Professor Joe Minta obtained BSc(HONS) (Biochemistry) from University of Ghana (1966), MSc (Biochemistry) from University of Guelph (1968) and PhD (Biochemistry) and MBA from University of Toronto in 1971 and 1994 respectively. He was awarded MRC (Canada) fellowship for post-doctoral research in immunopathology with Professor Irwin Lepow at the University of Connecticut Health Center, Farmington from 1971-1973. He was subsequently appointed Assistant Professor, Department of Pathology, Faculty of Medicine, University of Toronto, in 1973and Associate Professor in 1978. He was cross-appointed as Clinical Immunopathologist at the Toronto Western Hospital (1977-1979) and Research Scientist at the Toronto Wellesley Hospital Rheumatic Disease Research Unit (1979-1989). Dr. Minta was the recipient of the Canadian Heart Foundation Research Scholarship from 1973-1977 and the Canadian Arthritis and Rheumatism Society Research Associateship in Basic Science from 1979-1989. Dr. Minta was a visiting Professor in the Department of Molecular and Clinical Rheumatology, at The Johns Hopkins University School of Medicine, Baltimore, Maryland, from 1989-1990. He served as the coordinator of the graduate program in the Department of Pathology from 1991-1993 and was a member of the Langer Task Force that formulated the recommendations for the merger of the Departments of Clinical Biochemistry, Microbiology and Pathology to form the Department of Laboratory Medicine and Pathobiology in 1997.
Professor Minta designed and coordinated several undergraduate and advanced graduate courses in the Departments of Pathology (1973-1998) and Laboratory Medicine and Pathobiology (1998-2011) including "Skeletal Disorders" (LMP404); “Molecular Biology & Applications to Human Disease” (LMP1018); “Inflammation, Immunity & Immunopathology” (LMP1020); and “Cell Death Pathways in Development, Tissue Homeostasis & Pathobiology” (LMP1515). He was the recipient of the JP Walter Teaching Award in 1995.
Professor Minta’s research was initially centered on delineating the molecular mechanisms underlying genetically-determined complement deficiency states and the regulation of the complement system in health and disease. Research in the past 10 years has focused on bioinformatics and pathway analysis of bacterial lipopolysaccharide and oxidized cholesterol-induced human vascular smooth muscle cell phenotype transformation from the quiescent and contractile phenotype to the proliferative, synthetic and migratory phenotype which is a pivotal event in the development and pathogenesis of atherosclerosis and post-angioplasty restenosis. These pathway analyses provide novel biomarkers which are potential targets for diagnosis and drug discovery for therapeutic intervention in atherosclerosis and other cardiovascular diseases.
1. Integrative pathway dissection of molecular mechanisms of moxLDL-induced vascular smooth muscle phenotype transformation. BMC Cardiovasc Disord. 2013 Jan 16;13(1):4. Karagiannis GS, Weile J, Bader GD, Minta J. BMC Cardiovasc Disord. 2013 Jan 16;13(1):4, 1-19.
2. Microarray analysis of ox-LDL (oxidized low-density lipoprotein)-regulated genes in human coronary artery smooth muscle cells. Minta J, Jungwon Yun J, St Bernard R. Cell Biol Int Rep 2010;17(2) 33-45.
3. Microarray Analysis of Human Vascular Smooth Muscle Cell Responses to Bacterial Lipopolysaccharide. Joe Minta, James J. Yun, Sandy Der and Shikha Rana.American Journal of Immunology 2007 3:(2); 56 – 73.
4. mRNA differential display identification of vascular smooth muscle early response genes regulated by PDGF. Minta JO, Yun JJ, Kabiawu O, Jones J. Mol Cell Biochem. 2006 Jan;281(1-2):63-75.
5. Expression of gC1q-R/p33 and its major ligands in human atherosclerotic lesions. Peerschke EI, Minta JO, Zhou SZ, Bini A, Gotlieb A, Colman RW, Ghebrehiwet B. Mol Immunol. 2004 Jul;41(8):759-66.
6. An initiator element and a proximal cis-acting sequence are essential for transcriptional activation of the complement factor I (CFI) gene. Paramaswara B, Minta JO. Gene. 1999 Sep 3;237(1):71-80.
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