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Journal of Zhejiang University SCIENCE B 2010 Vol.11 No.8 P.599-607

http://doi.org/10.1631/jzus.B1001011


Evaluation of recombinant endostatin in the treatment of atherosclerotic plaques and neovascularization in rabbits


Author(s):  Wei Mao, Jing Kong, Jin Dai, Zhao-quan Huang, Dong-zhi Wang, Gui-bao Ni, Min-li Chen

Affiliation(s):  Department of Cardiology, Zhejiang Traditional Chinese Medical Hospital, Hangzhou 310006, China, First College of Clinical Medicine, Zhejiang Chinese Medical University, Hangzhou 310053, China, Department of Pathology, Zhejiang Traditional Chinese Medical Hospital, Hangzhou 310006, China, Center of Experimental Animal, Zhejiang Chinese Medical University, Hangzhou 310053, China

Corresponding email(s):   Maoweilw@163.com

Key Words:  Recombinant endostatin, Atherosclerosis, Neovessels


Wei Mao, Jing Kong, Jin Dai, Zhao-quan Huang, Dong-zhi Wang, Gui-bao Ni, Min-li Chen. Evaluation of recombinant endostatin in the treatment of atherosclerotic plaques and neovascularization in rabbits[J]. Journal of Zhejiang University Science B, 2010, 11(8): 599-607.

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author="Wei Mao, Jing Kong, Jin Dai, Zhao-quan Huang, Dong-zhi Wang, Gui-bao Ni, Min-li Chen",
journal="Journal of Zhejiang University Science B",
volume="11",
number="8",
pages="599-607",
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publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.B1001011"
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%T Evaluation of recombinant endostatin in the treatment of atherosclerotic plaques and neovascularization in rabbits
%A Wei Mao
%A Jing Kong
%A Jin Dai
%A Zhao-quan Huang
%A Dong-zhi Wang
%A Gui-bao Ni
%A Min-li Chen
%J Journal of Zhejiang University SCIENCE B
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%P 599-607
%@ 1673-1581
%D 2010
%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.B1001011

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T1 - Evaluation of recombinant endostatin in the treatment of atherosclerotic plaques and neovascularization in rabbits
A1 - Wei Mao
A1 - Jing Kong
A1 - Jin Dai
A1 - Zhao-quan Huang
A1 - Dong-zhi Wang
A1 - Gui-bao Ni
A1 - Min-li Chen
J0 - Journal of Zhejiang University Science B
VL - 11
IS - 8
SP - 599
EP - 607
%@ 1673-1581
Y1 - 2010
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.B1001011


Abstract: 
Objective: Atherosclerotic plaques and neovascularization play an important role in the course of coronary atherosclerosis. This study evaluated the effect of recombinant endostatin on experimental atherosclerotic plaques and neovascularization in rabbits. Methods: Eighteen healthy male rabbits were divided into three groups: control group, atherosclerotic model group, and recombinant endostatin treated group. The atherosclerotic model was established via a high-cholesterol diet after balloon catheter injury. The subject weights, serum total cholesterol, creatine kinase-myocardial band fraction (CKMB), and matrix metalloproteinase-2 (MMP-2) were measured. Six weeks after treatment, the aortic roots were taken for pathological assay. The thickness ratio of the intima to media was measured by hematoxylin and eosin (HE) staining, and the number of neovessels was measured by immunohistochemistry via monoclonal antibody CD31 staining. Results: The weight, plasma total cholesterol, and CKMB were not significantly different between the atherosclerotic model group and the recombinant endostatin treated group, but much higher than those of the control group (P<0.05). The thickness ratio of the intima to media in the recombinant endostatin treated group was distinctly less than that in the atherosclerotic model group (P<0.05). The number of neovessels decreased dramatically (P<0.05) and the content of MMP-2 decreased slightly without statistical difference (P>0.05) in the recombinant endostatin treated group, compared to the atherosclerotic model group. Conclusions: recombinant endostatin is able to inhibit the growth of neovascularization in the atherosclerotic plaque and the development of plaque.

Darkslateblue:Affiliate; Royal Blue:Author; Turquoise:Article

Reference

[1]Chadefaux, B., Ceballos, I., Hamet, M., Coude, M., Poissonnier, M., Kamoun, P., Allard, D., 1988. Is absence of atheroma in down syndrome due to decreased homocysteine levels? Lancet, 332(8613):741.

[2]Chen, F., Eriksson, P., Kimura, T., Herzfeld, I., Valen, G., 2005. Apoptosis and angiogenesis are induced in the unstable coronary atherosclerotic plaque. Coronary Artery Disease, 16(3):191-197.

