scholarly journals ANALYSIS OF THE INTERRELATION OF THE VASCULAR ENDOTHELIAL GROWTH FACTOR WITH PITUITARY ADENOMAS COMPLICATED BY PITUITARY APOPLEXY

2017 ◽  
Vol 22 (3) ◽  
pp. 131-135
Author(s):  
K. E Makhkamov ◽  
Miralib M. Azizov ◽  
T. A Vervekina ◽  
D. A Nishonov

Aim. Despite the fact that the pituitary adenoma is a relatively benign tumor, sometimes the course of the disease is complicated by intramedullary hemorrhage. In the world literature there are single data on the molecular mechanism of hemorrhage in the adenomas of the pituitary gland. Vascular endothelial growth factor (VEGF) plays an important role in angiogenesis and permeability of the endothelium in various brain tumors. There was made an analysis of the relationship between pituitary apoplexy and VEGF expression in pituitary adenomas. Material and methods. Immunohistochemical investigation of the level of expression of the molecular-biological marker - VEGF was performed with the use of monoclonal antibodies with the method of semiquantitative analysis in 30 pituitary adenoma patients. In the clinical study data about the age, gender, hormonal activity and X-ray study were studied. There was executed a statistical analysis of the relationship between clinical diagnostic data and VEGF expression. Results. Hormonal active tumors were detected in 12 (40%) cases, intratumoral hemorrhage - in 16 (53.3%), adenomas with cystic component - in 7 (23.3%) and invasion of cavernous sinus - in 22 (73.3%) of cases. Expression of VEGF was observed in 11 cases (36.6%). Based on the analysis the expression of VEGF was found to be closely related to pituitary apoplexy (PA) in pituitary adenomas (p < 0.001). However, there was no statistically significant relationship between VEGF and age, sex, tumor size, hormonal activity, cystic component presence, invasive tumor growth (p > 0.05). Conclusion. It was found that immunohistochemical examination of the level of expression of a molecular biological marker VEGF can be used in the evaluation of the prognosis of the disease or the identification of a risk group with a high probability of the development of pituitary apoplexy and recurrence of tumor growth.

1999 ◽  
Vol 10 (3) ◽  
pp. 229-235 ◽  
Author(s):  
Ricardo V. Lloyd ◽  
Bernd W. Scheithauer ◽  
Takao Kuroki ◽  
Sergio Vidal ◽  
Kalman Kovacs ◽  
...  

2002 ◽  
Vol 28 (1) ◽  
pp. 20-23 ◽  
Author(s):  
L ARTESE ◽  
C RUBINI ◽  
G FERRERO ◽  
M FIORONI ◽  
A SANTINELLI ◽  
...  

Circulation ◽  
1998 ◽  
Vol 98 (20) ◽  
pp. 2108-2116 ◽  
Author(s):  
Mayumi Inoue ◽  
Hiroshi Itoh ◽  
Makiko Ueda ◽  
Takahiko Naruko ◽  
Akiko Kojima ◽  
...  

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Hanna Lawnicka ◽  
Dorota Ptasinska-Wnuk ◽  
Slawomir Mucha ◽  
Jolanta Kunert-Radek ◽  
Marek Pawlikowski ◽  
...  

The aim of our study was to examine the involvement of renin-angiotensin system (RAS) in estrogen-induced lactotropes proliferation and vascular endothelial growth factor (VEGF) expression in rat pituitary. The study was performed on Fisher 344 rats underwent 8-day treatment with diethylstilboestrol (DES). The proliferation index (PCNA) and VEGF expression in pituitary sections were estimated using immunohistochemical methods. Treatment with DES increased the number of PCNA-positive cells, VEGF-positive cells, and VEGF-positive blood vessels in pituitary. Stimulatory effect of estrogen on cell proliferation and VEGF expression in blood vessels was attenuated by losartan, PD123319, and captopril. VEGF immunoreactivity in pituitary cells of DES-treated rats was decreased by AT1 antagonist and not changed by AT2 blocker and ACE inhibitor. Our findings suggest the involvement of RAS in DES-induced cell proliferation and VEGF expression in pituitary. Both the AT1 and AT2 receptors appear to mediate the estrogen-dependent mitogenic and proangiogenic effects in rat pituitary.


