scholarly journals The Effectiveness of Triamcinolone Injection on Risk of Postoperative Operations with the Conjunctiva Autograft Technique and Its Association with Change of VEGF mRNA Expression

2020 ◽  
Vol 13 (02) ◽  
pp. 543-549 ◽  
Author(s):  
Purnamanita Purnamanita ◽  
Budu Budu ◽  
Mochammad Hatta ◽  
Muhammad Nasrum Massi ◽  
Rosdiana Natzir ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Vegf Mrna ◽  
Triamcinolone Injection ◽  
Vegf Mrna Expression

scholarly journals Adenosine upregulates VEGF expression in cultured myocardial vascular smooth muscle cells

1999 ◽  
Vol 277 (2) ◽  
pp. H595-H602 ◽  
Author(s):  
Jian-Wei Gu ◽  
Ann L. Brady ◽  
Vivek Anand ◽  
Michael C. Moore ◽  
Whitney C. Kelly ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Mrna Expression ◽  
Vascular Smooth Muscle Cells ◽  
Vegf Expression ◽  
Vegf Mrna ◽  
Protein Levels ◽  
Hypoxic Conditions ◽  
Vegf Mrna Expression ◽  
Vegf Protein

We tested whether adenosine has differential effects on vascular endothelial growth factor (VEGF) expression under normoxic and hypoxic conditions, and whether A1 or A2 receptors (A1R; A2R) mediate these effects. Myocardial vascular smooth muscle cells (MVSMCs) from dog coronary artery were exposed to hypoxia (1% O2) or normoxia (20% O2) in the absence and presence of adenosine agonists or antagonists for 18 h. VEGF protein levels were measured in media with ELISA. VEGF mRNA expression was determined with Northern blot analysis. Under normoxic conditions, the adenosine A1R agonists, N 6-cyclopentyladenosine and R(-)- N 6-(2-phenylisopropyl)adenosine did not increase VEGF protein levels at A1R stimulatory concentrations. However, adenosine (5 μM) and the adenosine A2R agonist N 6-[2-(3,5-dimethoxyphenyl)-2-(2-methylphenyl)]ethyl adenosine (DPMA; 100 nM) increased VEGF protein levels by 51 and 132% and increased VEGF mRNA expression by 44 and 90%, respectively, in cultured MVSMCs under normoxic conditions. Hypoxia caused an approximately fourfold increase in VEGF protein and mRNA expression, which could not be augmented with exogenous adenosine, A2R agonist (DPMA), or A1R agonist [1,3-diethyl-8-phenylxanthine (DPX)]. The A2R antagonist 8-(3-chlorostyryl)-caffeine completely blocked adenosine-induced VEGF protein and mRNA expression and decreased baseline VEGF protein levels by up to ∼60% under normoxic conditions but only by ∼25% under hypoxic conditions. The A1R antagonist DPX had no effect. These results are consistent with the hypothesis that 1) adenosine increases VEGF protein and mRNA expression by way of A2R. 2) Adenosine plays a major role as an autocrine factor regulating VEGF expression during normoxic conditions but has a relatively minor role during hypoxic conditions. 3) Endogenous adenosine can account for the majority of basal VEGF secretion by MVSMCs under normoxic conditions and could therefore be a maintenance factor for the vasculature.

The relationship of EGFR and VEGF mRNA expression in ovarian carcinoma

2009 ◽  
Vol 6 (2) ◽  
pp. 100-103 ◽  
Author(s):  
Aiping Chen ◽  
Ruirui Yang ◽  
Hongling Zhang ◽  
Hui Song
Keyword(s):  
Ovarian Carcinoma ◽  
Mrna Expression ◽  
Vegf Mrna ◽  
Relationship Of ◽  
The Relationship ◽  
Vegf Mrna Expression

REAL TIME RT-PCR VEGF mRNA EXPRESSION AND ERK1 EXPRESSION AND ACTIVITY IN RENAL TUMORS

1999 ◽  
pp. 148
Author(s):  
Donata Villari ◽  
Giulio Nicita ◽  
Carmela Tricarico ◽  
Astrid Parenti ◽  
Alessandro Della Melina ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Real Time ◽  
Renal Tumors ◽  
Rt Pcr ◽  
Vegf Mrna ◽  
Vegf Mrna Expression ◽  
Expression And Activity

