Bcl-2 protects against Abeta(25-35)-induced oxidative PC12 cell death by potentiation of antioxidant capacity

Biochemical and Biophysical Research Communications
Jung-Hee Jang, Young-Joon Surh

Abstract

A substantial body of data indicates that reactive oxygen intermediates (ROIs) are implicated in pathogenesis of diverse human diseases. Oxidative stress induced by ROIs often causes cell death via apoptosis that is regulated by a plenty of functional genes and their protein products. Bcl-2 is one such protein that blocks apoptosis induced by various death stimuli. In spite of extensive research, the molecular mechanisms underlying antiapoptotic function of Bcl-2 are not fully clarified. In the present work, we have investigated the role of bcl-2 in protecting against beta-amyloid (Abeta)-induced oxidative death in rat pheochromocytoma (PC12) cells. Transfection with the antiapoptotic bcl-2 gene rescued PC12 cells from apoptotic death induced by Abeta. Addition of an NF-kappaB inhibitor, such as pyrrolidine dithiocarbamate or N-tosyl-l-phenylalanine chloromethyl ketone, to the media aggravated Abeta-induced PC12 cell death. PC12 cells overexpressing bcl-2 exhibited higher levels of constitutively activated NF-kappaB compared with vector-transfected controls, which appear to be mediated by the elevated activation of Akt/protein kinase B. The ectopic expression of bcl-2 enhanced both the expression and the activity of catalase, w...Continue Reading

References

Jan 1, 1992·Free Radical Research Communications·R SchreckP A Baeuerle
Apr 10, 1992·Science·J A Hardy, G A Higgins
May 15, 1993·Proceedings of the National Academy of Sciences of the United States of America·L T ZhongD E Bredesen
Oct 4, 1996·Cell·P A Baeuerle, D Baltimore
Jan 1, 1997·Free Radical Biology & Medicine·W R Markesbery
Sep 16, 1999·Experimental Neurology·G DengC W Cotman
Dec 2, 1999·Genes & Development·S R DattaM E Greenberg
May 8, 2000·Journal of Neuroscience Research·K HondaS Shimohama
Feb 28, 2002·Redox Report : Communications in Free Radical Research·P A AmstadP L Gutierrez
Apr 10, 2003·Free Radical Biology & Medicine·Jung-Hee Jang, Young-Joon Surh
Mar 24, 2004·Free Radical Biology & Medicine·Jung-Hee JangYoung-Joon Surh

❮ Previous
Next ❯

Citations

Mar 21, 2006·Apoptosis : an International Journal on Programmed Cell Death·J ChenP X Chen
Jul 27, 2007·Journal of Toxicology and Environmental Health. Part a·Kyoung Ah KangJin Won Hyun
Nov 6, 2012·Phytomedicine : International Journal of Phytotherapy and Phytopharmacology·Yan-Fang XianXiao-Ping Lai
Jan 16, 2009·The FEBS Journal·Ankur MaheshwariDeoki Nandan
May 11, 2005·Biochemical and Biophysical Research Communications·Jung-Hee Jang, Young-Joon Surh
Oct 6, 2005·The Journal of Biological Chemistry·Manuel J SantosNibaldo C Inestrosa
Oct 17, 2017·Oncotarget·Mathias TessonRobert Mairs
Jul 4, 2009·Molecular Reproduction and Development·Archana AggarwalDeoki Nandan
Aug 21, 2020·Neurochemical Research·Mithun Singh RajputRashmi Dahima
Jun 20, 2020·BMC Complementary Medicine and Therapies·Yan LinDuan-Fang Liao
Aug 9, 2008·Biochemical and Biophysical Research Communications·Susan J ThomsonMark B Hampton

❮ Previous
Next ❯

Related Concepts

Related Feeds

BCL-2 Family Proteins

BLC-2 family proteins are a group that share the same homologous BH domain. They play many different roles including pro-survival signals, mitochondria-mediated apoptosis and removal or damaged cells. They are often regulated by phosphorylation, affecting their catalytic activity. Here is the latest research on BCL-2 family proteins.

AKT Pathway

This feed focuses on the AKT serine/threonine kinase, which is an important signaling pathway involved in processes such as glucose metabolism and cell survival.

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis