Gene Expressions Associated with Ultrastructural Changes in Vascular Endothelium of Atherosclerotic Lesion
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Gene Expressions Associated with Ultrastructural Changes in Vascular Endothelium of Atherosclerotic Lesion

Authors: M. Maimunah, G.A. Froemming, H. Nawawi, M.I. Nafeeza, O. Effat, M.R. Rohayu Izanwati, M.S. Mohamed Saifulaman

Abstract:

Attachment of the circulating monocytes to the endothelium is the earliest detectable events during formation of atherosclerosis. The adhesion molecules, chemokines and matrix proteases genes were identified to be expressed in atherogenesis. Expressions of these genes may influence structural integrity of the luminal endothelium. The aim of this study is to relate changes in the ultrastructural morphology of the aortic luminal surface and gene expressions of the endothelial surface, chemokine and MMP-12 in normal and hypercholesterolemic rabbits. Luminal endothelial surface from rabbit aortic tissue was examined by scanning electron microscopy (SEM) using low vacuum mode to ascertain ultrastructural changes in development of atherosclerotic lesion. Gene expression of adhesion molecules, MCP-1 and MMP-12 were studied by Real-time PCR. Ultrastructural observations of the aortic luminal surface exhibited changes from normal regular smooth intact endothelium to irregular luminal surface including marked globular appearance and ruptures of the membrane layer. Real-time PCR demonstrated differentially expressed of studied genes in atherosclerotic tissues. The appearance of ultrastructural changes in aortic tissue of hypercholesterolemic rabbits is suggested to have relation with underlying changes of endothelial surface molecules, chemokine and MMP-12 gene expressions.

Keywords: Ultrastructure of luminal endothelial surface, Macrophage metalloelastase (MMP-12), Real-time PCR.