The Role Of PO2, HbO2 and Exercise in Human VEGF mRNA Expression

2004 ◽  
Vol 36 (Supplement) ◽  
pp. S52???s53
Author(s):  
Lesley Lawrenson ◽  
Jennifer G. Poole ◽  
I. Mark Olfert ◽  
Russell S. Richardson
Keyword(s):  
Mrna Expression ◽  
Vegf Mrna ◽  
Vegf Mrna Expression

scholarly journals Heart and lung VEGF mRNA expression in rats with monocrotaline- or hypoxia-induced pulmonary hypertension

1998 ◽  
Vol 275 (6) ◽  
pp. H1948-H1956 ◽  
Author(s):  
Chohreh Partovian ◽  
Serge Adnot ◽  
Saadia Eddahibi ◽  
Emmanuel Teiger ◽  
Micheline Levame ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Mrna Expression ◽  
Vascular Remodeling ◽  
Prolonged Exposure ◽  
Similar Degree ◽  
Vegf Expression ◽  
Vegf Mrna ◽  
Pulmonary Vascular Remodeling ◽  
The Right ◽  
Vegf Mrna Expression

Vascular endothelial growth factor (VEGF) is an endothelial cell-specific mitogen that is upregulated during exposure to hypoxia. In this study, we analyzed heart and lung VEGF mRNA expression and examined pulmonary vascular remodeling as well as myocardial capillary density in two rat models of pulmonary hypertension involving exposure to chronic hypoxia (CH) and treatment with monocrotaline (MCT), respectively. The rats were studied after 0.5, 1, 3, 15, and 30 days of exposure to 10% O2 or 1, 6, and 30 days after a subcutaneous MCT injection (60 mg/kg). Both CH and MCT induced pulmonary hypertension and hypertrophy of the right ventricle (RV) with increased RV weight and atrial natriuretic peptide mRNA expression. VEGF mRNA expression as assessed by Northern blot analysis was potently induced after 12 h of hypoxia in both the right and left ventricles. After prolonged exposure to hypoxia, VEGF mRNA returned to baseline in the left ventricle (LV) but remained increased in the RV, where it peaked after 30 days. In MCT rats, VEGF mRNA was unchanged in the LV but decreased by 50% in the RV and by 90% in the lungs after 30 days. VEGF mRNA remained unchanged in the lungs from CH rats. Pulmonary vascular remodeling was more pronounced in MCT than in CH rats. The number of capillaries per RV myocyte was increased in rats exposed to 30 days of hypoxia, whereas it remained unchanged in MCT rats despite a similar degree of RV hypertrophy. Our results suggest that the sustained increase in VEGF expression in the hypertrophied RV during CH may account for the increased number of capillaries per myocyte. In contrast, reduced VEGF expression in the lungs and RV of MCT rats may aggravate pulmonary vascular remodeling and compromise RV myocardial perfusion.

VEGF mRNA expression in bovine fetal cotyledons and maternal caruncles throughout gestation

2007 ◽  
Vol 115 (S 1) ◽  
Author(s):  
C Pfarrer ◽  
R Leiser ◽  
D Schams ◽  
HR Tinneberg ◽  
B Berisha
Keyword(s):  
Mrna Expression ◽  
Vegf Mrna ◽  
Vegf Mrna Expression

Human Cytomegalovirus Can Infect Multiple Myeloma Cells and Protect the Cells from Apoptosis.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 5059-5059
Author(s):  
Guoqing Wei ◽  
Maofang Lin ◽  
Guangsheng Zhao ◽  
He Huang ◽  
Zhen Cai
Keyword(s):  
Mrna Expression ◽  
Culture Medium ◽  
Cmv Infection ◽  
Pcr Assay ◽  
Vegf Mrna ◽  
Serum Free ◽  
Pp65 Antigen ◽  
Infected Cells ◽  
Rpmi 8226 ◽  
Vegf Mrna Expression

