My lab is focused on lipoprotein receptors and how such receptors contribute to or protect against atherosclerosis. My current research project is on the role of scavenger receptor B1 (SRB1) in the differential regulation of scavenger receptor class A (SR-A) in macrophages, under conditions such as lipid loading. I am interested in how the expression and functional activity of SR-A is modulated in SRB1 knockout mice model.
My research is focused on the cross-talk between adiposcytes and the inflammatory conditions that underlie Crohn's disease. The connective and adipose tissue changes observed in patients with Crohn's disease have received little attention although fat hypertrophy, fat wrapping and "creeping fat" have long been recognized by surgeons as a phenomenon suitable for delineating the extent of active disease. Obesity in patients with inflammatory bowel disease, ulcerative colitis and Chron's colitis is associated with more frequent complications and increased risk for the development of colorectal cancer.
Jill Cholewa, B.S., Post Lab Cardiovascular disease is the leading casue of death in our society. After much deliberating research, mechanisms involved in the initiation and progression remain unclear. Macrophages play a key role in the development and progression of atherosclerosis and the other inflammatory diseases. My work in macrophages relates to defining cytoplasmic amino acid sequences involved in class A macrophage scavenger receptor (SR-A) mediated functions such as macrophage adhesion and the uptake of modified low density lipoprotein. The functional importance of cytoplasmic sequences in coupling SR-A to either cell adhesion or ligand uptake is not clear. Therefore, the results of the structure-function studies we are completing will further our understanding of signals that regulate SR-A mediated functions and may lead to new treatments for preventing and /or controlling the progression of atherosclerosis. Manisha Gupte, B.S., M.S., Cassis Lab The focus of research in our lab is in the area of the Renin-angiotensin System (RAS) and its regulation/dysregulation in obesity associated with hypertension. Angiotensin ll (Angll) the most potent and vasoactive peptide of this system is produced by the conversion of angiotensin i (Angl) to Angll by an enzyme ACE produced primarily by the lung. ACE has been a favored target for pharmacological strategies in patients with hypertension, heart failure and kidney diseases. However, recently, tow independent groups have identified a homologue of ACE i.e. ACE2. ACE2 has been demonstrated to convert Angll (vasoconstrictor) to Ang1-7 (vasodilator peptide). Besides its vasodilatory properties, Ang1-7 has been demonstrated to exhibit a number of cardioprotective effects. Adipocytes express all of the components of the RAS, including angiotensinogen, renin-like activity, ACE and angiotensin receptors (type 1 and type 2) with some of the components shown to be nutritionally regulated. Hence, the focus of my research is to determine if ACE2 is expressed in adipose tissue. Further, I am interested in the mechanism and regulation of ACE2 in adipose tissue, and if the expression of ACE2 in adipose tissue is nutritionally regulated.
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