[3]Fleiner, M., Kummer, M., Mirlacher, M., Sauter, G., Cathomas, G., Krapf, R., Biedermann, B.C., 2004. Arterial neovascularization and inflammation in vulnerable patients: early and late signs of symptomatic atherosclerosis. Circulation, 110(18):2843-2850.

[4]Galis, Z.S., Khatri, J.J., 2002. Matrix metalloproteinases in vascular remodeling and atherogenesis: the good, the bad, and the ugly. Circulation Research, 90(3):251-262.

[5]Ignatescu, M.C., Gharehbaghi-Schnell, E., Hassan, A., Rezaie-Majd, S., Korschineck, I., Schleef, R.R., Glogar, H.D., Lang, I.M., 1999. Expression of the angiogenic protein, platelet-derived endothelial cell growth factor, in coronary atherosclerotic plaques: in vivo correlation of lesional microvessel density and constrictive vascular remodeling. Arteriosclerosis, Thrombosis, and Vascular Biology, 19(10):2340-2347.

[6]Kalluri, R., 2003. Basement membranes: structure, assembly and role in tumour angiogenesis. Nature Reviews Cancer, 3(6):422-433.

[7]Mason, D.P., Kenagy, R.D., Hasenstab, D., Bowen-Pope, D.F., Seifert, R.A., Coats, S., Hawkins, S.M., Clowes, A.W., 1999. Matrix metalloproteinase-9 overexpression enhances vascular smooth muscle cell migration and alters remodeling in the injured rat carotid artery. Circulation Research, 85(12):1179-1185.

[8]McDonald, D.M., Choyke, P.L., 2003. Imaging of angiogenesis: from microscope to clinic. Nature Medicine, 9(6):713-725.

[9]Moreno, P.R., Lodder, R.A., 2002. Detection of lipid pool, thin fibrous cap, and inflammatory cells in human aortic atherosclerotic plaques by near-infarcted spectroscopy. Circulation, 105(8):923-927.

[10]Moulton, K.S., Olsen, B.R., Sonn, S., Fukai, N., Zurakowski, D., Zeng, X., 2004. Loss of collagen XVIII enhances neovascularization and vascular permeability in atherosclerosis. Circulation, 110(10):1330-1336.

[11]Naghavi, M., Libby, P., Falk, E., Casscells, S.W., Litovsky, S., Rumberger, J., Badimon, J.J., Stefanadis, C., Moreno, P., Pasterkamp, G., et al., 2003a. From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies: Part I. Circulation, 108(14):1664-1672.

[12]Naghavi, M., Libby, P., Falk, E., Casscells, S.W., Litovsky, S., Rumberger, J., Badimon, J.J., Stefanadis, C., Moreno, P., Pasterkamp, G., et al., 2003b. From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies: Part II. Circulation, 108(15):1772-1778.

[13]Nyberg, P., Heikkila, P., Sorsa, T., Luostarinen, J., Heljasvaara, R., Stenman, U.H., Pihlajaniemi, T., Salo, T., 2003. Endostatin inhibits human tongue carcinoma cell invasion and intravasation and blocks the activation of matrix metalloprotease-2, -9, and -13. Journal of Biological Chemistry, 278(25):22404-22411.

[14]O′Reilly, M.S., Boehm, T., Shing, Y., Fukai, N., Vasios, G., Lane, W.S., Flynn, E., Birkhead, J.R., Olsen, B.R., Folkman, J., 1997. Endostatin: an endogenous inhibitor of angiogenesis and tumor growth. Cell, 88(2):277-285.

[15]Pang, R.Q., Wang, H.X., Pan, X.H., 2002. Inhibitory effect of panax notoginseng saponins on proliferation of cultured rat vascular smooth muscle cells stimulated by hypercholesterolemic serum. China Journal of Modern Medicine, 12(2):4-6 (in Chinese).

[16]Pels, K., Labinaz, M., O′Brien, E.R., 1997. Arterial wall neovascularization-potential role in atherosclerosis and restenosis. Japanese Circulation Journal, 61(11):893-904.

[17]Rekhter, M.D., 1999. Collagen synthesis in atheroselerosis: too much and not enough. Cardiovascular Research, 41(2):378-384.

[18]Schwartz, R.S., Bayes-Genis, A., Lesser, J.R., Sangiorgi, M., Henry, T.D., Conover, C.A., 2003. Detecting vulnerable plaque using peripheral blood: inflammatory and cellular markers. Journal of Interventional Cardiology, 16(3):231-242.

[19]Scott, P.A., Harris, A.L., 1994. Current approaches to targeting cancer using antiangiogenesis therapies. Cancer Treatment Reviews, 20(4):393-412.

[20]Waltenberger, J., 2001. Pathophysiological bases of unstable coronary syndrome. Herz, 26(Suppl. 1):2-8 (in German).

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