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Towards and understanding of the role of Bax on bile acid-mediated cytoprotection
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2019 (English)In: European Biophysics Journal, ISSN 0175-7571, E-ISSN 1432-1017, Vol. 48, p. S177-S177Article in journal, Meeting abstract (Other academic) Published
Abstract [en]

Cytoprotective bile acids such as ursodeoxycholic acid (UDCA) and tauroursodeoxycholic acid (TUDCA) are known for their ability to inhibit apoptosis at submicellar concentrations in both hepatic and nonhepatic cells. The exact mechanism by which they exert this cytoprotection is not yet entirely clear, but their effect seems to be related with the blockage of processes that converge on mitochondrial damage. Bcl-2-associated X protein (Bax) plays a key role in apoptosis, which is achieved through translocation of the protein to the mitochondria from the cytosol after an apoptotic stimulus and formation of pores in mitochondrial membranes. We show here that both UDCA and TUDCA inhibit the interaction of Bax with activator molecules such as the Bid-BH3 peptide and decrease the affinity of Bax for liposomes mimicking outer mitochondrial membrane composition. Importantly, UDCA and TUDCA are shown to dramatically inhibit Bax-induced permeabilization of model membranes. The direct impact of apoptotic and cytoprotective bile acids on Bax translocation is monitored in HCT116 Bax/Bak DKO cells expressing Bax-GFP. The findings presented here clearly show that at physiologically active submicellar concentrations, bile acids have the ability to inhibit Bax poreforming activity and suggest that the cytoprotective activity of UDCA and TUDCA could be the result of this process.

Place, publisher, year, edition, pages
Springer, 2019. Vol. 48, p. S177-S177
National Category
Biophysics
Identifiers
URN: urn:nbn:se:umu:diva-161706DOI: 10.1007/s00249-019-01373-4ISI: 000473420400584OAI: oai:DiVA.org:umu-161706DiVA, id: diva2:1340405
Conference
Joint 12th EBSA European Biophysics Congress / 10th IUPAP International Conference on Biological Physics (ICBP), Madrid, Spain, July 20-24, 2019
Note

Supplement: 1

Meeting Abstract: P-396

Available from: 2019-08-05 Created: 2019-08-05 Last updated: 2019-08-05Bibliographically approved

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Gröbner, Gerhard

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