2025
P-396 Improving post-ovarian transplant primordial follicle survival by neovascularizing approaches
Celik S, Erden M, Rho N, Molla W, Oktay K. P-396 Improving post-ovarian transplant primordial follicle survival by neovascularizing approaches. Human Reproduction 2025, 40: deaf097.702. DOI: 10.1093/humrep/deaf097.702.Peer-Reviewed Original ResearchPrimordial follicle lossPrimordial follicle densityFollicle lossSphingosine-1-phosphateFlexHD PliableFTY-720Follicle activationOvarian graftsPrimordial folliclesLoss of primordial folliclesSevere-combined-immunodeficient miceFollicle densitySevere-combined-immunodeficiencyOvarian tissue transplantationPrimordial follicle activationPrimordial follicle survivalOvarian cortical piecesAcellular dermal matrixParaffin-embedded tissuesFollicle survivalCortical piecesChorion allograftTransplant outcomesCadaveric organ donorsWIDER IMPLICATIONSSuppression of endothelial ceramide de novo biosynthesis by Nogo-B contributes to cardiometabolic diseases
Rubinelli L, Manzo O, Sungho J, Del Gaudio I, Bareja R, Marino A, Palikhe S, Di Mauro V, Bucci M, Falcone D, Elemento O, Ersoy B, Diano S, Sasset L, Di Lorenzo A. Suppression of endothelial ceramide de novo biosynthesis by Nogo-B contributes to cardiometabolic diseases. Nature Communications 2025, 16: 1968. PMID: 40000621, PMCID: PMC11862206, DOI: 10.1038/s41467-025-56869-9.Peer-Reviewed Original ResearchConceptsNogo-BEndothelial dysfunctionHFD miceCardiometabolic diseasesSphingolipid signalingDevelopment of therapeutic strategiesBioactive sphingolipidsCeramide degradationSphingosine-1-phosphateHepatic glucose productionIn vivo evidenceEndothelial cellsEndothelial specific deletionCeramideBiosynthesisHigh-fat dietPathological implicationsSphingolipidsGlucose productionHFDIn vivoMale miceMetabolic dysfunctionTherapeutic strategiesMetabolic disorders
2024
Sphingosine‐1‐Phosphate Signalling Inhibition Suppresses Th1‐Like Treg Generation by Reversing Mitochondrial Uncoupling
Coulombeau R, Selck C, Giang N, Al‐Mohammad A, Ng N, Maher A, Argüello R, Scalfari A, Varley J, Nicholas R, Dominguez‐Villar M. Sphingosine‐1‐Phosphate Signalling Inhibition Suppresses Th1‐Like Treg Generation by Reversing Mitochondrial Uncoupling. Immunology 2024, 174: 153-166. PMID: 39444366, PMCID: PMC11652410, DOI: 10.1111/imm.13870.Peer-Reviewed Original ResearchTh1-like TregsSphingosine-1-phosphateSuppressive functionMitochondrial uncouplingSignaling inhibitionIncreased suppressive functionMultiple sclerosisTreg plasticityTreg reprogrammingTreg frequencyTreg generationTregsAutoimmune conditionsExpression of genesInflammatory environmentMS patientsS1P inhibitionFTY720Defective functionS1PMTORC1 signalingInhibitionReprogrammingSiponimod Attenuates Neuronal Cell Death Triggered by Neuroinflammation via NFκB and Mitochondrial Pathways
Gurrea-Rubio M, Wang Q, Mills E, Wu Q, Pitt D, Tsou P, Fox D, Mao-Draayer Y. Siponimod Attenuates Neuronal Cell Death Triggered by Neuroinflammation via NFκB and Mitochondrial Pathways. International Journal Of Molecular Sciences 2024, 25: 2454. PMID: 38473703, PMCID: PMC10931690, DOI: 10.3390/ijms25052454.Peer-Reviewed Original ResearchConceptsSecondary progressive MSRelapsing-remitting MSCentral nervous systemMultiple sclerosisProgressive MSModulator of sphingosine-1-phosphateCytokine tumor necrosis factor-alphaEffects of siponimodTumor necrosis factor-alphaHeterogeneous clinical courseBouts of inflammationNeuroprotective effectsPreclinical animal modelsAutoimmune demyelinating diseaseNecrosis factor-alphaMitochondrial oxidative phosphorylationHuman induced pluripotent stem cell (iPSC)-derived neuronsSphingosine-1-phosphateCytokine signaling pathwaysClinical courseLive cell analysisProgressive diseaseOral treatmentMitochondrial pathwayFactor-alpha
