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Proteome profiling in obstructive sleep apnea severity and treatment response towards early diagnosis and prognosis prediction

2019-05-08Lecture Restricted access
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dc.contributor.advisorDeodália, Dias
dc.contributor.advisorPenque, Deborah
dc.contributor.authorCoelho-Valentim, Cristina
dc.date.accessioned2020-06-03T07:47:03Z
dc.date.available2020-06-03T07:47:03Z
dc.date.issued2019-05-08
dc.description.abstractObstructive Sleep Apnea (OSA) syndrome is a common public health concern characterized by recurrent episodes of apneas and hypopneas during sleep. These obstructive events result in recurrent intermittent hypoxia and sleep fragmentation that can lead to metabolic and cardiovascular diseases. We recently demonstrated that OSA syndrome can cause alterations in the red blood cells (RBC) proteome that may be associated with OSA outcomes. Here we intend to investigate whether the positive airway pressure (PAP) treatment can revert/modulate these proteome alterations. RBCs from Snorers and patients with severe OSA before/after 6 months of PAP treatment (n=10/condition) were depleted of hemoglobin, analyzed by 2D-DIGE using Progenesis SameSpots v4.5. The differentially abundant proteins were identified by MALDI-MS and protein annotations acquired by DAVIDv6.8. Western blotting (WB) validation was performed for Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and (overoxidized) GAPDHSO3 on a new Cohort (n=59). Statistical analysis including correlation studies with peroxiredoxin 2 (PRDX2) redox-oligomeric forms and several clinical parameters was carried out using SPSS software. Ten protein spots exhibited significant differences (Anova p<0.05) among groups and were associated with cell death, protein oligomerization and response to stress. Three proteoforms of GAPDH were identified decreased in OSA RBC (Anova p<0.05). Six months of PAP treatment increased these GAPDH proteoforms to the control levels. By WB, we confirmed these data by showing that the decreased GAPDH monomeric/tetrameric forms in OSA were increased by PAP treatment. PAP also increased GAPDHSO3 tetramers. In OSA, GAPDH monomers and GAPDHSO3 tetramers correlated positively with the respiratory disturbance index or triglycerides and adrenalin, respectively. After PAP, GAPDHSO3 tetramers correlated positively with PAP-induced PRDX2SO2/3 decameric forms, described having chaperone activity in cell protection. OSA induces alterations in the redox/oligomeric state of GAPDH and PRDX2 that can be reverted/modulated by PAP treatment. The clinical significant of these findings needs further validation and investigation. Selected Reaction Monitoring (SRM) and bioinformatics – based tools, will be used to validate the obtained data. The same proteomics workflow strategy will be applied to investigate the plasma proteome in OSA and OSA response to therapypt_PT
dc.description.versionN/Apt_PT
dc.identifier.urihttp://hdl.handle.net/10400.18/6894
dc.language.isoengpt_PT
dc.subjectObstructive Sleep Apneapt_PT
dc.subjectOSApt_PT
dc.subjectProteomicspt_PT
dc.subjectApneia Obstrutiva Sonopt_PT
dc.subjectGenómica Funcionalpt_PT
dc.subjectGenómica Funcional e Estruturalpt_PT
dc.titleProteome profiling in obstructive sleep apnea severity and treatment response towards early diagnosis and prognosis predictionpt_PT
dc.typelecture
dspace.entity.typePublication
oaire.citation.conferencePlaceLisboa, Portugalpt_PT
oaire.citation.titleSeminário Doutoral I (2º ano), no âmbito do Programa Doutoral de Biologia (Biologia Molecular), Faculdade de Ciências da Universidade de Lisboa, 8 maio 2019pt_PT
rcaap.rightsrestrictedAccesspt_PT
rcaap.typelecturept_PT

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