scholarly journals Enhanced Vascular Endothelial Growth Factor Gene Expression in Ischaemic Skin of Critical Limb Ischaemia Patients

2012 ◽  
Vol 2012 ◽  
pp. 1-4 ◽  
Author(s):  
Silvia Bleda ◽  
Joaquín de Haro ◽  
Francisco Acin ◽  
César Varela ◽  
Leticia Esparza
Keyword(s):  
Gene Expression ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Critical Limb Ischaemia ◽  
Control Group ◽  
Venous Disease ◽  
Vascular Endothelial ◽  
Vegf Gene ◽  
Vegf Expression ◽  
Endothelial Growth Factor

Objectives. To perform a quantitative analysis of the vascular endothelial growth factor (VEGF) gene transcription in the skin of ischemic legs and provide information for VEGF in the pathogenesis in critical limb ischemia (CLI).Methods. Skin biopsies were obtained from 40 patients with CLI. Control samples came from 44 patients with chronic venous disease. VEGF gene expression was analysed using quantitative polymerase chain reaction.Results. Patients with CLI had higher skin VEGF expression than control group (RQ: 1.3 ± 0.1 versus 1,P=0.04).Conclusions. We found an association between ischemic skin and an elevated VEGF expression in legs from patients with CLI. These data support that the mechanism for VEGF upregulation in hypoxia conditions is intact and acts appropriately in the ischaemic limbs from patients with CLI.

scholarly journals Endocrine gland-derived vascular endothelial growth factor in rat pancreas: genetic expression and testosterone regulation

2008 ◽  
Vol 197 (2) ◽  
pp. 309-314 ◽  
Author(s):  
Angélica Morales ◽  
Sumiko Morimoto ◽  
Lorenza Díaz ◽  
Guillermo Robles ◽  
Vicente Díaz-Sánchez
Keyword(s):  
Gene Expression ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Pancreatic Tissue ◽  
Endocrine Gland ◽  
Vascular Endothelial ◽  
Rinm5f Cells ◽  
Vegf Gene ◽  
Rat Pancreas ◽  
Endothelial Growth Factor

Endocrine gland-derived vascular endothelial growth factor (EG-VEGF) is an endothelial cell mitogen, expressed essentially in steroidogenic cells. Recently, the expression of EG-VEGF in normal human pancreas and pancreatic adenocarcinoma has been demonstrated. Epidemiologically, pancreatic carcinogenesis is more frequent in males than females, and given that androgen receptors and testosterone biotransformation have been described in pancreas, we hypothesized that testosterone could participate in the regulation of EG-VEGF expression. In this study, we investigated the regulation of EG-VEGF gene expression by testosterone in normal rat pancreatic tissue and rat insulinoma cells (RINm5F). Total RNA was extracted from rat pancreas and cultured cells. Gene expression was studied by real-time PCR and protein detection by immunohistochemistry. Serum testosterone was quantified by RIA. Results showed that EG-VEGF is expressed predominantly in pancreatic islets and vascular endothelium, as well as in RINm5F cells. EG-VEGF gene expression was lower in the pancreas of rats with higher testosterone serum levels. A similar effect that was reverted by flutamide was observed in testosterone-treated RINm5F cells. In summary, testosterone down-regulated EG-VEGF gene expression in rat pancreatic tissue and RINm5F cells. This effect could be mediated by the androgen receptor. To our knowledge, this is the first time that a direct effect of testosterone on EG-VEGF gene expression in rat pancreas and RINm5F cells is demonstrated.

scholarly journals Systemic Antibiotic and Nonsteroidal Anti-Inflammatory Drug Treatment Decreases the Level of Endogenous Angiogenic Vascular Endothelial Growth Factor in Inflamed Human Periapical Tissues

2021 ◽  
Vol 11 (11) ◽  
pp. 4976
Author(s):  
Aleksandra Palatyńska-Ulatowska ◽  
Marta Michalska ◽  
Anna Drelich ◽  
Aleksandra Sałagacka-Kubiak ◽  
Ewa Balcerczak ◽  
...  
Keyword(s):  
Gene Expression ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Control Group ◽  
Vascular Endothelial ◽  
Rt Pcr ◽  
Tissue Samples ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
Endothelial Growth Factor

