简介：MolecularmechanismsoftheKru?ppel-likefamilyoftranscriptionfactors(KLFs)havebeenstudiedmoreinproliferatingcellsthaninpost-mitoticcellssuchasneurons.WerecentlyfoundthatKLFsregulateintrinsicaxongrowthabilityincentralnervoussystem(CNS)neuronsincludingretinalganglioncells,andhippocampalandcorticalneurons.Withatleast15of17KLFfamilymembersexpressedinneuronsandatleast5structurallyuniquesubfamilies,itisimportanttodeterminehowthiscomplexfamilyfunctionsinneuronstoregulatetheintricategeneticprogramsofaxongrowthandregeneration.BycharacterizingthemolecularmechanismsoftheKLFfamilyinthenervoussystem,includingbindingpartnersandgenetargets,andcomparingthemtodefinedmechanismsdefinedoutsidethenervoussystem,wemaybetterunderstandhowKLFsregulateneuritegrowthandaxonregeneration.

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简介：BACKGROUND:Livedeliverylimitstheclinicalapplicationofmaggottherapy.TodateinChina,therearenoinvivoreportsregardingwoundhealingmechanismsofmaggottherapyortheeffectsofmaggothomogenateonwoundnerveregeneration.OBJECTIVE:Toavoidcomplicationsduetotheuseoflivemaggots,anasepticmaggothomogenatewasapplied.SubstanceP(SP)andgeneproteinproduct9.5expressioninacutaneouswoundwasanalyzedtoexplorepossiblemechanismsofneuralregenerationandwoundhealingintherat.DESIGN,TIMEANDSETTING:ArandomgroupingandcontrolledanimalstudywasperformedatthelaboratoryoftheDepartmentofOrthopedicSurgery,FirstAffiliatedHospital,DalianMedicalUniversityfromAugust2008toApril2009.MATERIALS:LivemaggotswereculturedandprovidedbythelaboratoryoftheDepartmentofOrthopedicSurgeryoftheFirstAffiliatedHospital,DalianMedicalUniversity,China.METHODS:Atotalof48adultratswereselectedandtwoacute,full-thicknesswounds(round,1.5cmdiameter)werecreatedonthebackofeachrat.Thetwowoundswererandomlyassignedtohomogenateproductandcontrolgroups.Followingtwo-stepdisinfectionofmaggots,ahomogenatewasproducedfrom10maggotsandappliedtothewoundareainthehomogenateproductgroup,whilethewoundsinthecontrolgroupweretreatedwithnormalsalinealone.MAINOUTCOMEMEASURES:Ondays1,3,7,10,14,and21followinginjury,thewoundtissuewasexcised.HistologicalexaminationofthewoundwasobservedbyhematoxylinandeosinstainingorMasson'sTrichromestaining.SPandproteingeneproduct9.5expressionswereexaminedbyimmunohistochemistrytoevaluatewoundneuralregeneration.RESULTS:Ondays7,10,and14,therateofwoundhealingwassignificantlygreaterinthehomogenateproductgroupcomparedwiththecontrolgroup(P<0.05),andhomogenatehealingwasbetterthanthatseeninthecontrolgroup.Ondays3,7,and10,SPexpressionincellsandregenerativenerveswassignificantlygreaterinthehomogenateproductgroupcomparedw

