简介：AIM:ToscreenmicroRNAs（miRNAs）andsetuptargetmiRNAsinpterygium.METHODS:PrimaryfibroblastswereisolatedfrompterygiumandTenon’scapsuleandcultured.ImmunocytochemicalanalysisandWesternblottingwereperformedtoconfirmthecultureoffibroblasts.Inall,1733miRNAswerescreenedinthefirststepbyusingGeneChip?miRNA3.0Array.SpecificmiRNAsinvolvedinthepathogenesisofpterygiumweresubsequentlydeterminedusingthefollowingcriteria:1)highreproducibilityinarepetitivetest;2)baselogvalueof>7.0forbothcontrolandpterygialfibroblasts;and3)logratioof>1.0betweenpterygialfibroblastsandcontrolfibroblasts.RESULTS:Primaryscreeningshowedthat887/1733miRNAswereup-regulatedand846/1733miRNAsweredown-regulatedinpterygialfibroblastscomparedwiththoseincontrolfibroblasts.Ofthe1733miRNAsscreened,4miRNAs,namely,miRNA-143a-3p,miRNA-181a-2-3p,miRNA-377-5pandmiRNA-411a-5p,mettheabove-mentionedcriteria.Primaryscreeningshowedthatthese4miRNAswereup-regulatedinpterygialfibroblastscomparedwithcontrolfibroblastsandthatmiRNA-143a-3phadthehighestmeanratiocomparedwiththemiRNAsincontrolfibroblasts.CONCLUSION:miRNA-143a-3p,miRNA-181a-2-3p,miRNA-377-5pandmiRNA-411a-5pareup-regulatedinpterygialfibroblastscomparedwithcontrolfibroblasts,suggestingtheirinvolvementinthepathogenesisofpterygium.

简介：理解空间飞行怎么影响细胞的发信号的小径的分子的机制，静止正常人的WI-38成纤维细胞在STS-93航天飞机使命上被飞。随后，RNA取样从飞空间并且地面控制房间被用来构造二个cDNA图书馆，它然后为抑制被处理减少性的杂交(SSH)识别spaceflight特定的基因表达。与氧化应力，DNA修理，和丰满的酸氧化有关的关键基因被空间飞行激活的SSH数据表演，建议细胞的氧化应力的正式就职。这被neuregulin的起来规定进一步证实1并且钙绑定蛋白质钙调蛋白2。另一个明显的压力符号是空间飞行唤起Ras/mitogen-activated蛋白激酶和phosphatidylinositol-3激酶发信号小径，与一起起来调整几个官方补给阶段的房间周期穿越基因。显示出表示的起来规定的另外的基因涉及蛋白质合成和pro-apoptosis，以及支持幸存。机能上地相关的基因的Interactome分析证明c-Myc为显示出重要变化的那些基因是“中心”。因此，我们的结果建议微严肃旅行可以在主要与细胞的应力发信号联系的基因表达影响变化，指导到apoptotic死亡或早熟的老朽的房间。

简介：客观：到从膝系带的文化成纤维细胞房间并且到学习这些房间的生物特征。方法：前面的十字形的系带(ACL)和从新西兰白兔子的中间的并行的系带(MCL)的房间在vitro是有教养的。骨胶原的细胞的生长和表示被分析。而且，一在里面vitro创伤闭合模型被建立，ACL和MCL房间愈合被比较。结果：为所有这些房间的最大的生长与Dulbecco的家被获得修改的鹰与10%胎儿的牛的浆液补充的媒介，而是RPMI1640和火腿是媒介不是合适的维持这些房间的F12。从新西兰白兔子的ACL和MCL房间的形态学在vitro是相似的，但是MCL房间变得比ACL房间快。两种房间类型在我由ACL房间生产了打III的大杂烩类型的文化，而是比率生产了骨胶原的类似的数量比由MCL房间生产了高。创伤闭合试金证明在在损害以后的36个小时，在ACL文化创造的没有房间的地区被ACL房间部分占据；相反，在MCL文化的受伤地区被房间几乎完全盖住。结论：尽管从新西兰白兔子的ACL细胞和MCL细胞在文化在形态学显示出类似的外观，细胞的生长和象在vitro愈合一样的骨胶原的生物化学的合成是显著地不同的。在在vitro的房间的二种类型的内在的性质的这些差别可能在vivo贡献这些系带的微分愈合潜力。

