bmd

Department of Biomedical Sciences

at the

University of South Alabama

DR. AZIN AGAH

Assistant Professor of Biomedical Sciences

Postdoctoral Studies: Harvard Medical School

Ph.D., Kansas State University

Phone: (251) 380-2710; Fax: (251) 380-2710

E-mail: aagah@usouthal.edu

Research Interests:

Inflammation induced angiogenesis, tissue repair and regeneration, matricellular proteins; scleroderma, fibrosis, extracellular matrix remodeling.

Representative Publications:

Agah, A, Kyriakides TR, Bornstein P. Proteolysis of cell-surface tissue transglutaminase by matrix metalloproteinase-2 contributes to the adhesive defect and matrix abnormalities in thrombospondin-2-null fibroblasts and mice. Am J Pathol. 2005; 167(1):81-8.  

Christopherson KS, Ullian EM, Mullowney CE, Stokes CCA, Agah A, Mosher  DF, Lawler J, Bornstein P, Barres BA. Thrombospondins 1 and 2 are astrocyte-secreted proteins that are necessary and sufficient to promote CNS synaptogenesis.  Cell. 2005; 120(3):421-33. 

Bornstein, P, Agah, A, Kyriakides TR. The role of Thrombospondins 1 and 2 in the regulation of cell-matrix interactions, collagen fibril formation, and the response to injury. Int. J. of Biochem Cell Biol. 2004; 36(6): 1115-25.  

Agah A, Kyriakides TR, Letrondo N, Bjorkblom B, Bornstein P. Thrombospondin 2 levels are increased in aged mice: consequences for cutaneous wound healing and angiogenesis. Matrix Biol. 2004; 22(7):539-47.  

Kokenyesi R, Armstrong LC, Agah A, Bornstein P, Ryerse JS, Artal R. Thrombospondin 2 deficiency in pregnant mice results in premature softening of the uterine cervix. Biol Reprod. 2004; 70(2): 385-390.  

Agah A, Kyriakides TR, Lawler J, Bornstein P. The lack of Thrombospondin-1 (TSP1) dictates the course of wound healing in double TSP1/TSP2-null mice. Am. J. Pathol. 2002;161(3):831-9.

Agah A, Montalto MC, Young K , Stahl GL.  Isolation, cloning and functional characterization of porcine mannose-binding lectin. Immunology 2001;102(3):338-343. Agah A, Montalto MC, Kiesecker CL, Morrissey M, Grover M, Whoolery KL, Rother RP, Stahl GL. Isolation, characterization and cloning of porcine complement component C7. J. Immunol. 2000;165: 1059-1065. 

Collard CD, Vakeva AP, Morrissey M, Agah A, Rollins SA, Reenstra WR, Buras JA, Meri S, Stahl GL. Complement activation following oxidative stress: Role of the Lectin Complement Pathway. Am. J. Pathol. 2000;156(5):1549-1556. 

Collard CD, Agah A, Reenstra WR, Buras JA, Stahl GL. Endothelial nuclear factor-κB translocation and vascular cell adhesion molecule-1 induction by complement: Inhibition with anti-human C5 therapy or cGMP analogues. Arteriosclerosis, Thrombosis Vascular Biol. 1999; 2623-2629. 

Collard CD, Bukusoglu C, Agah A, Colgan SP, Reenstra WR, Morgan BP, Stahl GL. Hypoxia-induced expression of complement receptor type 1 (CR1, CD35) in human vascular endothelial cells. Am. J. Physiol. Cell Physiol. 1999;276:C450-458. 

Taylor CT, Fueki N, Agah A, Hershberg RM, Colgan SP. Critical role of cAMP response element binding protein (CREB) expression in hypoxia-elicited induction of epithelial TNF-α. J. Biol. Chem. 1999;274(27):19447-54. 

Collard CD, Lekowski R, Jordan JE, Agah A, Stahl GL. Complement activation following oxidative stress. Molec. Immunol. 1999;36:941-948. 

Park KW, Tofukuji M, Metais C, Comunale ME, Dai HB, Simons M, Stahl GL, Agah A, Sellke FW.  Attenuation of endothelium-dependent dilation of pig pulmonary arterioles following cardiopulmonary bypass is mediated by complement C5a. Anesth. Analgesia 1999;89:42-48. 

Tofukuji M, Stahl GL, Metais C, Tomita M, Agah A, Bianchi C, Fink M, Sellke FW. Mesenteric dysfunction after extracorporeal circulation: Role of C5a-induced leukocyte sequestration. Ann. Thorac. Surg. 2000;69(3):799-807. 

Collard CD, Agah A, Stahl GL. Complement activation following reoxygenation of hypoxic human umbilical cells: Role of intracellular reactive oxygen species, NF-κB and new protein synthesis.  Immunopharmacology 1998;39:39-50. 

Vakeva AP, Agah A, Rollins SA, Matis LA, Li L, Stahl GL. Myocardial infarction and apoptosis after myocardial ischemia and reperfusion: Role of the terminal complement components and inhibition by anti-C5 therapy. Circulation 1998;97:2259-2267. 

Tofukuji M, Stahl GL, Agah A, Metais C, Simons M, Sellke FW. Anti-C5a monoclonal antibody reduces cardioplegia-induced coronary endothelial dysfunction. J. Thoracic Cardiovasc. Surg. 1998;116:1060-1068.

UNIVERSITY OF SOUTH ALABAMA
Department of Biomedical Sciences
UCOM 6000, Mobile, AL 36688
(251) 380-2710, fax: 380-2711
Last updated: January 25, 2008