Digital Object Identifier (DOI): doi.org/10.5281/zenodo.1055527

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[1] Walski, M., Chlopicki, S., Celary-Walska, R., Frontczak-Baniewicz, M. Ultrastructural alterations of endothelium covering advanced atherosclerotic plaque in human carotid artery visualised by scanning electron microscope. J Physiol Pharmacol, 53(4 Pt 1): p. 713-23, 2002.
[2] Wilhelm, M.G. and A.D. Cooper, Induction of atherosclerosis by human chylomicron remnants: a hypothesis. J Atheroscler Thromb, 10(3): p. 132-9, 2003.
[3] Cybulsky, M.I., Lichtman, A. H., Hajra, L., Iiyama, K. Leukocyte adhesion molecules in atherogenesis. Clin Chim Acta, 286(1-2): p. 207- 18, 1999.
[4] Fan, J. and T. Watanabe, Inflammatory reactions in the pathogenesis of atherosclerosis. J Atheroscler Thromb, 10(2): p. 63-71, 2003.
[5] Galkina, E. and K. Ley, Vascular adhesion molecules in atherosclerosis. Arterioscler Thromb Vasc Biol, 27(11): p. 2292-301, 2007.
[6] Kuzuya, M. and Iguchi, A. Role of matrix metalloproteinases in vascular remodeling. J Atheroscler Thromb, 10(5): p. 275-82, 2003.
[7] Katsuda, S. and Kaji, T. Atherosclerosis and extracellular matrix. J Atheroscler Thromb, 10(5): p. 267-74, 2003.
[8] Dollery, C.M. and Libby, P. Atherosclerosis and proteinase activation. Cardiovasc Res, 69(3): p. 625-35, 2006.
[9] Dollery, C.M., McEwan, J.R. and Henney, A.M. Matrix metalloproteinases and cardiovascular disease. Circ Res, 77(5): p. 863-8, 1995.
[10] Dollery, C.M., Owen, C. A., Sukhova, G. K., Krettek, A., Shapiro, S. D., and Libby, P. Neutrophil elastase in human atherosclerotic plaques: production by macrophages. Circulation, 107(22): p. 2829-36, 2003.
[11] Halpert, I., Sires, U. I., Roby, J. D., Potter-Perigo, S., Wight, T. N., Shapiro, S. D., Welgus, H. G., Wickline, S. A., and Parks, W. C. Matrilysin is expressed by lipid-laden macrophages at sites of potential rupture in atherosclerotic lesions and localizes to areas of versican deposition, a proteoglycan substrate for the enzyme. Proc Natl Acad Sci U S A, 93(18): p. 9748-53, 1996.
[12] Libby, P. and P.M. Ridker, Inflammation and atherosclerosis: role of Creactive protein in risk assessment. Am J Med, 116 Suppl 6A: p. 9S-16S, 2004.
[13] Zeng, B., Prasan, A., Fung, K. C., Solanki, V., Bruce, D., Freedman, S. B. and Brieger, D. Elevated circulating levels of matrix metalloproteinase-9 and -2 in patients with symptomatic coronary artery disease. Intern Med J, 35(6): p. 331-5, 2005.
[14] Fan, J., Wang, X.,Wu, L.,Matsumoto, S. I.,Liang, J.,Koike, T.,Ichikawa, T.,Sun, H.,Shikama, H.,Sasaguri, Y.,Watanabe, T. Macrophage-specific overexpression of human matrix metalloproteinase-12 in transgenic rabbits. Transgenic Res, 13(3): p. 261-9, 2004.
[15] Yu, Y., Koike, T., Kitajima, S., Liu, E., Morimoto, M., Shiomi, M., Hatakeyama, K., Asada, Y., Wang, K. Y., Sasaguri, Y., Watanabe, T. Temporal and quantitative analysis of expression of metalloproteinases (MMPs) and their endogenous inhibitors in atherosclerotic lesions. Histol Histopathol, 23(12): p. 1503-16, 2008.
[16] Morgan, A.R., Rerkasem, K., Gallagher, P. J., Zhang, B., Morris, G. E., Calder, P. C., Grimble, R. F., Eriksson, P., McPheat, W. L., Shearman, C. P., Ye, S. Differences in matrix metalloproteinase-1 and matrix metalloproteinase-12 transcript levels among carotid atherosclerotic plaques with different histopathological characteristics. Stroke, 35(6): p. 1310-5, 2004.
[17] Daley, S.J., Herderick, E. E., Cornhill, J. F., Rogers, K. A. Cholesterolfed and casein-fed rabbit models of atherosclerosis. Part 1: Differing lesion area and volume despite equal plasma cholesterol levels. Arterioscler Thromb, 14(1): p. 95-104, 1994.
[18] Daley, S.J., Klemp, K. F., Guyton, J. R., Rogers, K. A. Cholesterol-fed and casein-fed rabbit models of atherosclerosis. Part 2: Differing morphological severity of atherogenesis despite matched plasma cholesterol levels. Arterioscler Thromb, 14(1): p. 105-41, 1994.
[19] Aikawa, M., Rabkin, E., Okada, Y., Voglic, S. J., Clinton, S. K., Brinckerhoff, C. E., Sukhova, G. K., Libby, P. Lipid lowering by diet reduces matrix metalloproteinase activity and increases collagen content of rabbit atheroma: a potential mechanism of lesion stabilization. Circulation, 97(24): p. 2433-44, 1998.
[20] Ozer, N.K., Negis, Y., Aytan, N., Villacorta, L., Ricciarelli, R., Zingg, J. M., Azzi, A. Vitamin E inhibits CD36 scavenger receptor expression in hypercholesterolemic rabbits. Atherosclerosis, 184(1): p. 15-20. 2006.
[21] Riedmuller, K., Metz, S., Bonaterra, G. A., Kelber, O., Weiser, D., Metz, J., Kinscherf, R. Cholesterol diet and effect of long-term withdrawal on plaque development and composition in the thoracic aorta of New Zealand White rabbits. Atherosclerosis, 210(2): p. 407-13, 2010.
[22] de Bruijn, W.C. and W. van Mourik, Scanning electron microscopic observations of endothelial changes in experimentally induced atheromatosis of rabbit aortas. Virchows Arch A Pathol Anat Histol, 365(1): p. 23-40, 1975.
[23] Brevetti, G., V. Schiano, and M. Chiariello, Endothelial dysfunction: a key to the pathophysiology and natural history of peripheral arterial disease? Atherosclerosis, 197(1): p. 1-11, 2008.
[24] Reidy, M.A. and D.E. Bowyer, Scanning electron microscope studies of rabbit aortic endothelium in areas of haemodynamic stress during induction of fatty streaks. Virchows Arch A Pathol Anat Histol, 377(3): p. 237-48, 1978.
[25] Nitschmann, E., Berry, L., Bridge, S., Hatton, M. W., Richardson, M., Monagle, P., Chan, A. K., Andrew, M. Morphological and biochemical features affecting the antithrombotic properties of the aorta in adult rabbits and rabbit pups. Thromb Haemost, 79(5): p. 1034-40, 1998.
[26] Matsuda, J., Takahashi, S. Ohkoshi, K., Kaminaka, K., Kaminaka, S., Nozaki, C., Maeda, H., Tokunaga, T. Production of transgenic chimera rabbit fetuses using somatic cell nuclear transfer. Cloning Stem Cells, 4(1): p. 9-19, 2002.
[27] Mestas, J. and K. Ley, Monocyte-endothelial cell interactions in the development of atherosclerosis. Trends Cardiovasc Med, 18(6): p. 228- 32, 2008.
[28] Bobryshev, Y.V., Monocyte recruitment and foam cell formation in atherosclerosis. Micron, 37(3): p. 208-22, 2006.
[29] Lu, Z.Y., Jensen, L. E., Huang, Y., Kealey, C., Blair, I. A., Whitehead, A. S. The up-regulation of monocyte chemoattractant protein-1 (MCP-1) in Ea.hy 926 endothelial cells under long-term low folate stress is mediated by the p38 MAPK pathway. Atherosclerosis, 205(1): p. 48-54, 2009.
[30] Liang, J., Liu, E., Yu, Y., Kitajima, S., Koike, T., Jin, Y., Morimoto, M., Hatakeyama, K., Asada, Y., Watanabe, T., Sasaguri, Y., Watanabe, S., Fan, J. Macrophage metalloelastase accelerates the progression of atherosclerosis in transgenic rabbits. Circulation, 113(16): p. 1993-2001, 2006.