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dc.contributor.authorBANDYOPADHAYA, ARUNAVAen_US
dc.contributor.authorCONSTANTINOU, CATERINAen_US
dc.contributor.authorPSYCHOGIOS, NIKOLAOSen_US
dc.contributor.authorUEKI, RYUSUKEen_US
dc.contributor.authorYASUHARA, SHINGOen_US
dc.contributor.authorMARTYN, J.A. JEEVENDRAen_US
dc.contributor.authorWILHELMY, JULIEen_US
dc.contributor.authorMINDRINOS, MICHAELen_US
dc.contributor.authorRAHME, LAURENCE G.en_US
dc.contributor.authorTZIKA, A. ARIAen_US
dc.date.accessioned2016-04-01T15:47:40Z
dc.date.issued2016en_US
dc.identifier.citationBANDYOPADHAYA, ARUNAVA, CATERINA CONSTANTINOU, NIKOLAOS PSYCHOGIOS, RYUSUKE UEKI, SHINGO YASUHARA, J.A. JEEVENDRA MARTYN, JULIE WILHELMY, MICHAEL MINDRINOS, LAURENCE G. RAHME, and A. ARIA TZIKA. 2016. “Bacterial-excreted small volatile molecule 2-aminoacetophenone induces oxidative stress and apoptosis in murine skeletal muscle.” International Journal of Molecular Medicine 37 (4): 867-878. doi:10.3892/ijmm.2016.2487. http://dx.doi.org/10.3892/ijmm.2016.2487.en
dc.identifier.issn1107-3756en
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:26318559
dc.description.abstractOxidative stress induces mitochondrial dysfunction and facilitates apoptosis, tissue damage or metabolic alterations following infection. We have previously discovered that the Pseudomonas aeruginosa (PA) quorum sensing (QS)-excreted small volatile molecule, 2-aminoacetophenone (2-AA), which is produced in infected human tissue, promotes bacterial phenotypes that favor chronic infection, while also compromising muscle function and dampens the pathogen-induced innate immune response, promoting host tolerance to infection. In this study, murine whole-genome expression data have demonstrated that 2-AA affects the expression of genes involved in reactive oxygen species (ROS) homeostasis, thus producing an oxidative stress signature in skeletal muscle. The results of the present study demonstrated that the expression levels of genes involved in apoptosis signaling pathways were upregulated in the skeletal muscle of 2-AA-treated mice. To confirm the results of our transcriptome analysis, we used a novel high-resolution magic-angle-spinning (HRMAS), proton (1H) nuclear magnetic resonance (NMR) method and observed increased levels of bisallylic methylene fatty acyl protons and vinyl protons, suggesting that 2-AA induces skeletal muscle cell apoptosis. This effect was corroborated by our results demonstrating the downregulation of mitochondrial membrane potential in vivo in response to 2-AA. The findings of the present study indicate that the bacterial infochemical, 2-AA, disrupts mitochondrial functions by inducing oxidative stress and apoptosis signaling and likely promotes skeletal muscle dysfunction, which may favor chronic/persistent infection.en
dc.language.isoen_USen
dc.publisherD.A. Spandidosen
dc.relation.isversionofdoi:10.3892/ijmm.2016.2487en
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC4790710/pdf/en
dash.licenseLAAen_US
dc.subjecten
dc.subject2-aminoacetophenoneen
dc.subjectskeletal muscleen
dc.subjectoxidative stressen
dc.subjectapoptosisen
dc.subjectmitochondriaen
dc.subjectnuclear magnetic resonanceen
dc.subjectmicroarraysen
dc.subjectgenomicsen
dc.titleBacterial-excreted small volatile molecule 2-aminoacetophenone induces oxidative stress and apoptosis in murine skeletal muscleen
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden
dc.relation.journalInternational Journal of Molecular Medicineen
dash.depositing.authorBANDYOPADHAYA, ARUNAVAen_US
dc.date.available2016-04-01T15:47:40Z
dc.identifier.doi10.3892/ijmm.2016.2487*
dash.contributor.affiliatedBandyopadhaya, Arunava
dash.contributor.affiliatedTzika, A.
dash.contributor.affiliatedYasuhara, Shingo
dash.contributor.affiliatedRahme, Laurence


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