1628: Direct Regulation of Prostate Blood Flow By Vascular Endothelial Growth Factor and its Participation in The Signal Transduction Pathway of Androgenic Prostate Blood Flow Regulation

2004 ◽  
Vol 171 (4S) ◽  
pp. 430-430
Author(s):  
Seiji Arai ◽  
Yasuhiro Shibata ◽  
Bunzo Kashiwagi ◽  
Yoshitatsu Fukabori ◽  
Kazuhiro Suzuki ◽  
...  
2018 ◽  
Vol 4 (1) ◽  
pp. 71-76 ◽  
Author(s):  
Antonietta Gigante ◽  
Luca Navarini ◽  
Domenico Margiotta ◽  
Biagio Barbano ◽  
Antonella Afeltra ◽  
...  

Introduction: Since female sexual dysfunction in systemic sclerosis women is multifactorial, we can assume that vascular damage may play a role in pathogenesis. The aim of the study was to evaluate the clitoral blood flow, by Echo color Doppler, and to correlate it whit serum levels of vascular endothelial growth factor and endostatin. Methods: A total of 15 systemic sclerosis women and 10 healthy controls matched for sex and age were enrolled in this study. Serum VEGF165 and endostatin levels were determined in systemic sclerosis patients by commercial enzyme-linked immunosorbent assay kit. Clitoral blood flow was measured by Doppler indices of clitoral artery: pulsatile index, resistive index, and systolic/diastolic ratio were measured. Sexual dysfunction was assessed by Female Sexual Function Index. Results: Vascular endothelial growth factor (pg/mL) and endostatin (ng/mL) median values were significantly higher in systemic sclerosis women than healthy controls. Resistive index and systolic/diastolic ratio median values were significantly higher in systemic sclerosis women than healthy controls. Negative correlation exists between serum levels of vascular endothelial growth factor and resistive index (r = −0.55, p < 0.05). Positive correlation was observed between serum levels of endostatin and resistive index (r = 0.70, p < 0.01) and systolic/diastolic ratio (r = 0.77, p < 0.01). Discussion: We can suppose that clitoral blood flow in systemic sclerosis women is reduced not only for macro- and microvascular damage but also for impaired angiogenesis.


Blood ◽  
1997 ◽  
Vol 90 (9) ◽  
pp. 3507-3515 ◽  
Author(s):  
Jian-Feng Wang ◽  
Ramesh K. Ganju ◽  
Zhong-Ying Liu ◽  
Hava Avraham ◽  
Shalom Avraham ◽  
...  

Abstract We have recently identified a novel ligand of the vascular endothelial growth factor (VEGF) family termed VEGF-related protein (VRP), which specifically binds to the FLT4 receptor. To characterize the signaling events after VRP engagement of its cognate receptor in hematopoietic cells, a population of human erythroleukemia (HEL) cells, termed HEL-JW, expressing high levels of FLT4 receptor was isolated. Stimulation of HEL-JW cells with VRP alone and in combination with the c-kit ligand/stem cell factor increased cell growth. VRP induced tyrosine phosphorylation of various proteins, including the FLT4 receptor. Further characterization of these tyrosine phosphorylated molecules revealed that Shc, Grb2, and SOS form a complex with the activated FLT4 receptor. HEL-JW cells also expressed RAFTK, a recently identified member of the focal adhesion kinase family. RAFTK was phosphorylated and activated upon VRP treatment, and there was an enhanced association of this kinase with the adaptor protein Grb2. Furthermore, the c-Jun NH2-terminal kinase (JNK), involved in growth activation and shown to mediate RAFTK signaling in other cell types, was activated by VRP stimulation. We also observed that VRP treatment of HEL-JW cells resulted in the phosphorylation of the cytoskeletal protein paxillin. This treatment resulted in an increased association of paxillin with RAFTK, which was mediated by the C-terminal region of RAFTK. These studies indicate that VRP stimulation induced the formation of a signaling complex at its activated receptor as well as activation of RAFTK. VRP-mediated activation of RAFTK may facilitate signal transduction to the cytoskeleton and downstream to the JNK pathway in FLT4-expressing blood cells.


2019 ◽  
Vol 02 (02) ◽  
pp. 107-107 ◽  
Author(s):  
Margalef R. ◽  
Minaya Muñoz F. ◽  
Valera Garrido F. ◽  
Santafe MM

Abstract Background The action of galvanic currents (GC) includes the generation of vasoactive substances such as, for example the vascular endothelial growth factor (VEGF) and its receptor, VEGFR-2. Aim To evaluate modifications in blood flow by action of the galvanic current. Material and Methods The experiments have been performed in Swiss male mice (45-50 days old). The experiments were performed at controlled temperature and light settings. The hypodermis of the skin in the cranial area was used. The procedures were as follows: 1) A portion of skin was sectioned and lifted to obtain a control image; 2) the needle (Physio Invasiva 0.30 × 40mm) was placed over the surface of the skull and covered with skin; 3) treatment was applied using 3 mA, during 3 seconds and three applications (Physio Invasiva Prim); 4) the skin was immediately lifted once again and 3h later to obtain experimental images. In the case of the controls, process 1-4 was repeated, however without applying current. The images were binarized (Digimizer 4.6.1. MedCalc Software) and the area occupied by the vessels of the same surface for each image. Results In mice treated using the GC protocol 3mA, 3 seconds and 3 applications, an increase of 38.53% ± 0.006 was obtained immediately after the application of the GC. However, at three hours, this variation disappears (% of variation: 4.03 ± 0.01), recovering control values. In the control experiments there was no modification. Conclusions Galvanic currents provoke an immediate and transitory vasodilation in mid to small caliber vessels. An immediate and transitory vasodilation has two consequences: the arrival of cells responsible for the inflammatory reaction is accelerated (an essential and necessary step for the regeneration of tissues) and lavage of nociceptive substances is facilitated, which supports an analgesic effect.


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