scholarly journals Vascular endothelial growth factor is neuroprotective against ischemic brain injury by inhibiting scavenger receptor A expression on microglia

2017 ◽  
Vol 142 (5) ◽  
pp. 700-709 ◽  
Author(s):  
Zheng Xu ◽  
Kaiwei Han ◽  
Jigang Chen ◽  
Chunhui Wang ◽  
Yan Dong ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Brain Injury ◽  
Growth Factor ◽  
Scavenger Receptor ◽  
Ischemic Brain Injury ◽  
Vascular Endothelial ◽  
Ischemic Brain ◽  
Scavenger Receptor A ◽  
Endothelial Growth Factor

scholarly journals Class A1 scavenger receptor prevents obesity-associated blood pressure elevation through suppressing overproduction of vascular endothelial growth factor B in macrophages

2020 ◽  
Author(s):  
Xudong Zhu ◽  
Yan Wang ◽  
Liu Zhu ◽  
Ye Zhu ◽  
Kun Zhang ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Scavenger Receptor ◽  
Vascular Endothelial ◽  
Obese Mice ◽  
Blood Pressure Elevation ◽  
Perivascular Adipose Tissue ◽  
Factor B ◽  
Endothelial Growth Factor

Abstract Aims Dysfunctional innate immune function and inflammation contributes to the pathogenesis of obesity-associated hypertension, in which macrophage infiltration in the perivascular adipose tissue (PVAT) plays a key role. However, the mechanisms behind it are not well understood. Class A1 scavenger receptor (SR-A1) is one of the major pattern recognition receptors in modulating macrophage activity, and here, we aimed to investigate its role in obesity-associated hypertension. Methods and results Both diet-induced and genetic obesity were generated in mice. Deficiency in SR-A1 aggravated the obesity-induced blood pressure (BP) elevation and endothelial dysfunction in mice. The BP-elevating effect of SR-A1 deficiency was blocked by the down-regulation of vascular endothelial growth factor B (VEGF-B) in obese mice. Overexpression of VEGF-B raised BP in the obese mice but not in normal mice. Administration of fucoidan, a ligand of SR-A1, lowered BP, and VEGF-B levels in Sr-a1+/+ but not in Sr-a1−/− obese mice. Conclusion These results reveal a new link between PVAT and vascular biology in obesity orchestrated by the SR-A1/VEGF-B axis in macrophages. SR-A1 and VEGF-B may be promising therapeutic targets in the treatment of obesity-associated hypertension.

scholarly journals Vascular Endothelial Growth Factor Increases Neurogenesis after Traumatic Brain Injury

2010 ◽  
Vol 30 (5) ◽  
pp. 1008-1016 ◽  
Author(s):  
Orli Thau-Zuchman ◽  
Esther Shohami ◽  
Alexander G Alexandrovich ◽  
Ronen R Leker
Keyword(s):  
Traumatic Brain Injury ◽  
Vascular Endothelial Growth Factor ◽  
Brain Injury ◽  
Growth Factor ◽  
Functional Outcome ◽  
Vascular Endothelial ◽  
Proliferating Cells ◽  
Neuroprotective Effects ◽  
Neurologic Disorders ◽  
Endothelial Growth Factor

Activation of endogenous stem cells has been proposed as a novel form of therapy in a variety of neurologic disorders including traumatic brain injury (TBI). Vascular endothelial growth factor (VEGF) is expressed in the brain after TBI and serves as a potent activator of angiogenesis and neurogenesis. In this study, we infused exogenous VEGF into the lateral ventricles of mice for 7 days after TBI using mini-osmotic pumps to evaluate the effects on recovery and functional outcome. The results of our study show that VEGF significantly increases the number of proliferating cells in the subventricular zone and in the perilesion cortex. Fate analysis showed that most newborn cells differentiated into astrocytes and oligodendroglia and only a few cells differentiated into neurons. Functional outcome was significantly better in mice treated with VEGF compared with vehicle-treated animals after TBI. Injury size was significantly smaller at 90 days after TBI in VEGF-treated animals, suggesting additional neuroprotective effects of VEGF. In conclusion, VEGF significantly augments neurogenesis and angiogenesis and reduces lesion volumes after TBI. These changes are associated with significant improvement in recovery rates and functional outcome.

Sign in / Sign up

Export Citation Format

Share Document