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BMEBT Seminar by Dr. Ruhul Abid
|Category:||College Of Arts And Sciences|
|Date & Time:||
Tuesday , 11/13/2012
from 11:00 AM to 12:00 PM
|Location:||Textiles - 101E|
|Sponsored by:||Biomedical Engineering & Biotech Seminar Series|
Dr. Sankha Bhowmick
TOPIC: GENETIC MANIPULATION OF BLOOD VESSELS IN CORONARY HEART DISEASE
Increased levels of reactive oxygen species (ROS) are known to cause several cardiovascular and inflammatory diseases including hypertension, heart attack (MI), and stroke. However, recent findings show that ROS are also essential for proper functions of the blood vessels that carry blood from and to the heart. Currently, there is a widely held belief that there must be a certain level of ROS that need to be maintained in out body – below or above which level may be detrimental for the functions of our blood vessels. At present we do not know what is the required or beneficial ‘level’ of ROS. And, also how long our blood vessels can tolerate higher levels of ROS before becoming diseased. Using genetically manipulated animal models, this talk will show how scientists are approaching this critical question. The main aim of these studies are to find a therapeutic modality to regulate ROS levels in our blood vessels to keep them healthy in chronic diseases where ROS levels are high such as coronary artery disease, diabetes and arthritis.
Dr. Ruhul Abid obtained his MD from Dhaka Medical College and PhD in Molecular Biology and Genetics from Nagoya University in Japan in 1997. He did his postdoctoral training at Harvard Medical School, where he became an Instructor in Medicine in 2002 and Assistant Professor in Medicine in 2006. He joined Cardiothoracic Surgery division and Cardiovascular Research Center at Brown Medical School in 2011. His major research focus is to understand how redox content of the endothelium modulates signaling pathways in the endothelium and regulates microvascular functions in vivo.
Dr. Abid was the first to demonstrate that NADPH oxidase-derived reactive oxygen species (ROS) are essential for endothelial cell (EC) proliferation, migration and survival in 2000. Recently, he has demonstrated that endothelium-dependent coronary arteriolar vasodilatation requires NADPH oxidase-derived ROS to activate PI3K-Akt-eNOS and nitric oxide (NO) production (ATVB, 2010). This study was awarded the best scientific work (Werner Risau Investigator Award in Vascular Biology by AHA in 2011) among 650 original research work published in the Journal ATVB in 2011. Currently, he has been using binary (Tet-NOX2:VE-Cad-tTA and Tet-SOD2:VE-Cad-tTA) and ternary (Tet-NOX2:Tet-SOD2:VE-Cad-tTA) transgenic animals. His studies will have great impact as ROS regulation at a sub-cellular (mitochondrial) level to preserve endothelial functions in health and disease (acute myocardial infarction, cardioplegic arrest, transplant surgery) has great therapeutic potential. The outcome of his projects may also be extrapolated to study other oxidative insults resulting in vascular injuries including stroke.