2020
Impaired Mitochondrial Stress Response due to CLPP Deletion Is Associated with Altered Mitochondrial Dynamics and Increased Apoptosis in Cumulus Cells
Esencan E, Jiang Z, Wang T, Zhang M, Soylemez-Imamoglu G, Seli E. Impaired Mitochondrial Stress Response due to CLPP Deletion Is Associated with Altered Mitochondrial Dynamics and Increased Apoptosis in Cumulus Cells. Reproductive Sciences 2020, 27: 621-630. PMID: 31939198, DOI: 10.1007/s43032-019-00063-y.Peer-Reviewed Original ResearchConceptsCaseinolytic peptidase PCumulus cell functionClpP deletionMitochondrial unfolded protein responseMitochondrial stress responseCumulus cellsUnfolded protein responseRNA sequencing analysisAltered mitochondrial dynamicsCell functionProtein homeostasisMitochondrial dynamics genesCLPP resultsMitochondrial dynamicsDynamic genesPhagosome pathwayProtein responseCellular metabolismGene expressionWild typeStress responseCumulus oophorus complexesMitochondrial ultrastructureSequencing analysisApoptotic activity
2019
Mitofusin 1 is required for female fertility and to maintain ovarian follicular reserve
Zhang M, Bener MB, Jiang Z, Wang T, Esencan E, Scott III R, Horvath T, Seli E. Mitofusin 1 is required for female fertility and to maintain ovarian follicular reserve. Cell Death & Disease 2019, 10: 560. PMID: 31332167, PMCID: PMC6646343, DOI: 10.1038/s41419-019-1799-3.Peer-Reviewed Original ResearchConceptsOocyte-granulosa cell communicationDynamic organellesAccumulation of ceramideFemale reproductive agingMitofusin 1Secondary follicle stageMitochondrial dynamicsCell communicationReproductive phenotypesCeramide synthesis inhibitor myriocinDevelopmental arrestApoptotic cell lossMitochondrial dysfunctionTargeted deletionOvarian follicular reserveOocyte maturationFemale fertilityFollicle stageDeletionPhenotypeReproductive agingOocytesCadherinFollicular reserveOrganellesMitofusin 2 plays a role in oocyte and follicle development, and is required to maintain ovarian follicular reserve during reproductive aging
Zhang M, Bener MB, Jiang Z, Wang T, Esencan E, Scott R, Horvath T, Seli E. Mitofusin 2 plays a role in oocyte and follicle development, and is required to maintain ovarian follicular reserve during reproductive aging. Aging 2019, 11: 3919-3938. PMID: 31204316, PMCID: PMC6628992, DOI: 10.18632/aging.102024.Peer-Reviewed Original ResearchConceptsMitofusin 2Key regulatory proteinsImpaired oocyte maturationFollicle developmentMitochondrial fusionRegulatory proteinsEndoplasmic reticulumMitochondrial dysfunctionTargeted deletionOocyte maturationOocytesReproductive agingFemale subfertilityOocyte qualityOvarian follicular reserveTelomeresMitochondriaMetabolic milieuProteinReticulumDeletionFusionPhenotypeApoptosisMaturation
2007
Estrogen increases apoptosis in the arterial wall in a murine atherosclerosis model
Seli E, Guzeloglu-Kayisli O, Kayisli UA, Kizilay G, Arici A. Estrogen increases apoptosis in the arterial wall in a murine atherosclerosis model. Fertility And Sterility 2007, 88: 1190-1196. PMID: 17498707, DOI: 10.1016/j.fertnstert.2007.01.132.Peer-Reviewed Original ResearchConceptsHigh-cholesterol dietMurine atherosclerosis modelAtherosclerotic plaque formationCholesterol dietFemale LDLAtherosclerosis modelPlaque formationArterial wallPlacebo-treated miceMitotic activityEffects of estrogenEffects of ovariectomyAtherosclerotic plaque developmentVascular effectsFemale miceMAIN OUTCOMEVascular apoptosisC57BL/6 backgroundPlaque developmentAortic wallLDLLDL receptorMice resultsMiceDNA strand breaks
