7422

VEGFA

MVCD1|VEGF|VPF;vascular endothelial growth factor A;VEGFA;vascular endothelial growth factor A

vascular permeability factor

6p12

protein-coding

Count: Vegfa; 83785

AIM: To study the effects of endothelin-1 (ET-1) and vascular endothelial growth factor (VEGF) on the mechanism of hypoxic pulmonary hypertension (HPH). METHODS: We studied 4 groups of age-controlled male rats, i.e., normal control for 2 weeks group (N2), normal control for 3 weeks group (N3), exposed to hypoxia for 2 weeks group (H2) and for 3 weeks group (H3). Chronic HPH rat models were established by chronic hypobaric hypoxia [(10.0% +/- 0.5% O2] for 2 and 3 weeks, respectively. The rats were anesthetized and fixed, and the levels of mean pulmonary artery pressure (mPAP) and carotid arterial pressure (CAP) were measured using catheters by a microcomputer via transducers. The weight ratio of right ventricle (RV) and left ventricle and septum (LV + S) [RV/ (LV+S)] were determined. The contents of ET-1 in plasma of pulmonary artery and carotid artery and in homogenates of lung and systemic arteries were determined by radioimmunoassay, and the contents of VEGF in serum of pulmonary artery and carotid artery were determined by ABC-ELISA. RESULTS: HPH rat models were established successfully. Compared with control groups, the values of ET-1 were both enhanced in carotid artery and pulmonary artery plasma in model groups (P < 0.01). In the HPH groups, the level of pulmonary artery plasma ET-1 was significantly lower than that of carotid artery plasma, but just the reverse was ET-1 in control rats. The levels of ET-1 in homogenates of lungs from HPH models were significantly higher than those in homogenates of lungs from control groups (P < 0.01), and markedly higher than those in homogenates of systemic arteries from HPH rats (P < 0.01) SThe values of VEGF in serum of pulmonary artery from H3 group were significantly higher than those from control groups and H2 group (P < 0.01). In serum of carotid artery, the values of VEGF from the HPH models were higher than those from the control groups (P < 0.01). CONCLUSION: ET-1 and VEGF play important roles in the pathogenesis of HPH. The result that ET-1 concentration around pulmonary arteries was significantly higher than that around systemic arteries may be one of the mechanisms accounting for the different reaction of them to hypoxia.

AIM: To investigate the role of vascular endothelial growth factor (VEGF) and endothelin-1 (ET-1) on pulmonary vascular structural remodeling in rats and pika. METHODS: The Wistar rats which reside at 2 260 m were carried to 3 417 m. After they were fed 24 hours,2 weeks and 3 weeks respectively, the level of VEGF and ET-1 were measured using a kit by ELISA method. Pulmonary tissue was taken out to stain with elastica-Van Gieson. The amount of pulmonary arteries (< 100 microm) and the component ratio of MA, PMA,and NMA were calculated by using a light microscope. The ratio of right ventricle weight to left ventricle plus septum weight (RV/LV + S) were measured. RESULTS: The ET-1 was significantly different in pika as compared with 24 h, 2 weeks, 3 weeks hypoxic rats (P < 0.01) respectively. The levels of VEGF in 2 weeks, 3 weeks rats were much higher than that of pika but no difference was found between pika and 24 h hypoxic rats. The ratio of MA, PMA obviously increased, and NMA decreased significantly, right ventricular hypertrophy was developed in differ groups of hypoxic rats. CONCLUSION: The VEGF and ET-1 participate the muscularization of pulmonary vessels during hypoxia and play an important role in the process of hypoxic pulmonary hypertension in rats, however the VEGF and ET-1 may be maintainable only normal organic function in pika.