Vascular endothelial growth factor (VEGF)-induced angiogenesis contributes to inflammatory bone resorption in humans. Widely documented antagonists to resorption include antibiotics and non-steroidal anti-inflammatory drugs (NSAIDs). The purpose of this study was to investigate the effect of these drugs on proangiogenic VEGF levels in periradicular lesions. Periapical tissue biopsies were obtained from 42 patients with chronic periapical periodontitis. VEGF levels were measured using a commercial ELISA kit in patients divided into groups according to treatment: no drugs (control group, n = 25), NSAIDs (n = 7), antibiotics (n = 5), and NSAIDs and antibiotics (n = 5). Reverse transcriptase (RT) reaction was performed in all the samples under analysis. Presence of VEGFA and VEGFB gene expression was assessed using reverse-transcription-polymerase chain reaction (RT-PCR). ELISA analysis indicated that average VEGF levels in tissue samples of patients treated with NSAIDs (6.097 ± 1.930 ng/mL), antibiotics (5.661 ± 2.395 ng/mL), and NSAIDs and antibiotics (7.142 ± 2.601 ng/mL) were significantly lower than in samples of control patients (10.432 ± 4.257 ng/mL, ANOVA p = 0.008). The RT-PCR did not reveal VEGFA gene expression in any of the 42 samples. VEGFB gene expression was found in 26 of 42 samples (69.1%). The use of NSAIDs or antibiotics in patients with exacerbated chronic periodontitis decreases VEGF levels in periapical tissues. Pharmacotherapy may minimize the effects of VEGF on apical periodontitis progression in that way.

scholarly journals Hypoxic Regulation of Vascular Endothelial Growth Factor mRNA Stability Requires the Cooperation of Multiple RNA Elements

1999 ◽  
Vol 10 (4) ◽  
pp. 907-919 ◽  
Author(s):  
J. A. Dibbens ◽  
D. L. Miller ◽  
A. Damert ◽  
W. Risau ◽  
M. A. Vadas ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Vascular Endothelial ◽  
Coding Region ◽  
Vegf Gene ◽  
Vegf Expression ◽  
Vegf Mrna ◽  
Rapid Degradation ◽  
Multiple Regions ◽  
Endothelial Growth Factor

Vascular endothelial growth factor (VEGF) is a key regulator of developmental, physiological, and tumor angiogenesis. Upregulation of VEGF expression by hypoxia appears to be a critical step in the neovascularization of solid cancers. The VEGF mRNA is intrinsically labile, but in response to hypoxia the mRNA is stabilized. We have systematically analyzed the regions in the VEGF mRNA that are responsible for its lability under normoxic conditions and for stabilization in response to hypoxia. We find that the VEGF mRNA not only contains destabilizing elements in its 3′ untranslated region (3′UTR), but also contains destabilizing elements in the 5′UTR and coding region. Each region can independently promote mRNA degradation, and together they act additively to effect rapid degradation under normoxic conditions. Stabilization of the mRNA in response to hypoxia is completely dependent on the cooperation of elements in each of the 5′UTR, coding region, and 3′UTR. Combinations of any of two of these three regions were completely ineffective in responding to hypoxia, whereas combining all three regions allowed recapitulation of the hypoxic stabilization seen with the endogenous VEGF mRNA. We conclude that multiple regions in the VEGF mRNA cooperate both to ensure the rapid degradation of the mRNA under normoxic conditions and to allow stabilization of the mRNA in response to hypoxia. Our findings highlight the complexity of VEGF gene expression and also reveal a mechanism of gene regulation that could become the target for strategies of therapeutic intervention.

