alexa
Reach Us +44-1625-708989
The Role Of Endoplasmic Reticulum Stress In The Chronic Inflammatory Response In Kidney Disease | 9139
ISSN: 2161-0959

Journal of Nephrology & Therapeutics
Open Access

Like us on:

OMICS International organises 3000+ Global Conferenceseries Events every year across USA, Europe & Asia with support from 1000 more scientific Societies and Publishes 700+ Open Access Journals which contains over 50000 eminent personalities, reputed scientists as editorial board members.

Open Access Journals gaining more Readers and Citations
700 Journals and 15,000,000 Readers Each Journal is getting 25,000+ Readers

This Readership is 10 times more when compared to other Subscription Journals (Source: Google Analytics)
All submissions of the EM system will be redirected to Online Manuscript Submission System. Authors are requested to submit articles directly to Online Manuscript Submission System of respective journal.

The role of endoplasmic reticulum stress in the chronic inflammatory response in kidney disease

2nd International Conference on Nephrology & Therapeutics

Jeffrey G. Dickhout

ScientificTracks Abstracts: J Nephrol Therapeutic

DOI: 10.4172/2161-0959.S1.009

Abstract
E 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
Biography
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.
Relevant Topics
Top