简介：Acetylcholinesterase(AChE)playsakeyroleinterminatingneurotransmissionatcholinergicsynapses.AChEisalsofoundintissuesdevoidofcholinergicresponses,indicatingitspotentialfunctionbeyondneurotransmission.IthasbeensuggestedthatAChEmayparticipateindevelopment,differentiation,andpathogenicprocessessuchasAlzheimer'sdiseaseandtumorigenesis.WeexaminedAChEexpressioninhumanlungfibroblastcellline(HLF)uponinductionofapoptosisbyUVorG418.AChEisinducedinallapoptoticcellsexaminedasdeterminedbycytochemicalstaining,immunologicalanalysis,affinity

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简介：Studieshavebeencarriedouttotesttheassumptionthattheprimaryphotoreceptorsfortheradioprotectiveactionof633nmlaserradiationarethecytochrome-c-oxidases.Todothis,thedevicewascreatedforradiationprotectionofbiologicalobjectsbasedonlasermodulewithawavelengthof532nm.Experimentsconductedonmurinefibroblastcellsshowedthattheradioprotectioneffectoflaserirradiationwasobservedinthedoseintervalabout0.4-0.85mJ/cm2.Maximumradioprotectioneffectisobservedatlaserradiationenergydensity~0.56mJ/cm2.ThedeterminationofthecellsurvivalwiththeautomaticcounterСТ20aftertheactionoftheionizingandcombinedirradiationshowedthatradioprotectiveactionofthelaserradiationwiththewavelengthof533nm,aswellastheradiationwiththewavelengthof633nm,istransferredbythemechanismofthe“bystandereffect”.Inaddition,itwasfoundthatradioprotectioneffectoflaserirradiationobservedonthecriterionofnumberofsurvivingsinglecells,comparedwithcellsexposedto?-radiationLaserirradiation,produceseffectiveradioprotectingactionalsoonthecriterionofgrowncellcolonies.Thevalueofthedosemodificationfactor(DMF)calculatedon50%cellsurvival(LD50)isequalto1.4.Theresultssuggestthatinthecaseofradioprotectiveactionofsmalldosesoflaserradiationwithawavelengthof633nm,aswellas532nmprimaryphotoreceptorsisthecytochrome-c-oxidases.

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简介：Osteoblastsofratculturedinvitrowerestimulatedwithpulsed50Hzelectromagneticfieldandbasicfibroblastgrowthfactor(bFGF).TheMTTmethod,flowcytometryandhistochemistrystainingwereusedtodetectcellproliferation,cellcycleandalkalinephosphatase.Theresultsindicated:afterstimulatedby1mTelectromagneticfield,thecellsaremoreabundant,havemoreSphasepercentages,2mTelectromagneticfieldhavenoevidenteffectoncells'growth;comparedwithelectromagneticfield,thecellsstimulatedbybFGFaremoreabundantandhavelargerSphaseratios.ElectromagneticfieldandbFGFhavenoeffectoncells,alkalinephosphatase.Therefore,weconcludedthatelectromagneticfieldcanenhanceosteoblastsgrowthlikesomegrowthfactorsuchasbasicfibroblastgrowthfactor,andtheosteoblasts',characteristicswasnotchanged.

