S100A8/A9 induces autophagy and apoptosis via ROS-mediated cross-talk between mitochondria and lysosomes that involves BNIP3.

Cell Research
S GhavamiMarek Los

Abstract

The complex formed by two members of the S100 calcium-binding protein family, S100A8/A9, exerts apoptosis-inducing activity in various cells of different origins. Here, we present evidence that the underlying molecular mechanisms involve both programmed cell death I (PCD I, apoptosis) and PCD II (autophagy)-like death. Treatment of cells with S100A8/A9 caused the increase of Beclin-1 expression as well as Atg12-Atg5 formation. S100A8/A9-induced cell death was partially inhibited by the specific PI3-kinase class III inhibitor, 3-methyladenine (3-MA), and by the vacuole H(+)-ATPase inhibitor, bafilomycin-A1 (Baf-A1). S100A8/A9 provoked the translocation of BNIP3, a BH3 only pro-apoptotic Bcl2 family member, to mitochondria. Consistent with this finding, DeltaTM-BNIP3 overexpression partially inhibited S100A8/A9-induced cell death, decreased reactive oxygen species (ROS) generation, and partially protected against the decrease in mitochondrial transmembrane potential in S100A8/A9-treated cells. In addition, either DeltaTM-BNIP3 overexpression or N-acetyl-L-cysteine co-treatment decreased lysosomal activation in cells treated with S100A8/A9. Our data indicate that S100A8/A9-promoted cell death occurs through the cross-talk of mitoc...Continue Reading

References

Jan 27, 1999·Biochimica Et Biophysica Acta·C KerkhoffC Sorg
Oct 20, 1999·The Journal of Cell Biology·T KirisakoY Ohsumi
Mar 10, 2000·Biochimica Et Biophysica Acta·B TurkV Turk
Aug 31, 2000·Annual Review of Biochemistry·J Kim, D J Klionsky
Dec 2, 2000·Science·D J Klionsky, S D Emr
Mar 27, 2001·The Journal of Cell Biology·N MizushimaT Yoshimori
Aug 3, 2001·Nature Reviews. Molecular Cell Biology·M Leist, M Jäättelä
Sep 6, 2001·Cell Death and Differentiation·W Bursch
Sep 29, 2001·Archives of Histology and Cytology·Y Uchiyama
Nov 20, 2002·Biological Chemistry·Boris TurkVito Turk
Apr 12, 2003·The Journal of Biological Chemistry·Laurence LamyAlain Bernard
May 24, 2003·Biochemical and Biophysical Research Communications·Tilman GruneKelvin J A Davies
Aug 2, 2003·The Journal of Biological Chemistry·Takahiro NemotoEiki Kominami
Oct 17, 2003·Genes & Development·Jerry M Adams
Dec 20, 2003·Biochemical and Biophysical Research Communications·Tamotsu Yoshimori
Mar 25, 2004·Journal of Cellular Physiology·Guglielmo SorciRosario Donato
Apr 8, 2004·Developmental Cell·Beth Levine, Daniel J Klionsky
Apr 13, 2004·Journal of Leukocyte Biology·Saeid GhavamiFatemeh Karami-Tehrani
May 20, 2004·Kidney International·Sira SooparbHarold A Franch
Nov 6, 2004·Science·Takahiro Shintani, Daniel J Klionsky
Nov 24, 2004·Nature Cell Biology·Shigeomi ShimizuYoshihide Tsujimoto
Jan 12, 2005·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Claus KerkhoffJacques Doussiere
Jan 20, 2005·Molecular and Cellular Biology·Patricia BoyaGuido Kroemer
Jun 1, 2005·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Jean-Christophe PeterJean-Christophe Roegel
Sep 24, 2005·Cell·Sophie PattingreBeth Levine
Feb 21, 2006·Antioxidants & Redox Signaling·Roberta KiffinAna Maria Cuervo
Dec 16, 2006·European Journal of Pharmacology·Mohammad HashemiMarek Los

❮ Previous
Next ❯

Citations

Mar 5, 2011·American Journal of Nephrology·Joseph GawdzikMarion A Hofmann Bowman
Oct 23, 2010·Arteriosclerosis, Thrombosis, and Vascular Biology·Marion A Hofmann BowmanElizabeth M McNally
Jul 28, 2012·Current Molecular Medicine·R DonatoC L Geczy
Nov 21, 2012·Hepatitis Monthly·Claudia MaletzkiClaus Kerkhoff
Apr 25, 2013·Hepatitis Monthly·Behzad YeganehSaeid Ghavami
May 3, 2014·International Journal of Molecular Medicine·Parvaneh MehrbodAini Ideris
Aug 7, 2014·Tumour Biology : the Journal of the International Society for Oncodevelopmental Biology and Medicine·Hamideh AbediSima Hajiahmadi
Jan 25, 2013·Tumour Biology : the Journal of the International Society for Oncodevelopmental Biology and Medicine·Saeid ShiraliMarzieh Moeinifard
Dec 12, 2012·Archivum Immunologiae Et Therapiae Experimentalis·Wiem ChaabaneMarek J Los
Dec 18, 2012·Apoptosis : an International Journal on Programmed Cell Death·Mei ShiYu-Zhong Zhang
Jan 21, 2014·The Ocular Surface·Louis TongShyam S Chaurasia
Apr 6, 2016·Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie·Yuqing DuanXiaobo Sun
May 17, 2011·Cell Calcium·Jean-Paul DecuypereJan B Parys
Aug 5, 2015·Nature Reviews. Rheumatology·Georg VargaAnna Rubartelli
Feb 28, 2016·Biochemical and Biophysical Research Communications·Yu-Dong XuYong-Qing Yang
Aug 15, 2012·Immunological Reviews·Daolin TangMichael T Lotze
Jan 11, 2013·Journal of Cellular and Molecular Medicine·Mayur V JainMarek Łos
Nov 19, 2011·Journal of Viral Hepatitis·S M AlavianS Ghavami
Nov 19, 2013·Journal of Cellular and Molecular Medicine·Jing XiongPin-Lan Li
Mar 29, 2016·Journal of Proteomics·Lorenzo E Hernández-CastellanoAndre M de Almeida
Jul 23, 2015·Ageing Research Reviews·Ramar Perumal Samy, Lina H K Lim
Jun 5, 2016·Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie·Haihui ZhangXiaobo Sun
Oct 3, 2012·Biochimica Et Biophysica Acta·Saeid GhavamiIan M C Dixon
Dec 3, 2010·Biochimica Et Biophysica Acta·Diego RodriguezClaudio Hetz
Oct 23, 2012·Hepatitis Monthly·Jaganmohan Reddy Jangamreddy, Marek J Los

❮ Previous
Next ❯

Related Concepts

Related Feeds

ATP Synthases

ATP synthases are enzymes located in the inner mitochondrial membrane that catalyze the synthesis of ATP during cellular respiration. Discover the latest research on ATP synthases here.

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.

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

Autophagy & Model Organisms

Autophagy is a cellular process that allows degradation by the lysosome of cytoplasmic components such as proteins or organelles. Here is the latest research on autophagy & model organisms

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.