alexa Endoplasmic Reticulum Stress Causes Renal Epithelial Ce

Journal of Pharmacological Reports
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Research Article

Endoplasmic Reticulum Stress Causes Renal Epithelial Cell Disjunction

Dickhout JG*, Chahal J, Matthews A, Carlisle RE, Tat V and Safaa Naiel
Department of Medicine, Division of Nephrology, McMaster University and St. Joseph’s Healthcare Hamilton, Hamilton, Ontario, Canada
*Corresponding Author : Jeffrey G Dickhout
Department of Medicine, Division of Nephrology
McMaster University and St. Joseph’s Healthcare Hamilton, 50
Charlton Avenue East, Hamilton, ON, L8N 4A6, Canada
Tel: 905-522-1155 ext. 35334
Fax: 905-540-6589
E-mail: [email protected]
Received January 06, 2016; Accepted February 05, 2016; Published February 08, 2016
Citation: Dickhout JG, Chahal J, Matthews A, Carlisle RE, Tat V, et al. (2016) Endoplasmic Reticulum Stress Causes Renal Epithelial Cell Disjunction. J Pharma Reports 1:107. doi:10.4172/jpr.1000107
Copyright: © 2016 Dickhout JG, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
 

Abstract

Endoplasmic reticulum (ER) stress results from the accumulation of misfolded proteins in the ER. ER stress is associated with acute kidney injury (AKI) of various causes, including two of the major causes of AKI, nephrotoxic drugs and renal ischemia. AKI is a pathology affecting approximately 15% of all hospital stays. When AKI occurs, it results in both significantly increased mortality and increased length of hospital stay. If the patient survives to leave the hospital, it increases the likelihood of developing chronic kidney disease 10-fold, end stage kidney disease 3-fold, and the incidence of premature death 2-fold. An important pathological feature of AKI is the disruption of epithelial cell junctions in the proximal tubule. This loss of epithelial cell junctions disrupts cell polarity preventing the reabsorption of ultrafiltrate components, including sodium, back into the circulation. We hypothesized that ER stress causes epithelial cell disjunction in human proximal tubular cells by trapping the junctional components in the ER and preventing them from reaching the cell surface. ER stress was induced by a variety of stressors including tunicamycin, thapsigargin, and A23187, all of which differ in their mechanism of action. We found that induction of ER stress, by any means, caused epithelial cell disjunction in the renal tubular epithelium. Disjunction was determined by the translocation of β-catenin, which is both a structural component of epithelial cell adherens junctions and a molecular chaperone, from the cell periphery to the perinuclear region. Co-localization experiments found β-catenin to be trapped within the ER.

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