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Experimental Rat and Mouse Carotid Artery Surgery: Injury and Remodeling Studies

DOI: 10.1155/2013/167407

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Abstract:

In cardiovascular research, translation of benchtop findings to the whole body environment is often critical in order to gain a more thorough and comprehensive clinical evaluation of the data with direct extrapolation to the human condition. In particular, developmental and/or pathophysiologic vascular growth studies often employ in vitro approaches such as cultured cells or tissue explant models in order to analyze specific cellular, molecular, genetic, and/or biochemical signaling factors under pristine controlled conditions. However, validation of in vitro data in a whole body setting complete with neural, endocrine, and other systemic contributions provides an essential proof of concept from a clinical perspective. Several well-characterized experimental in vivo models exist that provide excellent proof-of-concept tools to examine vascular growth and remodeling in the whole body. This paper will examine the rat carotid artery balloon injury model, the mouse carotid artery wire denudation injury model, and rat and mouse carotid artery ligation models with particular emphasis on minimally invasive surgical access to the site of intervention. Discussion will include key scientific and technical details as well as caveats, limitations, and considerations for the practical use of each of these valuable experimental models. 1. Introduction Translation of basic research discoveries to clinical efficacy and utility requires experimental models that encompass the whole body environment complete with neural, hormonal, endocrine, and other systemic contributions from associated cell and tissue types. All of these factors potentially influence the outcomes witnessed when using in vitro preparations and single cell or isolated tissue model systems. Particularly regarding vascular growth and remodeling studies, numerous experimental animal models in a variety of vascular beds have been used over the years as proof-of-concept in vivo approaches. Considering the carotid artery as a model system, several rodent-based approaches are widely used and accepted as clinically relevant in terms of examining the in vivo responses to injury-induced growth and remodeling. The rat carotid artery balloon injury model utilizes mechanical damage caused by a balloon catheter which results in mural distension and removal of the intimal endothelial lining. The mouse wire injury model uses an angiocatheter guide wire to remove the endothelial lining and denude the vessel in the absence of medial wall distension. Ligation experiments, using the common carotid artery or one of its