OBJECTIVE: To assess the effects of hypoxia inducible factor-1alpha (HIF-1alpha) and vascular endothelial growth factor (VEGF) on hypoxic pulmonary hypertension(HPH) in patients with acute high altitude reaction(AHAR) and its change after return to lower altitude. METHODS: Ninety-six officers and soldier participating in rescue of Yushu megaseism on April 14th in 2010, leaving low altitude area (1 500 m) rapidly to high altitude area(3 700 m) to undertake strenuous physical work were enrolled for study. All of them were male, aged 18-35 years, and they were divided into three groups according to the symptomatic scores of AHAR: without AHAR(group B, n=25), mild to moderate AHAR (group C, n=47 ) and severe AHAR (group D, n=24). Mean pulmonary artery pressure (mPAP), levels in serum HIF-1alpha and VEGF were measured at high altitude area after a stay of 50 days, and also after their return to lower altitude area (1 500 m) for 12 hours and 15 days. Fifty healthy volunteers at low altitude area served as control (group A). RESULTS: Level of mPAP (mm Hg, 1 mm Hg=0.133 kPa), serum HIF-1alpha (pg/L) and VEGF (ng/L) in group B (24.23+/-1.56, 68.80+/-7.52 and 82.56+/-6.32) were significantly higher than those in group A (18.50+/-1.30, 50.95+/-3.33 and 65.78+/-4.03), respectively (all P<0.01). Moreover, the value of all the parameters increased with increase in severity of AHAR, the respective value in group C were 28.42+/-1.32, 88.10+/-9.20 and 104.82+/-10.36, and in group D were 34.70+/-2.94, 117.93+/-13.46 and 136.77+/-12.03, and there were significant differences in comparing two groups (all P<0.01). At high altitude area, AHAR total score was positively correlated with mPAP, serum HIF-1alpha and VEGF (r=0.672, 0.737 and 0.634, respectively, all P<0.01), mPAP was positively correlated with serum HIF-1alpha and VEGF (r=0.706, 0.638, both P<0.01). Compared with group A, level of mPAP (29.08+/-4.22), serum HIF-1alpha (91.16+/-20.58) and VEGF (107.11+/-10.32) were significantly increased in 96 officers and soldiers who stayed for 50 days at an altitude of 3 700 m (all P<0.01), and the values were significantly decreased after returning to lower altitude area for 12 hours(23.05+/-3.18, 70.99+/-8.22 and 78.65+/-6.47) and 15 days(18.96+/-1.75, 52.31+/-4.92 and 63.08+/-4.55). The values showed significant difference between 12 hours and 15 days stay at 1 500 m (all P<0.01). The values of the determined parameters 15 days after return to lower altitude area showed no difference compared with those of group A (all P>0.05). CONCLUSION: Strenuous physical work at high altitude area, AHAR becomes more serious, and it is accompanied by higher values of HIF-1alpha, VEGF and mPAP, indicating that HPH is closely associated with elevation of HIF-1alpha and VEGF. These changes are improved after returning to lower altitude area for 12 hours, and they recover to normal lever after 15 days.

AIM: To study the expression of vascular endothelial growth factor (VEGF) and proliferating cell nuclear antigen(PCNA) in aorta and pulmonary artery smooth muscle cells of rats with hypoxia pulmonary hypertension(HPH). METHODS: The rat chronically HPH models were set up in the hypobaric hypoxia cabin. The experimental rats were divided into 3 groups: control group (rearing in a normoxia environment), two hypoxia groups (oxygen-deficient time being 2 weeks and 3 weeks, respectively). expression of VEGF and PCNA were detected by immunohistochemical staining and image analysis. RESULTS: There was VEGF expression in vascular smooth muscle cells of aorta, pulmonary artery trunk and pulmonary arteriole in control group. In two hypoxia groups VEGF expression in vascular smooth muscle cells of pulmonary artery, trunk and pulmonary arteriole increased significantly, while no difference was found in smooth muscle cells of aorta. expression of PCNA was very little in vascular smooth muscle cells of aorta, pulmonary artery trunk and pulmonary arteriole in control group. In two hypoxia groups, the PCNA expression increased only in vascular smooth muscle cells of pulmonary arteriole; there was no difference of PCNA expression in vascular smooth muscle cells of aorta and pulmonary artery trunk between hypoxia groups and control group. CONCLUSION: There is difference of VEGF expression in pulmonary artery trunk and aorta smooth muscle cells during the formation of chronic HPH, suggesting that VEGF expression may play very important role in the formation of chronic HPH.