简介：Inthisstudy,weaimedtoexploretheroleofursolicacidintheneuralregenerationoftheinjuredsciaticnerve.BALB/cmicewereusedtoestablishmodelsofsciaticnerveinjurythroughunilateralsciaticnervecompletetransectionandmicroscopicanastomosisat0.5cmbelowtheischialtuberosity.Thesuccessfullygeneratedmodelmiceweretreatedwith10,5,or2.5mg/kgursolicacidviaintraperitonealinjection.Enzyme-linkedimmunosorbentassayresultsshowedthatserumS100proteinexpressionlevelgraduallyincreasedat1-4weeksaftersciaticnerveinjury,andsignificantlydecreasedat8weeks.Assuch,ursolicacidhasthecapacitytosignificantlyincreaseS100proteinexpressionlevels.Real-timequantitativePCRshowedthatS100mRNAexpressionintheL4-6segmentsontheinjurysidewasincreasedafterursolicacidtreatment.Inaddition,themuscularmassindexinthesoleusmusclewasalsoincreasedinmicetreatedwithursolicacid.Toluidinebluestainingrevealedthatthequantityandaveragediameterofmyelinatednervefibersintheinjuredsciaticnerveweresignificantlyincreasedaftertreatmentwithursolicacid.10and5mg/kgofursolicacidproducedstrongereffectsthan2.5mg/kgofursolicacid.Ourfindingsindicatethatursolicacidcandose-dependentlyincreaseS100expressionandpromoteneuralregenerationinBALB/cmicefollowingsciaticnerveinjury.

简介：Directexposuretointensivevisiblelightcanleadtosolarretinopathy,includingmacularinjury.Thesignsandsymptomsincludecentralscotoma,metamorphopsia,anddecreasedvision.However,therehavebeenfewstudiesexaminingretinalinjuryduetointensivelightstimulationatthecellularlevel.Neuralnetworkarrangementsandgeneexpressionpatternsinzebrafishphotoreceptorsaresimilartothoseobservedinhumans,andphotoreceptorinjuryinzebrafishcaninducestemcell-basedcellularregeneration.Therefore,thezebrafishretinaisconsideredausefulmodelforstudyingphotoreceptorinjuryinhumans.Inthecurrentstudy,thecentralretinalphotoreceptorsofzebrafishwereselectivelyablatedbystimulationwithhigh-intensitylight.Retinalinjury,cellproliferationandregenerationofconesandrodswereassessedat1,3and7dayspostlesionwithimmunohistochemistryandinsituhybridization.Additionally,alight/darkboxtestwasusedtoassesszebrafishbehavior.Theresultsrevealedthatphotoreceptorswereregeneratedby7daysafterthelight-inducedinjury.However,theregeneratedcellsshowedadisruptedarrangementatthelesionsite.Duringtheinjury-regenerationprocess,thezebrafishexhibitedreducedlocomotorcapacity,weakenedphototaxisandincreasedmovementangularvelocity.Thesebehaviorsmatchedthemorphologicalchangesofretinalinjuryandregenerationinanumberofways.Thisstudydemonstratesthatthezebrafishretinahasarobustcapacityforregeneration.Visualimpairmentandstressresponsesfollowinghigh-intensitylightstimulationappeartocontributetothealterationofbehaviors.

简介：Multiplesclerosis(MS)isachronicimmune-mediatedinnammatory-demyelinatingdisorderofthecentralnervoussystem,withastrongneurodegenerativecomponent.ThequestionwhetherneurodegenerationinMSisindependentorrelatedtoneuroinflammationhasbeenlongdebated,butnotyetfullyclarified.Furthermore,littleisstillknownonhowneuroinflammationandneurodegenerationinMSarerelatedtopotentialregenerativeprocesses.Inthisperspective,webrieflydiscussmainclinical,pathologicalandexperimentalevidenceontherelationshipbetweenneuroinflammationandneurodegenerationinMS,andontheirconnectionwithregeneration.WediscussthattheseprocessesinMSmightrepresentintercorrelatedmanifestationsoftheimmuneresponse,especiallyoftheinnateimmunity.

简介：Traumaticbraininjury(TBI)istheleadingcauseofdeathanddisabilityofpersonsunder45yearsoldintheUnitedStates,affectingover1.5millionindividualseachyear.Ithadbeenthoughtthatrecoveryfromsuchinjuriesisseverelylimitedduetotheinabilityoftheadultbraintoreplacedamagedneurons.However,recentstudiesindicatethatthematuremammaliancentralnervoussystem(CNS)hasthepotentialtoreplenishdamagedneuronsbyproliferationandneuronaldifferentiationofadultneuralstem/progenitorcellsresidingintheneurogenicregionsinthebrain.Furthermore,increasingevidenceindicatesthattheseendogenousstem/progenitorcellsmayplayregenerativeandreparativerolesinresponsetoCNSinjuriesordiseases.Insupportofthisnotion,heightenedlevelsofcellproliferationandneurogenesishavebeenobservedinresponsetobraintraumaorinsultssuggestingthatthebrainhastheinherentpotentialtorestorepopulationsofdamagedordestroyedneurons.Thisreviewwilldiscussthepotentialfunctionsofadultneurogenesisandrecentdevelopmentofstrategiesaimingatharnessingthisneurogeniccapacityinordertorepopulateandrepairtheinjuredbrain.

