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ndoplasmic reticulum (ER) stress and the unfolded protein response (UPR) have been shown to be important in the chronic
inflammatory process via activation of nuclear factor-κB and activating protein 1 (AP1) stimulation. UPR activation also has
been shown to occur or be required for the differentiation of a number of cellular components of the immune system including
T-cells, plasma cells, macrophages and in myofibroblast differentiation. We have determined the presence of both a UPR response
and a chronic inflammatory response in our models of acute and chronic kidney disease. We want to determine if ER stress and
subsequent UPR induction results in this chronic inflammatory response through IRE1 mediated nuclear factor-κB signaling.
The tunicamycin model is a model of ER stress induced acute kidney injury. We show that tunicamycin leads to a chronic
inflammatory response characterized by T-cell infiltration. Further, this T-cell infiltrate is reduced in mice treated with the ER
stress inhibitor 4-PBA along with down regulation of the expression of a number of UPR response genes including GRP78, CHOP
and TDAG51. Further, in a model of chronic kidney disease, the Dahl S rat, we have observed a similar chronic inflammatory
response characterized by T-cell infiltration and linked to the development of salt-sensitive hypertension and proteinuria. This
T-cell infiltrate was inhibited by the ER stress inhibitor, 4-PBA (1 g/kg/day) treatment. Thus, it appears that the ER stress response
and UPR activation are part of the chronic inflammatory response associated with renal injury in both acute and chronic disease
Jeffrey G. Dickhout received his Ph.D. from McMaster University. He was trained as a Postdoctoral Fellow with Dr. Allen W. Cowley Jr. in Physiology
at the Medical College of Wisconsin. He was the inaugural holder of the Division of Nephrology Junior Researcher award. He is currently an assistant
professor in the Department of Medicine, Division of Nephrology at McMaster University and St. Joseph?s Healthcare Hamilton. His research
program is currently supported by the Canadian Institutes of Health Research. He has published over 25 peer-reviewed papers. The overall goal of
his research is to better understand the relationship between renal dysfunction and cardiovascular disease.
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