2009 ◽  
Vol 137 (7-8) ◽  
pp. 379-383 ◽  
Author(s):  
Ana Vidovic ◽  
Gradimir Jankovic ◽  
Dragica Tomin ◽  
Maja Perunicic-Jovanovic ◽  
Irena Djunic ◽  
...  

Introduction. Increased angiogenesis in bone marrow is one of the characteristics of chronic myeloid leukaemia (CML), a clonal myeloproliferative disorder that expresses a chimeric bcr/abl protein. Vascular endothelial growth factor (VEGF) is one of the most potent and a specific regulator of angiogenesis which principally targets endothelial cells and regulates several of their functions, including mitogenesis, permeability and migration. The impact of elevated VEGF expression on the course of chronic myeloid leukaemia is unknown. Objective. The aim of this study was the follow-up of VEGF expression during the course of CML. Methods. We studied VEGF expression of 85 CML patients (median age 50 years, range 16-75 years). At the commencement of the study, 29 patients were in chronic phase (CP), 25 in an accelerated phase (AP), and 31 in the blast crisis (BC). The temporal expression (percentage positivity per 1000 analysed cells) VEGF proteins over the course of CML were studied using the immunohistochemical technique utilizing relevant monoclonal antibodies. It was correlated with the laboratory (Hb, WBC and platelet counts, and the percentage of blasts) and clinical parameters (organomegaly, duration of CP, AP, and BC) of disease progression. Results. The expression of VEGF protein was most pronounced in AP (ANOVA, p=0.033). The level of VEGF expression correlated inversely with the degree of splenomegaly (Pearson, r=-0.400, p=0.011). High expression of VEGF correlated with a shorter overall survival (log rank, p=0.042). Conclusion. Immunohistochemically confirmed significance of the expression of VEGF in dependence of the CML stage could be of clinical importance in deciding on the timing therapy. These data suggest that VEGF plays a role in the biology of CML and that VEGF inhibitors should be investigated in CML.


2010 ◽  
Vol 299 (4) ◽  
pp. R1059-R1067 ◽  
Author(s):  
I. Mark Olfert ◽  
Richard A. Howlett ◽  
Peter D. Wagner ◽  
Ellen C. Breen

We have previously shown, using a Cre-LoxP strategy, that vascular endothelial growth factor (VEGF) is required for the development and maintenance of skeletal muscle capillarity in sedentary adult mice. To determine whether VEGF expression is required for skeletal muscle capillary adaptation to exercise training, gastrocnemius muscle capillarity was measured in myocyte-specific VEGF gene-deleted (mVEGF−/−) and wild-type (WT) littermate mice following 6 wk of treadmill running (1 h/day, 5 days/wk) at the same running speed. The effect of training on metabolic enzyme activity levels and whole body running performance was also evaluated in mVEGF−/− and WT mice. Posttraining capillary density was significantly increased by 59% ( P < 0.05) in the deep muscle region of the gastrocnemius in WT mice but did not change in mVEGF−/− mice. Maximal running speed and time to exhaustion during submaximal running increased by 20 and 13% ( P < 0.05), respectively, in WT mice after training but were unchanged in mVEGF−/− mice. Training led to increases in skeletal muscle citrate synthase (CS) and phosphofructokinase (PFK) activities in both WT and mVEGF−/− mice ( P < 0.05), whereas β-hydroxyacyl-CoA dehydrogenase (β-HAD) activity was increased only in WT mice. These data demonstrate that skeletal muscle capillary adaptation to physical training does not occur in the absence of myocyte-expressed VEGF. However, skeletal muscle metabolic adaptation to exercise training takes place independent of myocyte VEGF expression.


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