Angiogenesis effect on rat liver after administration of expression vector encoding vascular endothelial growth factor D

AIM: To verify the expressing efficiency and angiogenesiseffect after administration of expression vector encodingfor vascular endothelial growth factor D in normal andischemic rat liver.METHODS: Ten female S-D rats were administrated withliver tissue dot injection of naked PCHO/hVEGF-D, 50 μg/dot, three dots for each. The same amount of physiologicalsaline was used as control in the neighboring lobe. ForteenS-D rats, using inflow occlusion of left lateral lobe, were dividedinto two groups, seven rats in each group. One was ischemicplasmid group, which received naked plasmid PCHO/hVEGF-D injection of 150 μg. The other received the equal amountof natural saline injection and designed as control. Theexpressions of hVEGF-D in mRNA and protein levels wereidentified by in situ hybridyzation and immunohistochemistry,respectively. Endothelial cells were labeled by the factor VIIIimmunohistochemistrically. The average number of peri-sinusoidal capillaries of each group was calculated andcompared statistically 8 days after injection.RESULTS: A large amount of hVEGF-D in mRNA level wasfound in both normal and ischemic plasmid groups and butnone in their corresponding control groups. The protein ofhVEGF was also highly expressed in both normal and ischemicplasmid groups than in the controls. The mean number ofcapillaries under microscopy (×200) of the plasmid group andcontrol was 10.2±2.78 vs7.1±2.02 (P＜0.05), and those ofischemic plasmid group and ischemic control were 7.43+1.72vs 4.71± 1.11 with statistical difference (P＜0.05).CONCLUSION; The naked PCHO/hVEGF-D dot injection tonormal, ischemic rat liver can produce comparatively highexpression of hVEGF in both protein and mRNA levels, andprominently increase the number of new capillaries aroundhepatic sinuses. Therefore, it could be another ideal choicefor the treatment of ischemic liver diseases.