2019
SPHK1 deficiency protects mice from acetaminophen-induced ER stress and mitochondrial permeability transition
Li L, Wang H, Zhang J, Sha Y, Wu F, Wen S, He L, Sheng L, You Q, Shi M, Liu L, Zhou H. SPHK1 deficiency protects mice from acetaminophen-induced ER stress and mitochondrial permeability transition. Cell Death & Differentiation 2019, 27: 1924-1937. PMID: 31827236, PMCID: PMC7244772, DOI: 10.1038/s41418-019-0471-x.Peer-Reviewed Original ResearchConceptsActivation of activating transcription factor 6Mitochondrial permeability transitionApoptosis signal-regulating kinase 1SphK1 deficiencyER stressPermeability transitionEndoplasmic reticulumLevels of activating transcription factor 4Inhibit mitochondrial permeability transitionTranscription factor 6Transcription of inflammatory genesGlycogen synthase kinase 3bSignal-regulated kinases 1Transcription factor 4Phosphorylation of JNKAcetylation of p65Levels of histone deacetylaseHistone deacetylasesSphingosine-1-phosphateImpaired phosphorylationKinase 1Factor 2AFactor 6Exogenous S1PSphK1Reciprocal Multifaceted Interaction Between HDL (High-Density Lipoprotein) and Myocardial Infarction
Sposito A, de Lima-Junior J, Moura F, Barreto J, Bonilha I, Santana M, Virginio V, Sun L, Carvalho L, Soares A, Nadruz W, Feinstein S, Nofer J, Zanotti I, Kontush A, Remaley A. Reciprocal Multifaceted Interaction Between HDL (High-Density Lipoprotein) and Myocardial Infarction. Arteriosclerosis Thrombosis And Vascular Biology 2019, 39: 1550-1564. PMID: 31189429, DOI: 10.1161/atvbaha.119.312880.Peer-Reviewed Original ResearchConceptsMyocardial infarctionHigh-density lipoproteinSphingosine-1-phosphateSpectrum of signaling pathwaysEndothelin-1Cardiac functionCardioprotective benefitsTherapeutic advancesClinical studiesIschemia/reperfusion injuryProinflammatory moleculesAnimal modelsInsulin sensitivityHDLInfarctionMitochondrial channelsFunctional changesOxidative stressSignaling pathway
2007
Cross-talk between PDGF and S1P signalling elucidates the inhibitory effect and potential antifibrotic action of the immunomodulator FTY720 in activated HSC-cultures
Brunati A, Tibaldi E, Carraro A, Gringeri E, D’Amico F, Toninello A, Massimino M, Pagano M, Nalesso G, Cillo U. Cross-talk between PDGF and S1P signalling elucidates the inhibitory effect and potential antifibrotic action of the immunomodulator FTY720 in activated HSC-cultures. Biochimica Et Biophysica Acta 2007, 1783: 347-359. PMID: 18157950, DOI: 10.1016/j.bbamcr.2007.11.008.Peer-Reviewed Original ResearchConceptsPlatelet-derived growth factorHepatic stellate cellsTyrosine phosphorylation of PDGF receptorsSignaling pathwayPlatelet-derived growth factor stimulationCross-talkPlatelet-derived growth factor signaling pathwaysPhosphorylation of PDGF receptorS1P signalingStimulation of chemotaxisPlasma membranePhosphorylated formSphingosine-1-phosphateEffect of FTY720Activation of hepatic stellate cellsReceptor-independent wayFTY720 phosphorylationDevelopment of hepatic fibrosisS1P signaling pathwayPDGF receptorsCell typesCell proliferationPhosphorylationAntifibrotic actionMechanism of action
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