简介：Theirretrievablefateofneuronsdominatedtheneurosciencerhetoricforthefirsthalfofthiscentury,apositionthatwasfiercelycontestedandrecentlydebunkedbyextensivestudiescarriedoutinthefieldofneuroregenerationresearch.Theturningpointcameintheyear1928,whenRamonY.Cajal’s(Lobato,2008)worksuggestedthattheregenerativecapacityof

简介：Tinnitus,thephenomenonofringingorbuzzingintheearswithoutanexternalsoundsourceisoneofthemostcommonlyreportedsymptomsinotorhinolaryngologyandaffects10–15%ofthegeneralpopulation.Modelshavebeendevelopedtoaccountforneuralbasisoftinnitus,itspathogenesisanditsconsequencesonmentalhealth(deRidderetal.,2013).Inmostcasestinnitusonsetfollowsapartialhearingimpairment.Peripheralsensorydeprivationduetocochleardamages

简介：Thisstudyaimedtoexploretheroleofmechanicaltensioninhypertrophicscarsandthechangeinnervedensityusinghematoxylin-eosinstainingandS100immunohistochemistry,andtoobservetheexpressionofnervegrowthfactorbywesternblotanalysis.Theresultsdemonstratedthatmechanicaltensioncontributedtotheformationofahyperplasticscarinthebackskinofrats,inconjunctionwithincreasesinbothnervedensityandnervegrowthfactorexpressioninthescartissue.Theseexperimentalfindingsindicatethatthecutaneousnervoussystemplaysaroleinhypertrophicscarformationcausedbymechanicaltension.

简介：TheRho/Rho-associatedcoiled-coilcontainingproteinkinase(Rho/ROCK)pathwayisamajorsignalingpathwayinthecentralnervoussystem,transducinginhibitorysignalstoblockregeneration.Aftercentralnervoussystemdamage,themaincauseofimpairedregenerationisthepresenceoffactorsthatstronglyinhibitregenerationinthesurroundingmicroenvironment.ThesefactorssignalthroughtheRho/ROCKsignalingpathwaytoinhibitregeneration.Therefore,athoroughunderstandingoftheRho/ROCKsignalingpathwayiscrucialforadvancingstudiesonregenerationandrepairoftheinjuredcentralnervoussystem.

简介：Peripheralnerveinjuries(PNI)areamajorclinicalproblem.Ingeneral,PNIresultsfrommotorvehicleaccidents,lacerationswithsharpobjects,penetratingtrauma(gunshotwounds)andstretchingorcrushingtraumaandfractures.ItisestimatedthatPNIoccurin2.8%oftraumapatientsandthisnumberreaches5%ifplexusandrootlesionsarein-

简介：Braindevelopmentisoneofthemostfascinatingsubjectsinthefieldofbiologicalsciences.Nonetheless,ourscientificcommunitystillfaceschallengesintryingtounderstandtheconceptsthatdefinetheunderlyingmechanismsofneuraltissuedevelopment.Afterall,itisaverycomplexsubjecttograspandmany

