Basic Research
Copyright ©The Author(s) 2003. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Feb 15, 2003; 9(2): 312-315
Published online Feb 15, 2003. doi: 10.3748/wjg.v9.i2.312
Angiogenesis effect on rat liver after administration of expression vector encoding vascular endothelial growth factor D
Bao-Min Shi, Xiu-Yan Wang, Qing-Ling Mu, Tai-Huang Wu, Hong-Jun Liu, Zhen Yang
Bao-Min Shi, Qing-Ling Mu, Tai-Huang Wu, Hong-Jun Liu, Department of General Surgery, Shandong Provincial Hospital, Clinical College of Shandong University, Jinan 250021, Shandong Province, China
Xiu-Yan Wang, Department of Ultrasonography, Shandong Provincial Hospital, Clinical College of Shandong University, Jinan 250021, Shandong Province, China
Zhen Yang, Department of General Surgery, Tongji Hospital, Huazhong University of Science and Technology, Wuhan 430030, Hubei Province, China
Author contributions: All authors contributed equally to the work.
Supported by the National Science Fund for Postdoctoral Fellows in China, No 2001.6; the Medical Science Found of Shandong Province, No. 2001CA1DBA10
Correspondence to: Dr. Bao-Min Shi, Department of General Surgery, Shandong Provincial Hospital, Clinical College of Shandong University, 324 Jingwu Road, Jinan 250021, Shandong Province, China. baomins@163.net
Telephone: +86-531-7938911-2363 Fax: +86-531-7937741
Received: July 12, 2002
Revised: August 4, 2002
Accepted: August 23, 2002
Published online: February 15, 2003
Abstract

AIM: To verify the expressing efficiency and angiogenesis effect after administration of expression vector encoding for vascular endothelial growth factor D in normal and ischemic rat liver.

METHODS: Ten female S-D rats were administrated with liver tissue dot injection of naked PCHO/hVEGF-D, 50 μg/dot, three dots for each. The same amount of physiological saline was used as control in the neighboring lobe. Forteen S-D rats, using inflow occlusion of left lateral lobe, were divided into two groups, seven rats in each group. One was ischemic plasmid group, which received naked plasmid PCHO/hVEGF-D injection of 150 μg. The other received the equal amount of natural saline injection and designed as control. The expressions of hVEGF-D in mRNA and protein levels were identified by in situ hybridyzation and immunohistochemistry, respectively. Endothelial cells were labeled by the factor VIII immunohistochemistrically. The average number of peri-sinusoidal capillaries of each group was calculated and compared statistically 8 d after injection.

RESULTS: A large amount of hVEGF-D in mRNA level was found in both normal and ischemic plasmid groups and but none in their corresponding control groups. The protein of hVEGF was also highly expressed in both normal and ischemic plasmid groups than in the controls. The mean number of capillaries under microscopy (× 200) of the plasmid group and control was 10.2 ± 2.78 vs 7.1 ± 2.02 (P < 0.05), and those of ischemic plasmid group and ischemic control were 7.43 ± 1.72 vs 4.71 ± 1.11 with statistical difference (P < 0.05).

CONCLUSION: The naked PCHO/hVEGF-D dot injection to normal, ischemic rat liver can produce comparatively high expression of hVEGF in both protein and mRNA levels, and prominently increase the number of new capillaries around hepatic sinuses. Therefore, it could be another ideal choice for the treatment of ischemic liver diseases.

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