). Apoptosis was identified by annexin V‑propidium iodide staining and cell death detection kit. Apoptosis was evaluated after and before adding of 10 μM pioglitazone on EC. Nitrite (NO2‑) levels were determined in the culture supernatants. Induced apoptosis by the serum of patients was inhibited markedly when pioglitazone used before treating HUVECs with the sera of AD. Also, the measurement of nitrite concentration showed significantly greater levels of dissolved NO2/NO3 metabolite in the culture media of HUVECs treated by sera of AD patients (P < 0.05), while the rate of nitric oxide significantly decreased when pioglitazone exists in culture media. Further studies are justified to investigate the novel role of the PPARs in the prevention of the neuronal and endothelial damage in neurological disorder and present a new therapeutic approach for Alzheimer`s patients.