References

[1]  A. W. Clowes, M. A. Reidy, and M. M. Clowes, “Mechanisms of stenosis after arterial injury,” Laboratory Investigation, vol. 49, no. 2, pp. 208–215, 1983.
[2]  A. W. Clowes, M. A. Reidy, and M. M. Clowes, “Kinetics of cellular proliferation after arterial injury. I. Smooth muscle growth in the absence of endothelium,” Laboratory Investigation, vol. 49, no. 3, pp. 327–333, 1983.
[3]  A. W. Clowes and M. M. Clowes, “Kinetics of cellular proliferation after arterial injury. II. Inhibition of smooth muscle growth by heparin,” Laboratory Investigation, vol. 52, no. 6, pp. 611–616, 1985.
[4]  A. W. Clowes, M. M. Clowes, and M. A. Reidy, “Kinetics of cellular proliferation after arterial injury. III. Endothelial and smooth muscle growth in chronically denuded vessels,” Laboratory Investigation, vol. 54, no. 3, pp. 295–303, 1986.
[5]  D. A. Tulis, “Rat carotid artery balloon injury model,” Methods in molecular medicine, vol. 139, pp. 31–66, 2007.
[6]  D. A. Tulis, “Histological and morphometric analyses for rat carotid balloon injury model,” Methods in molecular medicine, vol. 139, pp. 31–66, 2007.
[7]  V. Lindner, J. Fingerle, and M. A. Reidy, “Mouse model of arterial injury,” Circulation Research, vol. 73, no. 5, pp. 792–796, 1993.
[8]  T. R. Sullivan Jr., R. H. Karas, M. Aronovitz et al., “Estrogen inhibits the response-to-injury in a mouse carotid artery model,” Journal of Clinical Investigation, vol. 96, no. 5, pp. 2482–2488, 1995.
[9]  M. D. Iafrati, R. H. Karas, M. Aronovitz et al., “Estrogen inhibits the vascular injury response in estrogen receptor α-deficient mice,” Nature Medicine, vol. 3, no. 5, pp. 545–548, 1997.
[10]  A. Kumar and V. Lindner, “Remodeling with neointima formation in the mouse carotid artery after cessation of blood flow,” Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 17, no. 10, pp. 2238–2244, 1997.
[11]  Y. Yuan, L. Liao, D. A. Tulis, and J. Xu, “Steroid receptor coactivator-3 is required for inhibition of neointima formation by estrogen,” Circulation, vol. 105, no. 22, pp. 2653–2659, 2002.
[12]  B. L. Langille and F. O'Donnell, “Reductions in arterial diameter produced by chronic decreases in blood flow are endothelium-dependent,” Science, vol. 231, no. 4736, pp. 405–407, 1986.
[13]  B. L. Langille, M. P. Bendeck, and F. W. Keeley, “Adaptations of carotid arteries of young and mature rabbits to reduced carotid blood flow,” American Journal of Physiology, vol. 256, no. 4, pp. H931–H939, 1989.
[14]  X. Yang, D. P. Thomas, X. Zhang et al., “Curcumin inhibits platelet-derived growth factor-stimulated vascular smooth muscle cell function and injury-induced neointima formation,” Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 26, no. 1, pp. 85–90, 2006.
[15]  D. Nam, C. W. Ni, A. Rezvan et al., “Partial carotid ligation is a model of acutely induced disturbed flow, leading to rapid endothelial dysfunction and atherosclerosis,” American Journal of Physiology, vol. 297, no. 4, pp. H1535–H1543, 2009.
[16]  C. N. Joshi, D. N. Martin, J. C. Fox, N. N. Mendelev, T. A. Brown, and D. A. Tulis, “The soluble guanylate cyclase stimulator BAY 41-2272 inhibits vascular smooth muscle growth through the cAMP-dependent protein kinase and cGMP-dependent protein kinase pathways,” Journal of Pharmacology and Experimental Therapeutics, vol. 339, pp. 394–402, 2011.
[17]  D. A. Tulis, W. Durante, K. J. Peyton, A. J. Evans, and A. I. Schafer, “Heme oxygenase-1 attenuates vascular remodeling following balloon injury in rat carotid arteries,” Atherosclerosis, vol. 155, no. 1, pp. 113–122, 2001.
[18]  D. A. Tulis, W. Durante, X. Liu, A. J. Evans, K. J. Peyton, and A. I. Schafer, “Adenovirus-mediated heme oxygenase-1 gene delivery inhibits injury-induced vascular neointima formation,” Circulation, vol. 104, no. 22, pp. 2710–2715, 2001.
[19]  D. A. Tulis, W. Durante, K. J. Peyton, G. B. Chapman, A. J. Evans, and A. I. Schafer, “YC-1, a benzyl indazole derivative, stimulates vascular cGMP and inhibits neointima formation,” Biochemical and Biophysical Research Communications, vol. 279, no. 2, pp. 646–652, 2000.
[20]  D. A. Tulis, K. S. Bohl Masters, E. A. Lipke et al., “YC-1-mediated vascular protection through inhibition of smooth muscle cell proliferation and platelet function,” Biochemical and Biophysical Research Communications, vol. 291, no. 4, pp. 1014–1021, 2002.
[21]  A. N. Keswani, K. J. Peyton, W. Durante, A. I. Schafer, and D. A. Tulis, “The cyclic GMP modulators YC-1 and zaprinast reduce vessel remodeling through antiproliferative and proapoptotic effects,” Journal of Cardiovascular Pharmacology and Therapeutics, vol. 14, no. 2, pp. 116–124, 2009.
[22]  D. A. Tulis, Z. H. Mnjoyan, R. L. Schiesser et al., “Adenoviral gene transfer of fortilin attenuates neointima formation through suppression of vascular smooth muscle cell proliferation and migration,” Circulation, vol. 107, no. 1, pp. 98–105, 2003.
[23]  K. J. Peyton, D. Ensenat, M. A. Azam et al., “Arginase promotes neointima formation in rat injured carotid arteries,” Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 29, no. 4, pp. 488–494, 2009.
[24]  K. J. Peyton, A. R. Shebib, M. A. Azam, X. Liu, D. A. Tulis, and W. Durante, “Bilirubin inhibits neointima formation and vascular smooth muscle cell proliferation and migration,” Frontiers in Pharmacology, vol. 3, article 48, 2012.
[25]  J. D. Stone, A. Narine, P. R. Shaver, J. C. Fox, J. R. Vuncannon, and D. A. Tulis, “AMP-activated protein kinase inhibits vascular smooth muscle cell proliferation and migration and vascular remodeling following injury,” American Journal of Physiology, vol. 304, pp. H369–H381, 2013.
[26]  F. H. Sims, “A comparison of structural features of the walls of coronary arteries from 10 different species,” Pathology, vol. 21, no. 2, pp. 115–124, 1989.
[27]  C. Indolfi, G. Esposito, E. Di Lorenzo et al., “Smooth muscle cell proliferation is proportional to the degree of balloon injury in a rat model of angioplasty,” Circulation, vol. 92, no. 5, pp. 1230–1235, 1995.
[28]  D. W. Courtman, A. Cho, L. Langille, and G. J. Wilson, “Eliminating arterial pulsatile strain by external banding induces medial but not neointimal atrophy and apoptosis in the rabbit,” American Journal of Pathology, vol. 153, no. 6, pp. 1723–1729, 1998.
[29]  R. F. G. Booth, J. F. Martin, A. C. Honey, D. G. Hassall, J. E. Beesley, and S. Moncada, “Rapid development of atherosclerotic lesions in the rabbit carotid artery induced by perivascular manipulation,” Atherosclerosis, vol. 76, no. 2-3, pp. 257–268, 1989.
[30]  M. T. Kuhlmann, S. Cuhlmann, I. Hoppe et al., “Implantation of a carotid cuff for triggering shear-stress induced atherosclerosis in mice,” Atherosclerosis, vol. 223, pp. 314–320, 2012.
[31]  P. Carmeliet, L. Moons, J. M. Stassen et al., “Vascular wound healing and neointima formation induced by perivascular electric injury in mice,” American Journal of Pathology, vol. 150, no. 2, pp. 761–776, 1997.

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