scholarly journals Vascular endothelial growth factor plays a critical role in the formation of the pre-metastatic niche via prostaglandin E2

2014 ◽  
Vol 32 (6) ◽  
pp. 2477-2484 ◽  
Author(s):  
SHILI LIU ◽  
MAN JIANG ◽  
QIANG ZHAO ◽  
SHANCHENG LI ◽  
YANPING PENG ◽  
...  
Biomolecules ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 253
Author(s):  
Xi Guo ◽  
Hong Yi ◽  
Tin Chiu Li ◽  
Yu Wang ◽  
Huilin Wang ◽  
...  

Vascular endothelial growth factor (VEGF) is a well-known angiogenic factor that plays a critical role in various physiological and pathological processes. VEGF also contributes to the process of embryo implantation by enhancing embryo development, improving endometrial receptivity, and facilitating the interactions between the developing embryo and the endometrium. There is a correlation between the alteration of VEGF expression and reproductive failure, including recurrent implantation failure (RIF) and recurrent miscarriage (RM). In order to clarify the role of VEGF in embryo implantation, we reviewed recent literature concerning the expression and function of VEGF in the reproductive system around the time of embryo implantation and we provide a summary of the findings reported so far. We also explored the effects and the possible underlying mechanisms of action of VEGF in embryo implantation.


Author(s):  
Ayodeji Folorunsho Ajayi ◽  
Busuyi David Kehinde ◽  
Olubodun Micheal Lateef ◽  
Bolaji Aderibigbe Akorede

Objective: Nitric oxide (NO), prostaglandin E2 (PgE2), and vascular endothelial growth factor (VEGF) are fundamental regulators of epithelial restitution and angiogenesis. They play important roles in ulcer healing. Insights into their possible changes during gastric ulcer healing putting age into consideration could give a guide to the proper management of ulcers in the aging population. This study, therefore, examined alterations in the concentrations of PgE2, NO, and VEGF in the gastric mucosa of rats of different ages after induction of ulcer and during healing.Methods: Male Wister rats (aged 3, 6, and 18 months old) were divided into three groups according to their ages. The ulcer was induced using the acetic acid ulcer model. Healing indices studied on days 3, 7, and 14 were the macroscopic dimension of ulcer, stomach tissue concentration of PgE2, NO, and VEGF, with the immunohistochemical expression of VEGF.Results: Outcome of this study showed 100%, 88.36%, and 62.30% area of mucosa healed in 3-, 6-, and 18-month-old rats respectively, on day 14 post-induction of ulcer. PgE2, NO, and VEGF concentrations were inversely proportional to age during healing. Immunohistochemical staining showed that younger rat (3 and 6 months old) had higher expression of VEGF throughout the healing period.Conclusion: It was therefore concluded that the slower rate of healing in older rats could be due to reduced gastroprotection, epithelial restitution, and angiogenesis as age increases.


2000 ◽  
Vol 74 (22) ◽  
pp. 10699-10706 ◽  
Author(s):  
Loreen J. Savory ◽  
Steven A. Stacker ◽  
Stephen B. Fleming ◽  
Brian E. Niven ◽  
Andrew A. Mercer

ABSTRACT Infection by the parapoxvirus orf virus causes proliferative skin lesions in which extensive capillary proliferation and dilation are prominent histological features. This infective phenotype may be linked to a unique virus-encoded factor, a distinctive new member of the vascular endothelial growth factor (VEGF) family of molecules. We constructed a recombinant orf virus in which the VEGF-like gene was disrupted and show that inactivation of this gene resulted in the loss of three VEGF activities expressed by the parent virus: mitogenesis of vascular endothelial cells, induction of vascular permeability, and activation of VEGF receptor 2. We used the recombinant orf virus to assess the contribution of the viral VEGF to the vascular response seen during orf virus infection of skin. Our results demonstrate that the viral VEGF, while recognizing a unique profile of the known VEGF receptors (receptor 2 and neuropilin 1), is able to stimulate a striking proliferation of blood vessels in the dermis underlying the site of infection. Furthermore, the data demonstrate that the viral VEGF participates in promoting a distinctive pattern of epidermal proliferation. Loss of a functional viral VEGF resulted in lesions with markedly reduced clinical indications of infection. However, viral replication in the early stages of infection was not impaired, and only at later times did it appear that replication of the recombinant virus might be reduced.


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