Dr. Haidari graduated from Tehran University of Medical Sciences in Iran with a doctorate degree in Clinical Laboratory Sciences. After completing his doctoral studies, Dr. Haidari remained at Tehran University for four more years, receiving his Ph.D. in Clinical Biochemistry. He then pursued two post-doctoral study programs at the University of Toronto in Toronto, Canada. His first program focused on lipoprotein metabolism in diabetes, followed by a second one in vascular biology of atherosclerosis. Dr. Haidari joined the Department of Internal Medicine, Division of Cardiology, University of Texas Medical School at Houston as an Assistant Professor in 2007. In addition to basic science research, Dr. Haidari has extensive work experience in both fields of laboratory medicine and clinical chemistry.
Dr. Haidari has been a facilitator for problem based learning (PBL) course of medical students at UTHealth since 2009. He received three appreciation certificates from the dean of Medical School for his “outstanding performance” in PBL.
- Doctoral Degree
- Clinical Biochemistry, Tehran University of Medical Sciences
- Doctorate Degree
- Medical Laboratory Sciences, Tehran University of Medical Sciences
Areas of Interests
Transendothelial migration (TEM) of leukocytes is a crucial step in atherogenesis. Disruption of endothelial adherens junction precedes TEM of leukocytes. Dr. Haidari`s research focuses on elucidating molecular mechanisms underlying the role of endothelial adherens junction in TEM of leukocytes. Dr. Haidari`s group discovered that activation of HRas/Raf/MEK/ERK signaling cascade and phosphorylation of myosin light chain are critical for the induction of vascular endothelial cadherin (VE-cad) tyrosine phosphorylation by pro-inflammatory cytokines, and attachment of monocytes or invasive cancer cells to endothelial cells. It is well established that tyrosine phosphorylation of VE-cad leads to dismantling of adherens junction, impairment of endothelial barrier function and finally enhanced TEM of leukocytes. Based on his previous research Dr. Haidari developed a hypothetical model that explains how attachment of leukocyte to endothelial cells alters endothelial signal transduction that leads to enhanced TEM of leukocytes. Currently, the main objective of Dr. Haidari`s group is to test the validity of that model. Recently, Dr. Haidari started a new project to determine the molecular mechanism that underlies accelerated atherosclerosis in diabetic patients by investigating the impact of hyperglycemia on integrity of endothelial adherens junction.