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Bcl-2 protects against Abeta(25-35)-induced oxidative PC12 cell death by potentiation of antioxidant capacity.
Biochem Biophys Res Commun. 2004 Jul 30; 320(3):880-6.BB

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, which were attenuated by NF-kappaB blockers. These results suggest that NF-kappaB plays a role in bcl-2-mediated protection against Abeta-induced apoptosis in PC12 cells through augmentation of cellular antioxidant capacity.

Authors+Show Affiliations

Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University, Shinlim-dong, Kwanak-ku, Seoul 151-742, South Korea.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

15240130

Citation

Jang, Jung-Hee, and Young-Joon Surh. "Bcl-2 Protects Against Abeta(25-35)-induced Oxidative PC12 Cell Death By Potentiation of Antioxidant Capacity." Biochemical and Biophysical Research Communications, vol. 320, no. 3, 2004, pp. 880-6.
Jang JH, Surh YJ. Bcl-2 protects against Abeta(25-35)-induced oxidative PC12 cell death by potentiation of antioxidant capacity. Biochem Biophys Res Commun. 2004;320(3):880-6.
Jang, J. H., & Surh, Y. J. (2004). Bcl-2 protects against Abeta(25-35)-induced oxidative PC12 cell death by potentiation of antioxidant capacity. Biochemical and Biophysical Research Communications, 320(3), 880-6.
Jang JH, Surh YJ. Bcl-2 Protects Against Abeta(25-35)-induced Oxidative PC12 Cell Death By Potentiation of Antioxidant Capacity. Biochem Biophys Res Commun. 2004 Jul 30;320(3):880-6. PubMed PMID: 15240130.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Bcl-2 protects against Abeta(25-35)-induced oxidative PC12 cell death by potentiation of antioxidant capacity. AU - Jang,Jung-Hee, AU - Surh,Young-Joon, PY - 2004/05/12/received PY - 2004/7/9/pubmed PY - 2004/8/27/medline PY - 2004/7/9/entrez SP - 880 EP - 6 JF - Biochemical and biophysical research communications JO - Biochem Biophys Res Commun VL - 320 IS - 3 N2 - 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, which were attenuated by NF-kappaB blockers. These results suggest that NF-kappaB plays a role in bcl-2-mediated protection against Abeta-induced apoptosis in PC12 cells through augmentation of cellular antioxidant capacity. SN - 0006-291X UR - https://www.unboundmedicine.com/medline/citation/15240130/Bcl_2_protects_against_Abeta_25_35__induced_oxidative_PC12_cell_death_by_potentiation_of_antioxidant_capacity_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006291X04013002 DB - PRIME DP - Unbound Medicine ER -