Jie Du, Ph.D., Associate Professor
Current research interests include the evaluation of cellular mechanisms leading to vascular remodeling in several vascular diseases such as atherosclerosis, hypertension, vascular grafts and diabetes. We are also studying vascular remodeling in human patient tissues and transgenic animal models such as LDLR null, apoE null, type I and type II diabetic model. We have generated several smooth muscle conditional knock out mice with null mutation of insulin like growth factor I and its receptor to examine the role of IGF I in vascular remodeling. Angiotensin II (ang II) is a multifunctional peptide that plays a fundamental role in vascular remodeling. Currently, we are studying the crosstalk of ang II and IGF I-induced signals: to identify signaling pathway leading to ang II-induced proliferation in both cell culture and a smooth muscle specific IGF IR knockout model with hypertension. AV graft occlusion is a major cause of disability, mortality and the leading cause of hospitalization for hemodialysis patients. One of project is to understand the mechanism, we examine the cross talk between growth factor and integrin. Our hypothesis is that stimulation and activation of the IGF I signaling pathway in SMC, via synergistic interactions with the aVß3 integrin is an absolute requirement for other growth factors to stimulate vascular remodeling in the process of vein graft failure
In addition, the role of vascular stem cell in development of vascular complications such as diabetes-accelerated atherosclerosis is also a specific area of interest using the bone marrow transplant animal model. We are developing an efficient genetic strategy that promotes embryonic stem cell differentiation into vascular cells. We are also using bone-marrow transplant model to identify the signals that controls stem cell differentiation and proliferation in vascular remodeling process.
Another area of active interest in the laboratory is the better understanding of the signaling pathways which lead to tumor formation. Our laboratory has examined, in particular, downstream effectors of the IGF IR/PI3Kinase/ Serum glucocorticoids regulate kinase signaling pathway. We have shown that the SGK-induced pathway contributes to the activation of NFkappa B mediated survival pathway and cell cycle progression.