OBJECTIVE: pulmonary arterial hypertension (PH) is a progressive disease with a poor prognosis that ultimately leads to right ventricular failure and death. The pathogenesis of severe PH seems to be related to inflammatory responses and coagulation disturbances. Many diseases can develop PH in their course, thus aggravating their outcome. The objective was to investigate the values of vascular endothelial growth factor (VEGF), sP-selectin, lipoprotein-associated phospholipase A2 (PLA2-LDL), antiphospholipid antibodies (APLA) and their relation with PH, in systemic lupus erythematosus (SLE) and chronic obstructive pulmonary disease (COPD), two conditions in which the occurrence of PH is frequent. DESIGN: Prospective clinical study. SETTING: A University Department of Internal Medicine, a National Institute of Research. PATIENTS: 30 SLE patients (15 patients without PH (group I) and 15 patients with PH group II)), 30 patients with COPD (15 patients without PH (group III) and 15 patients with PH (group IV)) and 10 healthy controls, selected by clinical, immunological, echocardiographical criteria and pulmonary functional tests. MAIN OUTCOME MEASURES: VEGF, sP-selectin and PLA2-LDL level in plasma and presence of antiphospholipids antibodies (lupus anticoagulant, anticardiolipin and anti beta2 GPI) in plasma. - Results: In patients with PH, the values of VEGF were significantly increased [group II (1023.1) and IV (904.3)] compared with group I (744.2), III (356.4), and controls (330.3). The values of sP-selectin in group II (9.7), and IV (10.4) were also increased compared with controls (6). APLA were present in all patients in group II (100%), and in 8 patients in group IV (53%), while in the other groups the frequency was low (33% group I and 13% group III). PLA2-LDL activity was higher in group II (429.1) and group IV (394.5) than in group I (317.8), group III (343.2) and controls (256.3). CONCLUSION: PH is a severe complication in COPD and SLE. The increased values of VEGF, PLA2-LDL and P-selectin in patients with long standing PH are related to severe endothelial dysfunction and may have prognostic values. APLA may have pathogenic value in SLE patients with PH. APLA are possibly implicated in the pathogenesis of PH in these diseases. VEGF, APLA and sP-selectin may constitute new therapeutic targets for PH.

BACKGROUND: The association between systemic sclerosis and pulmonary arterial hypertension (PAH) is well recognized. Vascular endothelial growth factor (VEGF) has been reported to play an important role in pulmonary hypertension. The aim of the present study was to examine the relationship between systolic pulmonary artery pressure, clinical and functional manifestations of the disease and serum VEGF levels in systemic sclerosis. METHODS: Serum VEGF levels were measured in 40 patients with systemic sclerosis and 13 control subjects. All patients underwent clinical examination, pulmonary function tests and echocardiography. RESULTS: Serum VEGF levels were higher in systemic sclerosis patients with sPAP >or= 35 mmHg than in those with sPAP < 35 mmHg (352 (266, 462 pg/ml)) vs (240 (201, 275 pg/ml)) (p < 0.01), while they did not differ between systemic sclerosis patients with sPAP < 35 mmHg and controls. Serum VEGF levels correlated to systolic pulmonary artery pressure, to diffusing capacity for carbon monoxide and to MRC dyspnea score. In multiple linear regression analysis, serum VEGF levels, MRC dyspnea score, and D(LCO) were independent predictors of systolic pulmonary artery pressure. CONCLUSION: Serum VEGF levels are increased in systemic sclerosis patients with sPAP >or= 35 mmHg. The correlation between VEGF levels and systolic pulmonary artery pressure may suggest a possible role of VEGF in the pathogenesis of PAH in systemic sclerosis.

OBJECTIVES: HIF-1 alpha (hypoxia-inducible factor-1 alpha) mediates the responses of mammalian cells to hypoxia/ischemia by inducing the expression of adaptive gene products (e.g., vascular endothelial growth factor (VEGF) and erythropoietin (EPO)). Persistent pulmonary hypertension of the newborn (PPHN) and cyanotic congenital heart disease (CCHD) are common neonatal diseases considered as paradigms of hypoxemia. Since the expression HIF-1 alpha, VEGF and EPO in newborns diagnosed with these diseases has yet to be studied, we set out to define the expression of these genes in peripheral blood from newborn infants diagnosed with PPHN and CCHD. DESIGN AND METHODS: The mRNA transcripts encoding HIF-1 alpha, VEGF and EPO were measured by RT-PCR in healthy newborn infants and infants diagnosed with PPHN and CCHD. RESULTS: An important increase in HIF-1 alpha expression was observed in both pathological conditions, accompanied by significant increases in VEGF and EPO expression when compared to healthy infants. CONCLUSIONS: HIF-1 alpha mRNA expression increases in newborn infants with PPHN or CCHD, as does the expression of its target genes VEGF and EPO.CI - (c) 2009 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved.