Search results for "Semaphorin"

showing 10 items of 16 documents

Sema3a plays a role in the pathogenesis of CHARGE syndrome

2018

CHARGE syndrome is an autosomal dominant malformation disorder caused by heterozygous loss of function mutations in the chromatin remodeler CHD7. Chd7 regulates the expression of Sema3a, which also contributes to the pathogenesis of Kallmann syndrome, a heterogeneous condition with the typical features hypogonadotropic hypogonadism and an impaired sense of smell. Both features are common in CHARGE syndrome suggesting that SEMA3A may provide a genetic link between these syndromes. Indeed, we find evidence that SEMA3A plays a role in the pathogenesis of CHARGE syndrome. First, Chd7 is enriched at the Sema3a promotor in neural crest cells and loss of function of Chd7 inhibits Sema3a expression…

0301 basic medicineEmbryo NonmammalianKallmann syndromePHENOTYPIC SPECTRUMmedicine.disease_causeSeverity of Illness IndexEpigenesis GeneticPathogenesisAXON GUIDANCECHD7CHARGE syndromeXenopus laevis0302 clinical medicineHYPOGONADOTROPIC HYPOGONADISMPromoter Regions GeneticGenetics (clinical)GeneticsMutationGeneral MedicinePhenotypeDNA-Binding ProteinsNEURAL CREST CELLSNeural CrestHomeobox Protein Nkx-2.5MIGRATIONBiology03 medical and health sciencesHypogonadotropic hypogonadismKALLMANN-SYNDROMEGeneticsmedicineAnimalsHumansEpigeneticsSHORT STATUREMolecular BiologyLoss functionMUTATIONSGenetic Complementation TestDNA HelicasesSemaphorin-3AKallmann Syndromemedicine.diseaseDisease Models Animal030104 developmental biologyHEK293 CellsXENOPUS-EMBRYOSMutationCHARGE Syndrome030217 neurology & neurosurgery
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Semaphorins in Adult Nervous System Plasticity and Disease

2021

Semaphorins, originally discovered as guidance cues for developing axons, are involved in many processes that shape the nervous system during development, from neuronal proliferation and migration to neuritogenesis and synapse formation. Interestingly, the expression of many Semaphorins persists after development. For instance, Semaphorin 3A is a component of perineuronal nets, the extracellular matrix structures enwrapping certain types of neurons in the adult CNS, which contribute to the closure of the critical period for plasticity. Semaphorin 3G and 4C play a crucial role in the control of adult hippocampal connectivity and memory processes, and Semaphorin 5A and 7A regulate adult neuro…

0301 basic medicineNervous systemsemaphorinsanimal structuresautismNeurosciences. Biological psychiatry. NeuropsychiatryReviewHippocampal formationBiologymultiple sclerosisExtracellular matrix03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineSemaphorinNeuroplasticitymedicineMultiple sclerosisPerineuronal netNeurogenesisCell Biologymedicine.diseaseschizophrenia030104 developmental biologymedicine.anatomical_structurenervous systemplasticityembryonic structuresAlzheimer’s disease; autism; epilepsy; multiple sclerosis; perineuronal net; plasticity; schizophrenia; semaphorinsepilepsysense organsperineuronal netbiological phenomena cell phenomena and immunityNeuroscienceAlzheimer’s disease030217 neurology & neurosurgeryNeuroscienceRC321-571
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New functions of Semaphorin 3E and its receptor PlexinD1 during developing and adult hippocampal formation

2018

AbstractThe development and maturation of cortical circuits relies on the coordinated actions of long and short range axonal guidance cues. In this regard, the class 3 semaphorins and their receptors have been seen to be involved in the development and maturation of the hippocampal connections. However, although the role of most of their family members have been described, very few data about the participation of Semaphorin 3E (Sema3E) and its receptor PlexinD1 during the development and maturation of the entorhino-hippocampal (EH) connection are available. In the present study, we focused on determining their roles both during development and in adulthood. We determined a relevant role for…

0301 basic medicineNeurobiologia del desenvolupamentScienceHippocampusNerve Tissue ProteinsSemaphorinsBiologyHippocampal formationHippocampusArticle03 medical and health sciencesMice0302 clinical medicineSemaphorinmedicineAnimalsDevelopmental neurobiologyProgenitor cellReceptorCells CulturedGlycoproteinsNeuronsMultidisciplinaryMembrane GlycoproteinsHippocampus properDentate gyrusQRIntracellular Signaling Peptides and ProteinsGene Expression Regulation DevelopmentalMembrane ProteinsProteinsEmbryonic stem cellCytoskeletal Proteins030104 developmental biologymedicine.anatomical_structurenervous systemMutationMedicineNeuroscienceProteïnes030217 neurology & neurosurgerySignal Transduction
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Reduced Sympathetic Innervation in Endometriosis is Associated to Semaphorin 3C and 3F Expression

