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Deficit of p66ShcA restores redox-sensitive stress response program in cisplatin-induced acute kidney injury

Overwhelming oxidative stress and compromised tubular cell antioxidant response have been incriminated for cisplatin (Cis)-induced acute kidney injury (AKI). We hypothesized that Cis-induced AKI was the outcome of the deactivated redox-sensitive stress response program (RSSRP). Wild type (WT) and he...

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Published in:Experimental and molecular pathology 2013-06, Vol.94 (3), p.445-452
Main Authors: Rattanavich, Rungwasee, Plagov, Andrei, Kumar, Dileep, Rai, Partab, Lederman, Rivka, Salhan, Divya, Vashistha, Himanshu, Malhotra, Ashwani, Meggs, Leonard G., Singhal, Pravin C.
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creator Rattanavich, Rungwasee
Plagov, Andrei
Kumar, Dileep
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Meggs, Leonard G.
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description Overwhelming oxidative stress and compromised tubular cell antioxidant response have been incriminated for cisplatin (Cis)-induced acute kidney injury (AKI). We hypothesized that Cis-induced AKI was the outcome of the deactivated redox-sensitive stress response program (RSSRP). Wild type (WT) and heterozygous p66ShcA(p66+/−) mice in groups of six were administered either normal saline (WT) or Cis (12.5mg/kg, intraperitoneal, Cis/WT). Renal biomarkers were collected and kidneys were harvested for renal histology. Cis/WT showed elevated blood urea nitrogen levels and enhanced tubular cell apoptosis, necrosis, and dilated tubules filled with casts when compared to Cis/p66+/−. Cis/p66+/− developed only a clinically occult AKI (normal blood urea levels and only microscopic alterations). Immunoblots from the lysates of renal tissues of Cis/WT displayed enhanced expression of phospho-p66ShcA, and phospho-Foxo3A but attenuated expression of MnSOD and catalase; conversely, p66 deficit prevented these alterations in Cis milieu. In in vitro studies, Cis treated mouse proximal tubular cells (MPTCs) displayed enhanced phosphorylation of p66ShcA and no increase in tubular cell expression of MnSOD. In addition, renal tissues of Cis/WT and Cis-treated MPTCs displayed enhanced phosphorylation of p53 and Bax expression. However, MPTC partially silenced for p66ShcA displayed partial inhibition of Cis-induced tubular cell apoptosis as well as necrosis. These findings indicate that Cis-induced AKI is the outcome of the deactivated RSSRP (attenuated anti-oxidant response) and activation of pro-apoptotic (p53-induced Bax expression) pathway. •Kidney cells display compromised antioxidant response in cis-induced AKI.•Cis deactivated redox-sensitive stress response program (RSSRP) in tubular cells.•P66ShcA deficit in tubular cells restored RSSRP in cis milieu.
doi_str_mv 10.1016/j.yexmp.2013.03.001
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In in vitro studies, Cis treated mouse proximal tubular cells (MPTCs) displayed enhanced phosphorylation of p66ShcA and no increase in tubular cell expression of MnSOD. In addition, renal tissues of Cis/WT and Cis-treated MPTCs displayed enhanced phosphorylation of p53 and Bax expression. However, MPTC partially silenced for p66ShcA displayed partial inhibition of Cis-induced tubular cell apoptosis as well as necrosis. These findings indicate that Cis-induced AKI is the outcome of the deactivated RSSRP (attenuated anti-oxidant response) and activation of pro-apoptotic (p53-induced Bax expression) pathway. •Kidney cells display compromised antioxidant response in cis-induced AKI.•Cis deactivated redox-sensitive stress response program (RSSRP) in tubular cells.•P66ShcA deficit in tubular cells restored RSSRP in cis milieu.</abstract><cop>Netherlands</cop><pub>Elsevier Inc</pub><pmid>23506954</pmid><doi>10.1016/j.yexmp.2013.03.001</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record>
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ispartof Experimental and molecular pathology, 2013-06, Vol.94 (3), p.445-452
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source ScienceDirect Freedom Collection
subjects Acute kidney injury
Acute Kidney Injury - chemically induced
Acute Kidney Injury - metabolism
Acute Kidney Injury - pathology
Animals
Antineoplastic Agents - toxicity
Apoptosis
Apoptosis - drug effects
bcl-2-Associated X Protein - metabolism
Blood Urea Nitrogen
Cisplatin - toxicity
Cisplatinum
Female
Gene Silencing
Heterozygote
Kidney Tubules, Proximal - drug effects
Kidney Tubules, Proximal - metabolism
Kidney Tubules, Proximal - pathology
Male
Mice
Mice, Knockout
Necrosis - chemically induced
Oxidation-Reduction
Oxidative stress
Oxidative Stress - drug effects
Oxidoreductases - metabolism
p66ShcA
Phosphorylation
Redox-sensitive stress response program
Shc Signaling Adaptor Proteins - deficiency
Shc Signaling Adaptor Proteins - genetics
Shc Signaling Adaptor Proteins - metabolism
Tumor Suppressor Protein p53 - metabolism
title Deficit of p66ShcA restores redox-sensitive stress response program in cisplatin-induced acute kidney injury
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