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dc.contributor.authorRichardson, Adam
dc.contributor.authorMuir, Lewis
dc.contributor.authorMousdell, Sasha
dc.contributor.authorSexton, Darren
dc.contributor.authorJones, Sarah
dc.contributor.authorHowl, John
dc.contributor.authorRoss, Kehinde
dc.date.accessioned2018-02-01T11:51:23Z
dc.date.available2018-02-01T11:51:23Z
dc.date.issued2018-01-30
dc.identifier.citationRichardson A., Muir L., Mousdell S., Sexton D., Jones S., Howl J., Ross K. (2018) 'Modulation of mitochondrial activity in HaCaT keratinocytes by the cell penetrating peptide Z-Gly-RGD(DPhe)-mitoparan' BMC Research Notes, 11 (1) doi: 10.1186/s13104-018-3192-1
dc.identifier.issn1756-0500
dc.identifier.doi10.1186/s13104-018-3192-1
dc.identifier.urihttp://hdl.handle.net/2436/621065
dc.description.abstractObjective Biologically active cell penetrating peptides (CPPs) are an emerging class of therapeutic agent. The wasp venom peptide mastoparan is an established CPP that modulates mitochondrial activity and triggers caspase-dependent apoptosis in cancer cells, as does the mastoparan analogue mitoparan (mitP). Mitochondrial depolarisation and activation of the caspase cascade also underpins the action of dithranol, a topical agent for treatment of psoriasis. The effects of a potent mitP analogue on mitochondrial activity were therefore examined to assess its potential as a novel approach for targeting mitochondria for the treatment of psoriasis. Results In HaCaT keratinocytes treated with the mitP analogue Z-Gly-RGD(DPhe)-mitP for 24 h, a dose-dependent loss of mitochondrial activity was observed using the methyl-thiazolyl-tetrazolium (MTT) assay. At 10 μmol L−1, MTT activity was less than 30% that observed in untreated cells. Staining with the cationic dye JC-1 suggested that Z-Gly-RGD(DPhe)-mitP also dissipated the mitochondrial membrane potential, with a threefold increase in mitochondrial depolarisation levels. However, caspase activity appeared to be reduced by 24 h exposure to Z-Gly-RGD(DPhe)-mitP treatment. Furthermore, Z-Gly-RGD(DPhe)-mitP treatment had little effect on overall cell viability. Our findings suggest Z-Gly-RGD(DPhe)-mitP promotes the loss of mitochondrial activity but does not appear to evoke apoptosis in HaCaT keratinocytes.
dc.language.isoen
dc.publisherBioMed Central
dc.relation.urlhttps://bmcresnotes.biomedcentral.com/articles/10.1186/s13104-018-3192-1
dc.subjectCell penetrating peptides
dc.subjectBioportides
dc.subjectKeratinocytes
dc.subjectMitochondria
dc.titleModulation of mitochondrial activity in HaCaT keratinocytes by the cell penetrating peptide Z-Gly-RGD(DPhe)-mitoparan
dc.typeJournal article
dc.identifier.journalBMC Research Notes
dc.date.accepted2018-01-19
rioxxterms.funderUniversity of Wolverhampton
rioxxterms.identifier.projectUoW010218SJ
rioxxterms.versionVoR
rioxxterms.licenseref.urihttps://creativecommons.org/CC BY-NC-ND 4.0
rioxxterms.licenseref.startdate2018-02-01
dc.source.volume11
dc.source.issue82
refterms.dateFCD2018-10-19T09:24:43Z
refterms.versionFCDVoR
refterms.dateFOA2018-02-01T00:00:00Z
html.description.abstractObjective Biologically active cell penetrating peptides (CPPs) are an emerging class of therapeutic agent. The wasp venom peptide mastoparan is an established CPP that modulates mitochondrial activity and triggers caspase-dependent apoptosis in cancer cells, as does the mastoparan analogue mitoparan (mitP). Mitochondrial depolarisation and activation of the caspase cascade also underpins the action of dithranol, a topical agent for treatment of psoriasis. The effects of a potent mitP analogue on mitochondrial activity were therefore examined to assess its potential as a novel approach for targeting mitochondria for the treatment of psoriasis. Results In HaCaT keratinocytes treated with the mitP analogue Z-Gly-RGD(DPhe)-mitP for 24 h, a dose-dependent loss of mitochondrial activity was observed using the methyl-thiazolyl-tetrazolium (MTT) assay. At 10 μmol L−1, MTT activity was less than 30% that observed in untreated cells. Staining with the cationic dye JC-1 suggested that Z-Gly-RGD(DPhe)-mitP also dissipated the mitochondrial membrane potential, with a threefold increase in mitochondrial depolarisation levels. However, caspase activity appeared to be reduced by 24 h exposure to Z-Gly-RGD(DPhe)-mitP treatment. Furthermore, Z-Gly-RGD(DPhe)-mitP treatment had little effect on overall cell viability. Our findings suggest Z-Gly-RGD(DPhe)-mitP promotes the loss of mitochondrial activity but does not appear to evoke apoptosis in HaCaT keratinocytes.


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