BCR/ABL induces expression of vascular endothelial growth factor and its transcriptional activator, hypoxia inducible factor-1α, through a pathway involving phosphoinositide 3-kinase and the mammalian target of rapamycin

Blood ◽  
2002 ◽  
Vol 100 (10) ◽  
pp. 3767-3775 ◽  
Author(s):  
Matthias Mayerhofer ◽  
Peter Valent ◽  
Wolfgang R. Sperr ◽  
James D. Griffin ◽  
Christian Sillaber
Keyword(s):  
Gene Expression ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Mammalian Target Of Rapamycin ◽  
Hypoxia Inducible Factor ◽  
Vascular Endothelial ◽  
Vegf Gene ◽  
Vegf Mrna ◽  
Phosphoinositide 3 Kinase ◽  
Endothelial Growth Factor

Recent data suggest that vascular endothelial growth factor (VEGF), a cytokine involved in autocrine growth of tumor cells and tumor angiogenesis, is up-regulated and plays a potential role in myelogenous leukemias. In chronic myelogenous leukemia (CML), VEGF is expressed at high levels in the bone marrow and peripheral blood. We show here that the CML-associated oncogene BCR/ABL induces VEGF gene expression in growth factor–dependent Ba/F3 cells. Whereas starved cells were found to contain only baseline levels of VEGF mRNA, Ba/F3 cells induced to express BCR/ABL exhibited substantial amounts of VEGF mRNA. BCR/ABL also induced VEGF promoter activity and increased VEGF protein levels in Ba/F3 cells. Moreover, BCR/ABL was found to promote the expression of functionally active hypoxia-inducible factor-1 (HIF-1), a major transcriptional regulator of VEGF gene expression. BCR/ABL-induced VEGF gene expression was counteracted by the phosphoinositide 3-kinase (PI3-kinase) inhibitor LY294002 and rapamycin, an antagonist of mammalian target of rapamycin (mTOR), but not by inhibition of the mitogen-activated protein kinase pathway. Similarly, BCR/ABL-dependent HIF-1α expression was inhibited by the addition of LY294002 and rapamycin. Together, our data show that BCR/ABL induces VEGF- and HIF-1α gene expression through a pathway involving PI3-kinase and mTOR. BCR/ABL-induced VEGF expression may contribute to the pathogenesis and increased angiogenesis in CML.

scholarly journals Comparison of Menstrual Effluent Vascular Endothelial Growth Factor Immunocytochemistry Expression Between Endometriosis and Non-Endometriosis Patients

2020 ◽  
Vol 9 (3) ◽  
pp. 182-189
Author(s):  
Ruswana Anwar ◽  
Sunardi Sunardi ◽  
Siti Salima ◽  
Setyorini Irianti ◽  
Benny Hasan Purwara ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Study Groups ◽  
Pain Scale ◽  
Control Group ◽  
Vascular Endothelial ◽  
Vegf Expression ◽  
Cyst Size ◽  
Significant Difference ◽  
Endothelial Growth Factor

Objectives: This study aimed to measure the vascular endothelial growth factor (VEGF) expression in menstrual effluent from patients with endometriosis compared to non-endometriosis through immunocytochemical methods. We also measured the degree of pain level, endometrioma cyst size, and infertility status whether it is affected by VEGF expression. Materials and Methods: The present case-control study was conducted in Hasan Sadikin General Hospital, Bandung. Thirty productive-age women diagnosed with endometrioma and 30 productive-age women without endometriosis as the control group were included in this study. Menstrual effluent was taken from the posterior fornix on the second day of menstruation and stained using immunocytochemistry staining for VEGF. Results: The results demonstrated a significant difference between the two study groups in terms of VEGF intensity and histoscore although no difference was found in VEGF distributions between the study groups. The subjects in the endometriosis group had significantly higher VEGF intensity and significantly higher VEGF histoscore compared to the control group. Women with VEGF histoscore more than 6 has 9.33 times risk of developing endometriosis compared to those with lower histoscore. There were no significant correlations between VEGF and pain scale, infertility, and the cyst size. Finally, the cyst size was proportionally related to pain. Conclusions: VEGF distribution and expression in endometriosis women were significantly higher than VEGF levels in non-endometriosis women. Women with menstrual effluent containing higher VEGF levels had more chances of developing endometriosis compared to those with lower VEGF levels. Eventually, larger endometrioma size was proportionally related to higher pain levels in subjects with endometrioma.

scholarly journals Effects of hyperthyroidism on expression of vascular endothelial growth factor (VEGF) and apoptosis in fetal adrenal glands