简介：Objective:ToexplorereciprocalactionbetweenBMP-2(bonemorphogeneticprotein-2)andBMP-3forbetterunderstandingofthemechanismofBMPduringbonefractureunion.Methods:rhBMP-2wasaddedintotheculturedfibroblastswiththeconcentrationof1200ng/ml.TheexpressionofBMP-3infibroblastswasdetectedbyimmunohistochemistry.EukaryoticexpressionvectorpcDNA3-BMP-3wastransfectedintothefibroblasts.AftertheeffectiveexpressionofBMP-3wasidentified,BMP-2wasalsodetectedbyimmunohistochemistryinBMP-3expressioncells.ThefibroblaststransfectedwithemptyvectorpcDNA3wereusedasthecontrol.Results:ExogenousrhBMP-2couldpromotetheexpressionofBMP-3infibroblasts.BMP-3alsocouldbedetectedinthesecells.Conclusions:BMP-2andBMP-3couldreciprocallyadjusttheexpressioninfibroblasts.

简介：AbstractBackground:Fibroblast-like synoviocytes (FLSs), resident mesenchymal cells of synovial joints, play an important role in the pathogenesis of rheumatoid arthritis (RA). Dickkopf-1 (DKK-1) has been proposed to be a master regulator of bone remodeling in inflammatory arthritis. Here, potential impairation on the activity of FLSs derived from RA to small interfering RNAs (siRNAs) targeting DKK-1 was investigated.Methods:siRNAs targeting DKK-1 were transfected into FLSs of patients with RA. Interleukin (IL)-1β, IL-6, IL-8, matrix metalloproteinase (MMP) 2, MMP3, MMP9, transforming growth factor (TGF)-β1, TGF-β2 and monocyte chemoattractant protein (MCP)-1 levels in the cell culture supernatant were detected by enzyme-linked immunosorbent assay (ELISA). Invasion assay and 3H incorporation assay were utilized to investigate the effects of siRNAs targeting DKK-1 on FLSs invasion and cell proliferation, respectively. Western blotting was performed to analyze the expression of nuclear factor (NF)-κB, interleukin-1 receptor-associated kinase (IRAK)1, extracellular regulated protein kinases (ERK)1, Jun N-terminal kinase (JNK) and β-catenin in FLSs.Results:DKK-1 targeting siRNAs inhibited the expression of DKK-1 in FLSs (P < 0.01). siRNAs induced a significant reduction of the levels of IL-6, IL-8, MMP2, MMP3 and MMP9 in FLSs compared to the control group (P < 0.05). DKK-1 targeting siRNAs inhibited the proliferation and invasion of FLSs (P < 0.05). Important molecules of pro-inflammatory signaling in FLSs, including IRAK1 and ERK1, were decreased by the inhibition of DKK-1 in FLSs. In contrast, β-catenin, a pivotal downstream molecule of the Wnt signaling pathway was increased.Conclusions:By inhibiting DKK-1, we were able to inhibit the proliferation, invasion and pro-inflammatory cytokine secretion of FLSs derived from RA, which was mediated by the ERK or the IRAK-1 signaling pathway. These data indicate the application of DKK-1 silencing could be a potential therapeutic approach to RA.