2016

Endometriosis is a chronic inflammatory disease and one of the most common causes of pelvic pain. The mechanisms underlying pain emergence or chronic inflammation during endometriosis remain unknown. Several chronic inflammatory diseases including endometriosis show reduced amounts of noradrenergic nerve fibers. The source of the affected innervation is still unclear. Semaphorins represent potential elicitors, due to their known role as axonal guidance cues, and are suggested as nerve repellent factors in different chronic inflammatory diseases. Therefore, semaphorins might influence the progress of neuroinflammatory mechanisms during endometriosis. Here, we analyzed the noradrenergic inner…

AdultMale0301 basic medicineNeuroimmunomodulationNeurogenesisEndometriosisNeuroscience (miscellaneous)EndometriosisPainInflammationSemaphorinsYoung Adult03 medical and health sciencesCellular and Molecular NeuroscienceNerve Fibers0302 clinical medicineImmune systemSemaphorinHumansMedicineSecretionEndometriosiReceptorbusiness.industryMacrophagesPelvic painInnervationNeurogenesisMiddle Agedmedicine.disease030104 developmental biologyNeurologyImmunologyFemaleSympathetic nerve fibermedicine.symptomSemaphorinCarrier Proteinsbusiness030217 neurology & neurosurgery
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Semaphorin and plexin gene expression is altered in the prefrontal cortex of schizophrenia patients with and without auditory hallucinations

2015

Auditory hallucinations (AH) are clinical hallmarks of schizophrenia, however little is known about molecular genetics of these symptoms. In this study, gene expression profiling of postmortem brain samples from prefrontal cortex of schizophrenic patients without AH (SNA), patients with AH (SA) and control subjects were compared. Genome-wide expression analysis was conducted using samples of three individuals of each group and the Affymetrix GeneChip Human-Gene 1.0 ST-Array. This analysis identified the Axon Guidance pathway as one of the most differentially expressed network among SNA, SA and CNT. To confirm the transcriptome results, mRNA level quantification of seventeen genes involved i…

Adultmedicine.medical_specialtyHallucinationsSEMA4DDown-RegulationPrefrontal CortexNerve Tissue ProteinsSemaphorinsTranscriptomeMolecular geneticsInternal medicineNeuroplasticitymedicineHumansRNA MessengerPrefrontal cortexBiological PsychiatryAgedOligonucleotide Array Sequence AnalysisAged 80 and overNeuronal PlasticitybiologyGene Expression ProfilingPlexinBrainMiddle Agedmedicine.diseaseAxonsbody regionsGene expression profilingPsychiatry and Mental healthEndocrinologySchizophreniaSchizophreniabiology.proteinPsychologyCell Adhesion MoleculesNeurosciencePsychiatry Research
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Mice lacking Plexin-B3 display normal CNS morphology and behaviour

2009

Semaphorins and their receptors, plexins, have emerged as important regulators of a multitude of biological processes. Plexin-B3 has been shown to be selectively expressed in postnatal oligodendrocytes. In contrast to the well-characterized Plexin-A family and the Plexin-B family members Plexin-B1 and -B2, no data are available on the functional role of Plexin-B3 in the central nervous system in vivo. Here we have elucidated the functional significance of Plexin-B3 by generating and analyzing constitutive knock-out mice. Plexin-B3-deficient mice were found to be viable and fertile. A systematic histological analysis revealed no morphological defects in the brain or spinal cord of mutant ani…

Central Nervous Systemanimal structuresCentral nervous systemNerve Tissue ProteinsReceptors Cell SurfaceAnxietyMotor ActivityNeuropsychological TestsBiologyMiceCellular and Molecular NeuroscienceSemaphorinmedicineAnimalsReceptorMolecular BiologyCells CulturedMice KnockoutBehavior AnimalPlexinAge FactorsCell BiologySpinal cordMotor coordinationOligodendrogliamedicine.anatomical_structureSpinal Cordembryonic structuresbiology.proteinMotor learningNeuroscienceBiomarkersFunction (biology)Molecular and Cellular Neuroscience
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Semaphorin 6A Improves Functional Recovery in Conjunction with Motor Training after Cerebral Ischemia

2010

Stroke is a major health problem in industrialized societies. Despite numerous attempts at developing acute stroke therapies aimed at minimizing acute infarct development, the only approved therapy so far is recombinant tissue plasminogen activator (rtPA). In recent years, the attention of the stroke community has therefore also put increased emphasis on understanding processes of post-stroke recovery, and their potential exploitability for therapeutic purposes. The brain has a remarkable ability to adapt to changes after stroke. Mechanisms that contribute to this plasticity are re-mapping and expansion of cortical areas to neighboring regions of functional motor cortex areas after injury […