Abstract Tumor relapse and cytomegalovirus(CMV) infection are very important concerns in the therapy of hematopoietic malignancies by bone marrow transplantation.It was reported that there was a higher rate of CMV reactivation in patients with multiple myeloma(MM) after autologous or CD34+ stem cell selected transplantation,but no attention so far has been given to a possible pathogenetic interplay between CMV and MM cells.CMV could infect many kinds of cells, and could inhibit apoptotic responses in several cell systems.Our studies were to investigate the alteration of apoptosis in MM cell line cells infected by CMV as well as the possible mechanism. After CMV AD169 was propagated in HF fibroblasts,MM cell line KM3 and RPMI 8226 cells were infected by 100,10,1 TCID50 of CMV,then were cultured with serum-free RPMI 1640.RT-PCR assay was used to detect the mRNA expression of CMV immediate early (IE) gene,Flow Cytometry was used to detect the CMV pp65 antigen positive cells and transmission electron microscope was used to detect CMV particles in the cells as well as the morpholoy and inner structure of the apoptotic MM cells. AnnexinV-FITC and Propidium Iodide Staining Solution were added to MM cells and apoptotic cells were detected with Flow Cytometry.To explore the possible mechanism that CMV infection inhibit the apoptotic responses in MM cells,RT-PCR assay was used to detecte the mRNA expression of IL-6 and VEGF in CMV-infected and mock-infected cells; ELISA assay was used to detecte the protein expression of IL-6 in the culture medium; EMSA assay was used to detecte the NF-κB activity of the cells.We got these results as below: CMV-infected MM cells could express IE mRNA compared with the uninfected;CMV particles could be found in the cells infected by 100 TCID50 of CMV compared with the mock-infected cells,and there were much more CMV pp65 antigen positive cells when KM3 cells were infected by 100,10 TCID50 of CMV,which was significant higher than the control group P<0.01. As to RPMI 8226 cells,CMV pp65 antigen positive cells were 4.3% when cells were infected by 100 TCID50 of CMV,while there were no CMV pp65 antigen positive cells in the mock-infected RPMI 8226 cells. There were less apoptotic KM3 cells which were infected with 100,10 TCID50 of CMV compared with the uninfected when cells were cultured in serum-free cultures P<0.05. As to RPMI 8226 cells, percent of apoptotic cells infected with 100,10,1 TCID50 of CMV were higher than the mock infected cells(21.2%,44.0%,53.2% vs 58.9%). Few apoptotic MM cells with typical character could be found in the CMV infected cells compared with the uninfected. CMV could increase the expression of IL-6 mRNA in MM cells in a titer-dependent way,While VEGF mRNA expression was not different between the infected and mock-infected group. On the other hand, CMV infection could increase the IL-6 protein and this protein in the culture medium increased as the CMV titer increased as well as time prolonged.With EMSA assay It was found that NF-κB was reactivated by the CMV infection. In conclusion, the results suggest: CMV can infect MM cells and replicate in the cells. CMV can protect MM cells from apoptosis induced by serum-free culture. CMV can activate NF-κB and increase the level of IL-6(mRNA and protein)in MM cells while not affect the VEGF mRNA expression. These results indicate that CMV may protect MM cells from apoptosis,which means that CMV infection maybe has very close relationship with tumor relapse or resistance to chemotherapeutic agents.

scholarly journals Vascular endothelial growth factor increases messenger RNAs encoding cyclooxygenase-II and membrane-associated prostaglandin E synthase in rat luteal cells

2004 ◽  
Vol 183 (3) ◽  
pp. 527-533 ◽  
Author(s):  
T Sakurai ◽  
K Tamura ◽  
H Kogo
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Mrna Expression ◽  
Corpus Luteum ◽  
Prostaglandin E ◽  
Vascular Endothelial ◽  
Vegf Mrna ◽  
Luteal Cells ◽  
Endothelial Growth Factor ◽  
Vegf Mrna Expression

Vascular endothelial growth factor (VEGF) is known to be necessary for the vascularization of the developing corpus luteum. Our recent data suggested that cyclooxygenase-II (COX-II) may play a role in the formation of vascular plexuses in developing corpora lutea of the rat. Here we examined the relationship between VEGF and the expression of prostaglandin (PG)- metabolizing enzymes in rat ovarian luteal cells. VEGF treatment caused a dose-dependent increase in the expression of COX-II and membrane-associated PGE synthase (mPGES) mRNA in cultured rat luteal cells. However, pretreatment of the luteal cells with a selective COX-II inhibitor, NS-398, abolished the VEGF-enhanced mPGES mRNA expression. VEGF also increased PGE2 secretion. Conversely, PGE2 dose-dependently stimulated VEGF mRNA expression. Furthermore, VEGF induced VEGF mRNA expression, but this effect was abolished by NS-398 pretreatment. These findings suggest that VEGF enhances PGE2 production by stimulating COX-II and mPGES expression in rat corpus luteum and that the effect of VEGF on luteal cells may be partially mediated by this stimulation of PGE2 production.

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