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.

Expression of local renin and angiotensinogen mRNA in cirrhotic portal hypertensive patient

AIM: To investigate the expression of local renin and angiotensinogen mRNA in cirrhotic portal hypertensive patients.METHODS: The expression of local renin and angiotensinogen mRNA in the liver, splenic artery and vein of PH patients was detected by RT-PCR analysis.RESULTS: Expression of local renin mRNA in the liver of control group was (0.19±0.11), significantly lower than that in splenic artery(0.45±0.17)or splenic vein(0.39±0.12)respectively, (P＜0.05). Expression of local angiotensinogen mRNA in the liver was (0.64±0.21), significantly higher than that in splenic artery(0.41±0.15) or in splenic vein (0.35±0.18)respectively, (P＜0.05). Expression of local renin mRNA in the liver, splenic artery and vein of PH group was (0.78±0.28),(0.86±0.35) and (0.81±0.22) respectively, significantly higher than that in the control group, (P＜0.05). Expression of local angiotensinogen mRNA in the liver, splenic artery and vein of PH group was (0.96±0.25), (0.83±0.18) and (0.79±0.23)respectively, significantly higher than that in the control group,(P＜0.05). There was no significant difference between the liver, splenic artery and vein in the expression of local renin or local angiotensinogen mRNA in PH group, (P＜0.05).CONCLUSION: In normal subjects the expression of local renin and angiotensinogen mRNA was organ specific, but with increase of the expression of LRAS, the organ-specificity became lost in cirrhotic patients. LRAS may contribute to increased resistance of portal vein with liver and formation of splanchnic vasculopathy.