简介：BacgroundPercutaneouscoronaryintervention(PCI)hasbecomeoneofthemosteffectivetreatmentsincoronaryheartdisease(CHD).However,thebottleneckproblemofPCIisthein-stentrestenosis(ISR).TheaimofthisstudywastoexploretheeffectsofastragalosideIV(ASTIV)onsuppressionofintimalhyperplasiamodulationoftheexpressionofbasicfibroblastgrowthfactor(b-FGF)inaratcarotidarteryballooninjurymodel.MethodsFiftyhealthymaleSprague-Dawley(SD)ratswererandomlydividedintofivegroups:asham-operationgroup(sham),amodelgroup(model),andthreeastragalosideIV-treatedgroups.Threedaysbeforethesurgery,1%carboxymethylcellulose(CMC)orASTIV(20,40or60mg·kg~(-1)·d~(-1))wasintragastricallyadministeredintoshamor3astragaloside-treatedgroupsonceadayfor17days.Hematoxylin-elsinstainingwascarriedouttodeterminethepathomorphologicalchangesandtheneointimalandmediaarearatio.Immunohistochemistrystainingwasperformedtomeasuretheexpressionsofproliferatingcellnuclearantigen(PCNA)andbasicfibrolastgrowthfactor(b-FGF).PCNAandb-FGFwereanalyzedwithIamage-ProPlus.Results(1)Thecarotidarteryintimalhyperplasiaintheratsofmodelwassimilartolumenstenosis.Comparedwiththeshamoperationgroup,theareaofthenewintimaandtheratiooftheintimatomedia(I/M)wereincreasedandthelumenareawasdecreased(P<0.01)inthemodelgroup.AstragalosideIVincreasedthelumenintimaldimensionanddecreasedtheareaofnewintimaandtheratioofintimatomediainadose-dependentmanner.(2)Comparedwiththesham-operationgroup,theexpressionsofPCNAandb-FGFincarotidarteryofmodelgroupweresignificantlyincreased(P<0.01).ASTIVdecreasedexpressionsofPCNAandb-FGFinthecarotidarteryofratsinadosedependentmanner.ConclusionAstragalosideIVsignificantlyinhibitsneointimalhyperplasiaofratcarotidarterythroughdown-regulatingtheexpressionsofPCNAandb-FGF.

简介：AbstractThere have been recent extensive studies and rapid advancement on the pathogenesis underlying idiopathic pulmonary fibrosis (IPF), and intricate pathogenesis of IPF has been suggested. The purpose of this study was to clarify the logical relationship between these mechanisms. An extensive search was undertaken of the PubMed using the following keywords: "etiology," "pathogenesis," "alveolar epithelial cell (AEC)," "fibroblast," "lymphocyte," "macrophage," "epigenomics," "histone," acetylation," "methylation," "endoplasmic reticulum stress," "mitochondrial dysfunction," "telomerase," "proteases," "plasminogen," "epithelial-mesenchymal transition," "oxidative stress," "inflammation," "apoptosis," and "idiopathic pulmonary fibrosis." This search covered relevant research articles published up to April 30, 2020. Original articles, reviews, and other articles were searched and reviewed for content; 240 highly relevant studies were obtained after screening. IPF is likely the result of complex interactions between environmental, genetic, and epigenetic factors: environmental exposures affect epigenetic marks; epigenetic processes translate environmental exposures into the regulation of chromatin; epigenetic processes shape gene expression profiles; in turn, an individual’s genetic background determines epigenetic marks; finally, these genetic and epigenetic factors act in concert to dysregulate gene expression in IPF lung tissue. The pathogenesis of IPF involves various imbalances including endoplasmic reticulum, telomere length homeostasis, mitochondrial dysfunction, oxidant/antioxidant imbalance, Th1/Th2 imbalance, M1-M2 polarization of macrophages, protease/antiprotease imbalance, and plasminogen activation/inhibition imbalance. These affect each other, promote each other, and ultimately promote AEC/fibroblast apoptosis imbalance directly or indirectly. Excessive AEC apoptosis and impaired apoptosis of fibroblasts contribute to fibrosis. IPF is likely the result of complex interactions between environmental, genetic, and epigenetic factors. The pathogenesis of IPF involves various imbalances centered on AEC/fibroblast apoptosis imbalance.

