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S100A8/A9 induces autophagy and apoptosis via ROS-mediated cross-talk between mitochondria and lysosomes that involves BNIP3
Department of Physiology, University of Manitoba, Winnipeg, MB, Canada; National Training Program in Allergy and Asthma, University of Manitoba, Winnipeg, MB, Canada; Biology of Breathing Group, Manitoba Institute of Child Health, Winnipeg, MB, Canada.
Department of Biochemistry and Medical Genetics, Manitoba Institute of Cell Biology, CancerCare Manitoba, Winnipeg, Canada.
Department of Biochemistry and Medical Genetics, Manitoba Institute of Cell Biology, CancerCare Manitoba, Winnipeg, Canada.
Department of Biochemistry and Chemistry, Center for Structural Biology, Vanderbilt University, Nashville, USA.
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2010 (English)In: Cell Research, ISSN 1001-0602, E-ISSN 1748-7838, Vol. 20, no 3, 314-331 p.Article in journal (Refereed) Published
Abstract [en]

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, ΔTM-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 ΔTM-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 mitochondria and lysosomes via ROS and the process involves BNIP3.

Place, publisher, year, edition, pages
2010. Vol. 20, no 3, 314-331 p.
Keyword [en]
S100A8/A9, Calprotectin, lysosomal activation, mitochondrial membrane potential, BNIP3, Beclin-1
National Category
Biochemistry and Molecular Biology Cell Biology
Identifiers
URN: urn:nbn:se:liu:diva-86904DOI: 10.1038/cr.2009.129ISI: 000275816300008PubMedID: 19935772OAI: oai:DiVA.org:liu-86904DiVA: diva2:583053
Available from: 2013-01-07 Created: 2013-01-07 Last updated: 2017-12-06

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Los, Marek Jan

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