简介：Qian-Zheng-San,atraditionalChineseprescriptionconsistingofTyphoniiRhizoma,BombyxBatryticatus,Scorpio,hasbeenfoundtoplayanactivetherapeuticroleincentralnervoussystemdiseases.However,itisunclearwhetherQian-Zheng-Sanhastherapeuticvalueforperipheralnerveinjury.Therefore,weusedSprague-Dawleyratstoinvestigatethis.Asciaticnervecrushinjurymodelwasinducedbyclampingtherightsciaticnerve.Subsequently,ratsinthetreatmentgroupwereadministered2mLQian-Zheng-San(1.75g/mL)dailyassystemictherapyfor1,2,4,or8weeks.RatsinthecontrolgroupwerenotadministeredQian-Zheng-San.Ratsinshamgroupdidnotundergosurgeryandsystemictherapy.Footprintanalysiswasusedtoassessnervemotorfunction.Electrophysiologicalexperimentswereusedtodetectnerveconductionfunction.Immunofluorescencestainingwasusedtoassessaxoncountsandmorphologicalanalysis.Immunohistochemicalstainingwasusedtoobservemyelinregenerationofthesciaticnerveandthenumberofmotoneuronsintheanteriorhornofthespinalcord.At2and4weekspostoperatively,thesciaticnervefunctionindex,nerveconductionvelocity,thenumberofdistantregeneratedaxonsandtheaxondiameterofthesciaticnerveincreasedintheQian-Zheng-Santreatmentgroupcomparedwiththecontrolgroup.At2weekspostoperatively,nervefiberdiameter,myelinthickness,andthenumberofmotorneuronsinthelumbarspinalcordanteriorhornincreasedintheQian-Zheng-Santreatmentgroupcomparedwiththecontrolgroup.TheseresultsindicatethatQian-Zheng-Sanhasapositiveeffectonperipheralnerveregeneration.

简介：Recentstudieshaveshownthattheglycation-associateddamageisnotlimitedtopatientswithdiabetes.Becauseoftheirassociationwithoxidativestress,advancedglycationend-products(AGEs)havealsobeenimplicatedinmanyneurodegenerativediseases,suchasHuntingtondisease,amyotrophiclateralsclerosis,andAlzheimerdisease(Yanetal.,

简介：ExogenoussubstancePaccelerateswoundhealingindiabetes,butthemechanismremainspoorlyunderstood.Here,weestablishedaratmodelbyintraperitoneallyinjectingstreptozotocin.Fourwounds(1.8cmdiameter)weredrilledusingaself-madepunchontotheback,bilateraltothevertebralcolumn,andthentreatedusingamnioticmembranewithepidermalstemcellsand/orsubstanceParoundandinthemiddleofthewounds.Withthecombinedtreatmentthewound-healingratewas100%at14days.Withprolongedtime,typeIcollagencontentgraduallyincreased,yettypeIIIcollagencontentgraduallydiminished.Abundantproteingeneproduct9.5-andsubstanceP-immunoreactivenervefibersregenerated.Partialnervefiberendingsextendedtotheepidermis.ThetherapeuticeffectsofcombinedsubstancePandepidermalstemcellswerebetterthanwithamnioticmembraneandeitherfactoralone.OurresultssuggestthatthecombinationofsubstancePandepidermalstemcellseffectivelycontributestonerveregenerationandwoundhealingindiabeticrats.

简介：Theextracellularmatrix,whichincludescollagens,laminin,orfibronectin,playsanimportantroleinperipheralnerveregeneration.Recently,aSchwanncell-derivedextracellularmatrixwithclassicalbiomaterialwasusedtomimictheneuralniche.However,extensiveclinicaluseofSchwanncellsremainslimitedbecauseofthelimitedorigin,lossofanautologousnerve,andextendedinvitroculturetimes.Inthepresentstudy,humanumbilicalcord-derivedmesenchymalstemcells(hUCMSCs),whichareeasilyaccessibleandmoreproliferativethanSchwanncells,wereusedtoprepareanextracellularmatrix.WeidentifiedthemorphologyandfunctionofhUCMSCsandinvestigatedtheireffectonperipheralnerveregeneration.Comparedwithanon-coateddishtissueculture,thehUCMSC-derivedextracellularmatrixenhancedSchwanncellproliferation,upregulatedgeneandproteinexpressionlevelsofbrain-derivedneurotrophicfactor,glialcell-derivedneurotrophicfactor,andvascularendothelialgrowthfactorinSchwanncells,andenhancedneuriteoutgrowthfromdorsalrootganglionneurons.ThesefindingssuggestthatthehUCMSC-derivedextracellularmatrixpromotesperipheralnerverepairandcanbeusedasabasisfortherationaldesignofengineeredneuralniches.

