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S100A8/A9 induces a...
S100A8/A9 induces autophagy and apoptosis via ROS-mediated cross-talk between mitochondria and lysosomes that involves BNIP3
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- Ghavami, Saeid (author)
- 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
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- Eshragi, Mehdi (author)
- Department of Biochemistry and Medical Genetics, Manitoba Institute of Cell Biology, CancerCare Manitoba, Winnipeg, Canada
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- Ande, Sudharsana R (author)
- Department of Biochemistry and Medical Genetics, Manitoba Institute of Cell Biology, CancerCare Manitoba, Winnipeg, Canada
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- Chazin, Walter J (author)
- Department of Biochemistry and Chemistry, Center for Structural Biology, Vanderbilt University, Nashville, USA
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- Klonisch, Thomas (author)
- Department of Human Anatomy and Cell Science, University of Manitoba, Winnipeg, Canada
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- Halayko, Andrew J. (author)
- Department of Physiology, University of Manitoba, Winnipeg, MB, Canada; Manitoba Institute of Child Health, Winnipeg, MB, Canada; Department of Internal Medicine, University of Manitoba, Winnipeg, MB, Canada
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- Mcneill, Karol D (author)
- Manitoba Institute of Child Health, University of Manitoba, Winnipeg, Canada
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- Hashemi, Mohammad (author)
- Department of Clinical Biochemistry, Zahedan University of Medical Sciences, Zahedan, Iran
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- Kerkhoff, Claus (author)
- Institute of Immunology, University of Muenster, Roentgenstr. 21, Muenster, Germany
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- Los, Marek Jan (author)
- Interfaculty Institute for Biochemistry, University of Tübingen, Germany
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(creator_code:org_t)
- 2009-11-24
- 2010
- English.
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In: Cell Research. - : Springer Science and Business Media LLC. - 1001-0602 .- 1748-7838. ; 20:3, s. 314-331
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Abstract
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- 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.
Subject headings
- NATURVETENSKAP -- Biologi -- Biokemi och molekylärbiologi (hsv//swe)
- NATURAL SCIENCES -- Biological Sciences -- Biochemistry and Molecular Biology (hsv//eng)
- NATURVETENSKAP -- Biologi -- Cellbiologi (hsv//swe)
- NATURAL SCIENCES -- Biological Sciences -- Cell Biology (hsv//eng)
Keyword
- S100A8/A9
- Calprotectin
- lysosomal activation
- mitochondrial membrane potential
- BNIP3
- Beclin-1
Publication and Content Type
- ref (subject category)
- art (subject category)
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- By the author/editor
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Ghavami, Saeid
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Eshragi, Mehdi
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Ande, Sudharsana ...
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Chazin, Walter J
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Klonisch, Thomas
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Halayko, Andrew ...
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show more...
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Mcneill, Karol D
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Hashemi, Mohamma ...
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Kerkhoff, Claus
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Los, Marek Jan
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show less...
- About the subject
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- NATURAL SCIENCES
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NATURAL SCIENCES
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and Biological Scien ...
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and Biochemistry and ...
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- NATURAL SCIENCES
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NATURAL SCIENCES
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and Biological Scien ...
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and Cell Biology
- Articles in the publication
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Cell Research
- By the university
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Linköping University