CerebellumPathologymedicine.medical_specialtyanimal structures610lcsh:MedicineSemaphorinsMotor ActivityBiologyBrain IschemiaCell LineNeuroscience/Motor SystemsSemaphorinPhysical Conditioning AnimalCortex (anatomy)NeuroplasticitymedicineAnimalsHumanslcsh:ScienceMultidisciplinarylcsh:RNeurogenesisNeurological Disorders/Cerebrovascular DiseaseRecovery of FunctionDependovirusRatsStrokemedicine.anatomical_structurenervous systemembryonic structuresCorticospinal tractlcsh:QAxon guidancesense organsNeuroscience/Neurobiology of Disease and RegenerationNeurosciencePsychomotor PerformanceResearch ArticleMotor cortexPLoS ONE
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A de novo microdeletion of SEMA5A in a boy with autism spectrum disorder and intellectual disability.

2016

AbstractSemaphorins are a large family of secreted and membrane-associated proteins necessary for wiring of the brain. Semaphorin 5A (SEMA5A) acts as a bifunctional guidance cue, exerting both attractive and inhibitory effects on developing axons. Previous studies have suggested that SEMA5A could be a susceptibility gene for autism spectrum disorders (ASDs). We first identified a de novo translocation t(5;22)(p15.3;q11.21) in a patient with ASD and intellectual disability (ID). At the translocation breakpoint on chromosome 5, we observed a 861-kb deletion encompassing the end of the SEMA5A gene. We delineated the breakpoint by NGS and observed that no gene was disrupted on chromosome 22. We…

Male0301 basic medicinemedicine.medical_specialtyAutism Spectrum DisorderChromosomes Human Pair 22Translocation BreakpointNerve Tissue ProteinsSemaphorinsBiology[SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human geneticsBioinformaticsArticleTranslocation GeneticautismeChromosome Breakpoints03 medical and health sciencesSemaphorin[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyIntellectual Disabilitymental disordersIntellectual disabilityGeneticsmedicineHumans[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsChildGenetics (clinical)Genetics[SDV.MHEP] Life Sciences [q-bio]/Human health and pathologyNeurosciencesMembrane Proteinsmedicine.disease030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsAutism spectrum disorderNeurons and CognitionPaternal InheritancecerveauChromosomes Human Pair 5AutismMedical geneticsChromosome DeletionmicrodélétionhumainChromosome 22[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyGenetic screen
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Expression of semaphorin 3A and neuropilin 1 with clinicopathological features and survival in human tongue cancer

2012

Objective: To investigate the association between semaphorin 3A (SEMA 3A) and its receptor neuropilin 1 (NRP1) and the clinicopathologic characteristics of patients with tongue cancer. Study Design: Forty-three tongue squamous cell carcinoma specimens were included. Immunohistochemical staining of SEMA3A and NRP1 was performed on 15 normal tongue epithelium specimens and the 43 tumour specimens. Immunoreactivity was evaluated based on the staining intensity and distribution score. Statistical analyses were performed using Chi-squared and Spearman tests and Kaplan-Meier analysis. Results: SEMA3A was significantly down-regulated in tongue cancer compared with normal tongue (P=0.025), while NR…

MalePathologymedicine.medical_specialtyOdontologíaSemaphorinTongueNeuropilin 1medicineHumansGeneral DentistryOral Medicine and Pathologybusiness.industryCancerSemaphorin-3ASEMA3AMiddle AgedPrognosismedicine.disease:CIENCIAS MÉDICAS [UNESCO]Ciencias de la saludNeuropilin-1EpitheliumTongue NeoplasmsStainingSurvival Ratemedicine.anatomical_structureOtorhinolaryngologyUNESCO::CIENCIAS MÉDICASCarcinoma Squamous CellImmunohistochemistryResearch-ArticleFemaleSurgerybusiness
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Genetic dissection of plexin signaling in vivo

2014

Mammalian plexins constitute a family of transmembrane receptors for semaphorins and represent critical regulators of various processes during development of the nervous, cardiovascular, skeletal, and renal system. In vitro studies have shown that plexins exert their effects via an intracellular R-Ras/M-Ras GTPase-activating protein (GAP) domain or by activation of RhoA through interaction with Rho guanine nucleotide exchange factor proteins. However, which of these signaling pathways are relevant for plexin functions in vivo is largely unknown. Using an allelic series of transgenic mice, we show that the GAP domain of plexins constitutes their key signaling module during development. Mice …

MultidisciplinaryRHOAanimal structuresbiologyTransgenePlexinMutantMice TransgenicNerve Tissue ProteinsBiological SciencesPhenotypeCell biologyMiceSemaphorinembryonic structuresbiology.proteinAnimalsGuanine nucleotide exchange factorSignal transductionSignal Transduction
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