简介：ASchwanncellhasregenerativecapabilitiesandisanimportantcellintheperipheralnervoussystem.ThismicroarraystudyispartofabioinformaticsstudythatfocusesmainlyonSchwanncells.Microarraydataprovideinformationondifferencesbetweenmicroarray-basedandexperiment-basedgeneexpressionanalyses.Accordingtomicroarraydata,severalgenesexhibitincreasedexpression(foldchange)buttheyareweaklyexpressedinexperimentalstudies(basedonmorphology,proteinandmRNAlevels).Incontrast,somegenesareweaklyexpressedinmicroarraydataandhighlyexpressedinexperimentalstudies;suchgenesmayrepresentfuturetargetgenesinSchwanncellstudies.Thesestudiesallowustolearnaboutadditionalgenesthatcouldbeusedtoachievetargetedresultsfromexperimentalstudies.Inthecurrentbigdatastudybyretrievingmorethan5000scientificarticlesfromPubMedorNCBI,GoogleScholar,andGoogle,1016(up-anddownregulated)genesweredeterminedtoberelatedtoSchwanncells.However,noexperimentwasperformedinthelaboratory;rather,thepresentstudyispartofabigdataanalysis.OurstudywillcontributetoourunderstandingofSchwanncellbiologybyaidingintheidentificationofgenes.Basedonacomparativeanalysisofallmicroarraydata,weconcludethatthemicroarraycouldbeagoodtoolforpredictingtheexpressionandintensityofdifferentgenesofinterestinactualexperiments.

简介：BACKGROUND:Previousstudieshaveshownthatp75neurotrophinreceptorplaysanimportantroleinperipheralnerveinjury.However,theroleofp75neurotrophinreceptorintheregenerationofperipheralnervesremainspoorlyunderstood.OBJECTIVE:Tostudytheeffectofp75neurotrophinreceptoronfacialnerveregeneration.DESIGN,TIMEANDSETTING:ArandomizedcontrolledexperimentwasperformedintheRegenerationLaboratoryofFlindersUniversity,AustraliaandtheBiomedicalLaboratoryofDentistrySchool,ShandongUniversityfromMarch2005toFebruary2006.MATERIALS:CholeratoxinBsubunit,fastblue,andbiotinrabbit-antigoatIgGwereprovidedbySigma,USA;goat-anticholeratoxinBsubunitantibodywasprovidedbyListBiologicals,USA.METHODS:Inp75neurotrophinreceptorknockoutandwildtype129/svmice,thefacialnervesononesidewerecrushed.Atdays2and4followinginjury,regeneratingmotorneuronsinthefacialnucleiwerelabeledbyfastblue,andtheregeneratingaxonwaslabeledbytheanterogradetracercholeratoxinBsubunit.MAINOUTCOMEMEASURES:AxonalregenerativevelocityandnumberweredetectedbyimmunohistochemicalstainingofcholeratoxinBsubunit,growth-associatedprotein,proteingeneproduct9.5,andcalcitonin-gene-relatedpeptide;survivalofmotorneuronsinthefacialnucleiwasdetectedbyretrogradefastblue.RESULTS:Axonalgrowthinthefacialnerveofp75neurotrophinreceptorknockoutmicewassignificantlylessthaninwildtypemice.Atday7afterinjury,thenumberofregeneratingmotorneuronsinp75neurotrophinreceptorknockoutmiceremainedsignificantlylessthaninwildtypemice(P<0.05).Thenumberofpositivelystainedfibersforgrowth-associatedprotein-43,proteingeneproduct9.5,andcalcitonin-gene-relatedpeptideinp75neurotrophinreceptorknockoutmicewassignificantlylessthaninwildtypemice(P<0.01).CONCLUSION:p75neurotrophinreceptorpromotedaxonalregenerationandenhancedthesurvivalrateofmotorneuronsfollowingfacialnerveinjury.