2015 ◽  
Vol 59 (4) ◽  
Author(s):  
T. Karaca ◽  
Y. Hulya Uz ◽  
R. Karabacak ◽  
I. Karaboga ◽  
S. Demirtas ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Adrenocorticotropic Hormone ◽  
Adrenal Glands ◽  
Control Group ◽  
Vascular Density ◽  
Vascular Endothelial ◽  
Vegf Expression ◽  
Fetal Rat ◽  
Endothelial Growth Factor

<p>This study investigated the expression of vascular endothelial growth factor (VEGF), vascular density, and apoptosis in fetal rat adrenal glands with hyperthyroidism in late gestation. Twelve mature female Wistar albino rats with the same biological and physiological features were used for this study. Rats were divided into two groups: control and hyperthyroidism. Hyperthyroidism was induced by daily subcutaneous injections of L-thyroxine (250 μg/kg) before pregnancy for 21 days and during pregnancy. Rats in the control and hyperthyroidism groups were caged according to the number of male rats. Zero day of pregnancy (Day 0) was indicated when the animals were observed to have microscopic sperm in vaginal smears. Pregnant rats were sacrificed on the 20th day of pregnancy; blood from each animal was collected to determine the concentrations of maternal adrenocorticotropic hormone and thyroxine. Rat fetuses were then quickly removed from the uterus, and the adrenal glands of the fetuses were dissected. VEGF expression, vascular density, and apoptosis were analyzed in fetal rat adrenal glands. Maternal serum levels of the adrenocorticotropic hormone and free thyroxine were significantly higher in the hyperthyroidism group than in the control group. Immunohistochemistry revealed that the number of VEGF positive cells and vessel density significantly increased in the hyperthyroidism rat fetal adrenal group compared with the control group. Hyperthyroidism did not change the fetal and placental weights and the number of fetuses. This study demonstrates that hyperthyroidism may have an effect on the development of rat adrenal glands mediated by VEGF expression, angiogenesis, and apoptosis. </p>

Quantitative Analysis of Gene Expression for Vascular Endothelial Growth Factor and Its Application.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 3912-3912
Author(s):  
Xia Bai ◽  
Jianxin Fu ◽  
Kaiyang Ding ◽  
Jiannong Cen ◽  
Zhaoyue Wang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Leukemia Cell ◽  
Reduction Rate ◽  
Leukemia Cell Line ◽  
Vascular Endothelial ◽  
Vegf Gene ◽  
Nbt Reduction ◽  
Endothelial Growth Factor

Abstract Vascular endothelial growth factor (VEGF) is a crucial mediator of angiogenesis, and plays an important role in pathogenesis of leukemia. However, the importance of VEGF in differentiation or apoptosis of leukemic cells remains to be evaluated. A competitor DNA fragment template of VEGF gene mimic was constructed with the method of gene recombinant technologies, and a competitive quantitative reverse transcriptase-polymerase chain reaction (cQRT-PCR) for analyzing VEGF gene expression was performed to assess the regulation of VEGF gene expression in the process of all-trans retinoic acid (ATRA)-induced differentiation of an acute promyelocytic leukemia cell line NB4. In construction of a standard curve from which the amount of target cDNA was derived, serial dilutions of the target were co-amplified with a constant amount of mimic, and the intensities of bands corresponding to the target and the mimic were measured. CD11b antigen and nitroblue tetrazolium (NBT) reduction rate of NB4 cells were also assayed at different time points. cQRT-PCR was a sensitive and reliable tool for analysis of VEGF gene expression, with a detectable range from 1 to 2 times 10 the fifth power molecules. The number of VEGF gene transcripts detected by means of cQRT-PCR assay was 42.3, 12.6, 3.6, and less than 1.0 times 10 the fifth powder per microgram of NB4 total RNA at 0, 12, 24 and 48 hours after ATRA treatment, respectively. The rapid down-regulation of VEGF gene expression during ATRA-induced NB4 cell differentiation was accompanied by an upregulation of CD11b expression and an increased NBT reduction rate. In conclusion, cQRT-PCR could be used as an efficient method of qualitative analysis of VEGF gene expression. ATRA significantly depresses VEGF expression and its antileukemic effect can be brought through the two ways of differentiation induction and angiogenesis inhibition.

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