2006
Estradiol Increases Apoptosis in Human Coronary Artery Endothelial Cells by Up-Regulating Fas and Fas Ligand Expression
Seli E, Guzeloglu-Kayisli O, Cakmak H, Kayisli UA, Selam B, Arici A. Estradiol Increases Apoptosis in Human Coronary Artery Endothelial Cells by Up-Regulating Fas and Fas Ligand Expression. The Journal Of Clinical Endocrinology & Metabolism 2006, 91: 4995-5001. PMID: 17003091, DOI: 10.1210/jc.2006-1225.Peer-Reviewed Original ResearchConceptsHuman coronary artery endothelial cellsCultured human coronary artery endothelial cellsHormone replacement therapyCoronary artery endothelial cellsArtery endothelial cellsReplacement therapyE2 treatmentPlaque stabilityPostmenopausal hormone replacement therapyEndothelial cellsFas/FasL pathwayEffects of E2Effects of estrogenAtherosclerotic plaque formationSignificant concentration-dependent increaseConcentration-dependent increaseFas ligand expressionCardiovascular eventsCardioprotective effectsInhibits atherogenesisMAIN OUTCOMEAnimal modelsFasL pathwayUp-regulating FasLigand expression
2004
Extent of nuclear DNA damage in ejaculated spermatozoa impacts on blastocyst development after in vitro fertilization
Seli E, Gardner DK, Schoolcraft WB, Moffatt O, Sakkas D. Extent of nuclear DNA damage in ejaculated spermatozoa impacts on blastocyst development after in vitro fertilization. Fertility And Sterility 2004, 82: 378-383. PMID: 15302287, DOI: 10.1016/j.fertnstert.2003.12.039.Peer-Reviewed Original ResearchConceptsBlastocyst developmentInfertility treatmentPregnancy rateTUNEL positivityIVF clinicsDNA strand breaksPrivate IVF clinicClinical pregnancy rateProspective comparative studyNick end labeling techniqueBlastocyst development ratePregnancy outcomesVs. 44MAIN OUTCOMESperm samplesLarge seriesSignificant negative correlationStrand breaksFlow cytometryTUNEL reactivityEnd-labeling techniqueIVFApoptotic cell deathPositivityNuclear DNA fragmentationThe presence of abnormal spermatozoa in the ejaculate: Did apoptosis fail?
Sakkas D, Seli E, Manicardi GC, Nijs M, Ombelet W, Bizzaro D. The presence of abnormal spermatozoa in the ejaculate: Did apoptosis fail? Human Fertility 2004, 7: 99-103. PMID: 15223758, DOI: 10.1080/14647270410001720464.Peer-Reviewed Original ResearchMeSH KeywordsApoptosisCell NucleusDNA DamageDNA FragmentationEjaculationHumansMaleSpermatogenesisSpermatozoaConceptsIntracytoplasmic sperm injectionNuclear DNA strand breaksDNA strand breaksAbnormal semen parametersAbnormal spermatozoaInfertile couplesMale infertilitySperm injectionSemen parametersQuality of spermatozoaAssisted reproductionStrand breaksCertain causesHuman spermatozoaSuch spermApoptosisSuccessful useNumerous studiesSpermatozoaPatients
2003
Abnormal spermatozoa in the ejaculate: abortive apoptosis and faulty nuclear remodelling during spermatogenesis
Sakkas D, Seli E, Bizzaro D, Tarozzi N, Manicardi GC. Abnormal spermatozoa in the ejaculate: abortive apoptosis and faulty nuclear remodelling during spermatogenesis. Reproductive BioMedicine Online 2003, 7: 428-432. PMID: 14656403, DOI: 10.1016/s1472-6483(10)61886-x.Peer-Reviewed Original ResearchConceptsNuclear DNA strand breaksDNA strand breaksAbnormal semen parametersAbnormal spermatozoaMale infertilitySemen parametersAbnormal persistenceApoptotic marker proteinsStrand breaksCertain causesHuman spermatozoaMarker proteinsApoptosisNumerous studiesSpermatogenesisSpermatozoaHumansInfertilityAbnormalities