In my laboratory, I am interested in how the larger blood vessels of the body are injured by toxic chemicals in our environment. The area of greatest concentration for this work is the muscular wall of blood vessels, or the "media." Experimental drugs and other chemicals that protect against injury - or predispose to injury - are under investigation in the hope that someday we may be able to manipulate the blood vessel wall to delay the commonest degenerative diseases, with the greatest human morbidity and mortality, including atherosclerosis and aneurysm.

My laboratory has been defining the cellular and biochemical events that occur during vascular injury by toxic chemicals that are relevant to the environment, or to cigarette smoke components. Past emphasis has been on the metabolism of vasculotoxic amines to aldehydes, but recent work has defined how glutathione-S-transferases act in the defense of vascular wall against reactive molecules both in vivo and in vitro. The role of these defense mechanisms during cellular injury of the vascular wall by atherosclerosis has been a longterm objective. New directions have been undertaken into the area of "developmental vasculotoxicity," or injury occurring in utero, or during development of immature individuals.

Perhaps the most exciting new direction of the laboratory has been the development of a model of dissecting aortic aneurysm. Our initial studies into this small animal model have revealed several pathways of fibrillogeneisis of collagen and elastin that may prove to be targets of toxic insult early in life, or even during embryologic development, resulting in this deadly disease which is just now coming to be recognized as a common killer of young persons. An important aspect of these studies are recent experiments with the industrial compound n-(2-aminoethyl)ethanolamine. or AEEA, which we have recently shown to induce dissecting aneurysms. These studies are being coordinated with and are partially funded by an industrial source that includes the DOW and BASF chemical companies.

• American Heart Association
• Galveston County Medical Society
• Houston Society of Clinical Pathologists
• International Society for Heart Research
• International Society for the Study of Xenobiotics
• Society for Cardiovascular Pathology (Founding Member)
• Society of Toxicologic Pathology
• Society of Toxicology
• Texas Medical Association
• Texas Society of Pathologists
• U.S. and Canadian Academy of Pathology

1. Gong, B, Trent, MB, Srivastava, D, Boor, PJ. Chemical-induced, nonlethal, developmental model of dissecting aortic aneurysm. Birth Defects Res. 73: 2005.
2. Boor, PJ, Yang, Y, Gong, B. Role of the media in vascular injury: atherosclerosis and dissection. Toxicol Path. 34:1-6, 2006.
3. Gong, B., Boor, PJ. The role of amine oxidases in xenobiotic metabolism. Expert Opin Drug Metab Toxicol. 2:559-571, 2006.
4. Conklin DJ, Bhatnagar A, Cowley HR, Johnson GH, Wiechmann RJ, Sayre LM, Trent MB, Boor PJ. Acrolein Generation Stimulates Hypercontraction in Isolated Human Blood Vessels. Toxicol. Appl. Pharm. 217(3):277-288, 2006.
5. Wang L, Yang Y, Dwivedi S, Xu Y, Chu ET, Li J, Fitchett K,  Boor PJ. Manipulating Glutathione-S-Transferases May Prevent the Development of Tolerance to Nitroglycerin Cardiovasc. Toxicol. 6(2):121-144, 2006.
6. Gong B, Asimakis GK, Chen Z, Albrecht TB, Boor PJ, Pappas TC, Bell B, Motamedi M. Whole-Body Hyperthermia Induces Up-Regulation of Vascular Endothelial Growth Factor Accompanied by Neovascularization in Cardiac Tissue. Life Sciences,79:1781-1788, 2006.
7. Yang Y, Boor PJ. Glutathione-S-Transferases and Oxidative Injury of Cardiovascular Tissues. In Toxicology of Glutathione Transferases, edited by Y.C. Awasthi. Taylor & Francis, pp. 257-276, 2006.
8. Singhal SS, Singhal J, Yadav S, Dwivedi S, Boor PJ, Awasthi YC, Awasthi S. Regression of Lung and Colon Cancer Xenografts by Depleting or Inhibiting RLIP76 (Ral-Binding Protein 1). Cancer Res. 67(9):4382-4389, 2007.
9. Cai P, Konig R, Boor PJ, Khan MF, Kaphalia BS, Ansari GAS. Immuno- and Hepato-toxicity of Dichloroacetic Acid in MRL +/+ and B6C3F1 Mice. J. Immunotox. 4:107-115, 2007
10. Huang M-H, Wang H-Q, Roeske W, Birnbaum Y, Wu Y, Yang N-P, Lin Y, Ye Y, McAdoo D, Hughes M, Lick S, Boor P, Lui C, Uretsky B. Mediating 2-Adrenergic Receptor: Role of Intrinsic Cardiac Adrenergic Cells. Am J Physiol: Heart and Circ Physiol 293: 376-384, 2007.
11. Xu Y, Gong B, Yang Y, Awasthi YC, Woods ME, Boor PJ. Glutathione-S-Transferase Protects against Oxidative Injury of Endothelial Cell Tight Junctions. Endothelium 14: 333-343, 2007.
12. Gong B, Sun J, Vargas G, Chang Q, Xu Y, Srivastava D, Boor PJ. Nonlinear Imaging Study of Extracellular Matrix in Chemical-Induced, Developmental Dissecting Aortic Aneurysm: Evidence for Defective Collagen Type III. Birth Defects Res (Part A) 82: 16-24, 2008.
13. Vertrees RA, Zwischenberger JB, Boor PJ, Popov V, McCarthy M, Solley TN, Goodwin T. Cellular Differentiation in Three-Dimensional Lung Cell Cultures. Cancer Biol Therapy 7: 1-8, 2008.
14. Gong B, Bell B, Boor PJ, Albrecht TB, Asimakis GK, Motamedi M. Cardiac preconditioning with local laser-induced hyperthermia J Surg Res. 149(2):177-183. 2008
15. Yang Y, Yang Y, Xu Y, Lick SD, Awasthi YC, Boor PJ. Endothelial Glutathione-S-Transferase A4-4 Protects Against Oxidative Stress and Modulates iNOS Expression through NF- κB Translocation. Toxicol. Appl. Pharmacol. 230: 187-196, 2008
16. Boor, PJ, Conklin, DJ. The Arterial Media as a Target of Structural and Functional Injury by Chemicals" in Cardiovascular Toxicology, 4th Edition, Daniel Acosta, ed; Informa Healthcare Publishing, New York, New York. pp. 667-691, 2008.
17. Xu Y, Gong B, Yang Y, Awasthi YC, Boor PJ. Adenovirus-Mediated Overexpression of Glutathione-S-Ttransferase Mitigates Transplant Arteriosclerosis in Rabbit Carotid Allografts. Transplantation (in press)
18. Boor, PJ. Methods of Analysis: Morphological Evaluation of the Heart and Blood Vessels, in Cardiovascular Toxicology, 2010 (in press)

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