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Proteomics of Obstructive Sleep Apnea with type 2 Diabetes Mellitus

2019-02-21Lecture Restricted access
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dc.contributor.authorVaz, Fátima
dc.contributor.authorValentim-Coelho, Cristina
dc.contributor.authorNeves, Sofia
dc.contributor.authorPenque, Deborah
dc.date.accessioned2019-05-30T10:17:33Z
dc.date.available2019-05-30T10:17:33Z
dc.date.issued2019-02-21
dc.description.abstractBackground: We previously showed that Obstructive sleep apnea (OSA), a common public health concern causing deleterious cardiometabolic dysfunction, induces alterations in red blood cell (RBC) proteome (Feliciano et al 2017). Herein, we aimed to investigate redox state of PRDX2 in OSA patients with Type 2 Diabetes Mellitus before and after positive airway pressure (PAP) treatment to better understand the basic mechanisms associated with OSA and OSA outcomes. Methods: RBC samples from control snorers (n=22 being 3 diabetics) and OSA patients before and after six month of PAP-treatment (n=29 being 8 diabetics) were analysed by non-reducing western blot using antibody against PRDX2 or PRDXSO2 to measure the total and overoxidized levels of monomeric/dimeric/multimeric forms of PRDX2. Non-reducing SDS-PAGE coomassie gel band corresponding to PRDX2 monomers from the different groups where trypsinized and investigation by LC/MS/MS for additional post-translational modifications (PTMs) are under process. Results: We confirmed previously data showing higher overoxidation on monomeric forms of PRDX2 in OSA RBC without comorbidity compared to Snorer controls. After PAP treatment, this overoxidation decreased followed by an increase of multimeric-overoxidized forms associated with chaperone protective function. In contrast, the level of PRDX2 monomers in RBC diabetic OSA, although the most abundant its overoxidation level was much lower than OSA without comorbidity and did not significant change after treatment. Moreover, the level of PAP-induced PRDX2-overoxidized-multimers was also lower in these diabetic OSA patients. The level of PRDX2 overoxidized monomeric/dimeric forms in RBC correlated negatively with levels of insulin / triglycerides and HbA1C, respectively.After PAP, PRDX2SO2 / 3 decamer levels correlated positively with adrenaline levels. Conclusions: The redox/oligomeric state of RBC PRDX2 regulated by overoxidation of the active cysteines were differentially modulated in diabetic OSA patients compared to OSA without this comorbidity. PAP-induced overoxidized oligo forms of PRDX2 associated with chaperone protective function showed decreased in OSA patients with diabetes. Preliminary data pointed to polyglutamylation on PRDX2 glutamic acid91 that can be differentially modulated in OSA with and without diabetes and/or in response to PAP treatment. The clinical impact of these findings needs further investigation and validation. My perspective future encompasses the complete identification of these PTM by MS based strategies and validation by SRM approaches.pt_PT
dc.description.versionN/Apt_PT
dc.identifier.urihttp://hdl.handle.net/10400.18/6413
dc.language.isoengpt_PT
dc.peerreviewednopt_PT
dc.subjectProteomicspt_PT
dc.subjectObstructive Sleep Apneapt_PT
dc.subjectDiabetes Mellituspt_PT
dc.subjectProteómicapt_PT
dc.subjectGenómica Funcional e Estruturalpt_PT
dc.subjectGenómica Funcionalpt_PT
dc.titleProteomics of Obstructive Sleep Apnea with type 2 Diabetes Mellituspt_PT
dc.typelecture
dspace.entity.typePublication
oaire.citation.conferencePlaceLisboa, Portugalpt_PT
oaire.citation.titleIV Genetics Workshop, Universidade Nova de Lisboa, 21 março 2019pt_PT
rcaap.rightsrestrictedAccesspt_PT
rcaap.typelecturept_PT

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