简介：Thepurposeofthepresentstudywastodetermineprotectivieeffectsofbasicfibroblastgrowthfactor(bFGF)oncochlearneuronsandhaircellsinvitroandinvivo.InexperimentI,culturedspiralganglionneurons(SGNs)preparedfromP3micewereexposedto20mMglutamatefor2hoursbeforetheculturemediumwasreplacedwithfreshmediumcontaining0,25,50,and100ng/mlbFGF,respectively.Fourteendayslater,allcultureswerefixedwith4%paraformaldehyde,andstainedwith1%toluidineblue.ThenumberofsurvivingSGNswerecountedandthelengthofSGNsneuritesweremeasured.Exposureto20mMglutamatefor24hoursresultedinaninhibitiononneuriteoutgrowthofSGNsandelevatedcelldeath.TreatmentofthecultureswithbFGFledtopromotionofneuriteoutgrowthandelevatednumberofsurvivingSGNs.EffectsofbFGFweredosedependentwiththehighestpotencyat100ng/ml.InexperimentⅡ,invivostudieswerecarriedoutwithguineapigsinwhichbFGForartificialperilymphwasperfusedintothecochleatoassesspossibleprotectiveeffectsofbFGFoncochlearhaircellsandcompoundactionpotentials(CAP).TheCAPsweremeasuredbefore,immediatlyand48hoursafterexposuretonoise.SignificantdifferencesinCAPwereobserved(p＜0.05)amongthebFGFperfusedgroup,controlgroup(t=3.896)andartificialperilymphperfusedgroup(t=2.520)at48hoursafternoiseexposure,CochleaewereremovedandhaircellLosswasanalyzedinsurfacepreparationspreparedfromallexperimentalanimals.Acoustictraumacausedlossof651and687innerhaircellsinthecontrolandartificialperilymphperfusedgroup,respectively.Insharpcontrast,only31innerhaircellswerelostinthebFGFperfusedears.Similarly,moreouterhaircellsdiedinthecontrolandperilymphperfuesedgroup(41830and41968,respectively)thaninthegrouptreatedwithbFGF(34258).OurresultsdemonstratethatbFGFprotectedSGNsagainstglutmateneurotoxicityinvitro.Inaddition,treatmentwithbFGFalso

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简介：BACKGROUND:Culturesfrommultipleportionsofumbilicalcordbloodmesenchymalstemcellshavebeenshowntoundergomorerapidproliferationandattachmentthansingleportions.OBJECTIVE:Toobservegrowthofbasicfibroblastgrowthfactor(bFGF)-inducedculturesofhumanamnion-derivedmesenchymalstemcells(AMSCs)anddifferentiationintoneuronal-likecells.DESIGN,TIMEANDSETTING:Comparativeobservation.ThestudywasperformedattheLaboratoryofMicrobiologyandImmunology,BasicMedicalSchoolofZhengzhouUniversityfromJanuarytoMay2008.METHODS:Amniafromfull-term,uterine-incisiondeliveryweredonatedby12healthywomen.AMSCswereobtainedbycellseparationandculturetechniques,andwerepassagedandinducedbybFGF.Fromthethirdpassage,atotalof1mLAMSCs,atadensityof1.0×10~4/mL,wasseparatelyharvestedfromsixsamples,whichservedasgroupA.Atotalof1mLAMSCs,atadensityof1.0×10~4/mL,washarvestedseparatelyfromtheremainingsixsamples,whichservedasgroupB.Atotalof0.5mLfromthesixsamplesofgroupAand0.5mLfromthesixsamplesofgroupBwerecombinedtoformgroupC.MAINOUTCOMEMEASURES:Differencesincellquantityamongthethreegroupswerecomparedbycellquantificationand3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide(MTT)analysis.Expressionofaglialcellmarker,neuron-specificenolase,andnestinwasdetectedinthethreegroupsbyimmunocytochemistry.RESULTS:CellquantificationandMTTanalysisoflivecells,aswellasAMSCabsorbance,weresignificantlygreateringroupCcomparedwithgroupsAandBat18daysofculture(P<0.05),andnosignificantdifferencewasobservedbetweengroupsAandB.Glialfibrillaryacidicprotein,neuron-specificenolase,andnestinwereexpressedinallgroupsfollowingbFGFinduction.CONCLUSION:MixedAMSCculturespromotedproliferation,andbFGF-inducedAMSCsdifferentiatedintoneuronal-likecells.