p66Shc signaling does not contribute to tubular damage induced by renal ischemia-reperfusion injury in rat. Biochem Biophys Res Commun 2022 May 07;603:69-74
Date
03/13/2022Pubmed ID
35278882Pubmed Central ID
PMC8969123DOI
10.1016/j.bbrc.2022.03.020Scopus ID
2-s2.0-85125835040 (requires institutional sign-in at Scopus site)Abstract
Renal ischemia-reperfusion (IR) injury is one of the major causes of acute kidney injury and represents a significant risk factor for renal transplantation. The level of renal damage is influenced by the ischemic duration and is caused by excessive amounts of produced reactive oxygen species (ROS). Adaptor protein p66Shc is known to regulate cellular and organ's sensitivity to oxidative stress and to contribute significantly to mitochondrial production of hydrogen peroxide in stress conditions. Studies carried out in cultured renal cells suggest that p66Shc-mediated mitochondrial dysfunction and ROS production are responsible for renal ischemic injury. We used our genetically modified rats, which either lack p66Shc expression, or express p66Shc variant, which constitutively generates increased quantities of hydrogen peroxide, to evaluate potential contribution of p66Shc signaling to renal damage in ischemia reperfusion rat model. Analysis of outer medulla tubule damage revealed the lack of contribution of either p66Shc expression or its constitutive signaling to IR injury in rat model.
Author List
Miller B, Regner K, Sorokin AAuthors
Kevin R. Regner MD Interim Chair, Professor in the Medicine department at Medical College of WisconsinAndrey Sorokin PhD Professor in the Medicine department at Medical College of Wisconsin
MESH terms used to index this publication - Major topics in bold
AnimalsOxidative Stress
Rats
Reactive Oxygen Species
Reperfusion Injury
Shc Signaling Adaptor Proteins
Src Homology 2 Domain-Containing, Transforming Protein 1
