Volumetric changes in transplanted vascularized fat flaps after ischemic or congestive stresses and their relationship to capillary density in a zucker fatty rat model

Microsurgery ◽  
2015 ◽  
Vol 35 (8) ◽  
pp. 653-661
Author(s):  
Kentaro Tanaka ◽  
Mutsumi Okazaki ◽  
Tomoyuki Yano ◽  
Masako Akiyama ◽  
Hiroki Mori ◽  
...  
Diabetologia ◽  
2011 ◽  
Vol 54 (8) ◽  
pp. 2192-2201 ◽  
Author(s):  
T. Takenaka ◽  
T. Inoue ◽  
H. Okada ◽  
Y. Ohno ◽  
T. Miyazaki ◽  
...  

2018 ◽  
Vol 46 (6) ◽  
pp. 2325-2334 ◽  
Author(s):  
Chun Gui ◽  
Zhi-yu  Zeng ◽  
Qi Chen ◽  
Ya-wei Luo ◽  
Lang Li ◽  
...  

Background/Aims: Microvascular insufficiency takes a critical role in the development of diabetic cardiomyopathy (DCM). So this study was designed to investigate the effects of Neuregulin-1 (NRG-1) treatment on myocardial angiogenesis and the changes of VEGF/Flk1 and Ang-1/Tie-2 signaling in the rat model of DCM. Methods: Diabetic rats were induced by a single intraperitoneal injection of Streptozotocin. 12 weeks after the diabetes induction, the rats with NRG-1 treatment were treated with tail vein injection of NRG-1 at the dose of 10µg/kg/d for consecutive 10 days. Cardiac function was assessed using catheter MPA cardiac function analysis system. Myocardial blood flow (MBF) was assessed with stable-isotope labeled microspheres. Capillary density was measured by CD31 immunohistochemistry. The protein expression and receptors phosphorylation were assessed using western blot. Results: Left ventricular function, capillary density and MBF were significantly reduced in DCM group when compared with those in the control group (P< 0.01, P< 0.01 and P< 0.05 respectively). Left ventricular function and capillary density were significantly increased in NRG-1 treatment group when compared with those in the DCM group (P< 0.05 and P< 0.05 respectively). The expression of VEGF and Ang-1 and the phosphorylation of Flk1 and Tie-1 were significantly decreased in DCM group as compared with those in the control group. However, those in the NRG-1 treatment group were significantly increased as compared with those in the DCM group. In vitro, NRG-1 treatment increased significantly the expression of VEGF and Ang-1 in human coronary artery smooth muscle cells. Conclusions: NRG-1 can increase the myocardial angiogenesis of DCM, probably via the direct effects of NRG-1 and via the increasing expression of VEGF and Ang-1. These findings may contribute to developing a novel approach to reverse the impaired angiogenic responses in diabetes or coronary artery disease.


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