简介：AbstractPurpose:The incidence of acute lung injury (ALI) in severe trauma patients is 48% and the mortality rate following acute respiratory distress syndrome evolved from ALI is up to 68.5%. Alveolar epithelial type 1 cells (AEC1s) and type 2 cells (AEC2s) are the key cells in the repair of injured lungs as well as fetal lung development. Therefore, the purification and culture of AEC1s and AEC2s play an important role in the research of repair and regeneration of lung tissue.Methods:Sprague-Dawley rats (3-4 weeks, 120-150 g) were purchased for experiment. Dispase and DNase I were jointly used to digest lung tissue to obtain a single-cell suspension of whole lung cells, and then magnetic bead cell sorting was performed to isolate T1α positive cells as AEC1s from the single-cell suspension by using polyclonal rabbit anti-T1a (a specific AEC1s membrane protein) antibodies combined with anti-rabbit IgG microbeads. Afterwards, alveolar epithelial cell membrane marker protein EpCAM was designed as a key label to sort AEC2s from the remaining T1α-neg cells by another positive immunomagnetic selection using monoclonal mouse anti-EpCAM antibodies and anti-mouse IgG microbeads. Cell purity was identified by immunofluorescence staining and flow cytometry.Results:The purity of AEC1s and AEC2s was 88.3% ± 3.8% and 92.6% ± 2.7%, respectively. The cell growth was observed as follows: AEC1s stretched within the 12-16 h, but the cells proliferated slowly; while AEC2s began to stretch after 24 h and proliferated rapidly from the 2nd day and began to differentiate after 3 days.Conclusion:AEC1s and AEC2s sorted by this method have high purity and good viability. Therefore, our method provides a new approach for the isolation and culture of AEC1s and AEC2s as well as a new strategy for the research of lung repair and regeneration.

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简介：AbstractType 1 diabetes (T1D) results from dysfunction of pancreatic islets β cells. Recent studies supported that endoplasmic reticulum (ER) stress takes an important role in pancreatic β cell excessive loss, resulting in T1D. Here, we aimed to review the relationship between ER stress and T1D. Additionally, we also reviewed the potential mechanisms underlying ER stress mediated T1D. Studies have shown that severe ER stress is directly involved in the pancreatic β cells destruction and pathogenesis of T1D. ER stress plays a key part in pancreatic β cells and T1D, which will help in developing new effective therapeutics for T1D.

简介：AbstractObjective:This study aimed to investigate the differentiation of human adipose-derived stem cells (hASCs) into endometrial epithelial cells (EECs) under certain induction conditions and to a further step provide a promising approach for ASCs in clinical practice to the treatment of severe intrauterine adhesion.Methods:Four groups of hASCs were separately cultured as follows: in Group 1, hASCs were cultured in a control medium (5% fetal bovine serum [FBS] + α-minimum Eagle’s medium [α-MEM]); in Group 2, hASCs were cultured in an induction medium (5% FBS + α-MEM + [1 × 10-7 mol/L 17β-estradiol] + 10 ng/mL transforming growth factor β1 [TGF-β1] + 10 ng/mL epidermal growth factor [EGF] + 10 ng/mL platelet-derived growth factor BB [PDGF-BB]); in Group 3, hASCs and human endometrium cells (hEMCs) were cocultured in the control medium; and in Group 4, hASCs and hEMCs were cocultured in the induction medium.Results:When cocultured with hEMCs, the morphology of hASCs became similar with EECs, and the addition of factors such as EGF, TGFβ, PDGF-BB, and 17β-estradiol promoted differentiation. This study, for the first time, demonstrated estrogen receptor (ER)α and ERβ expression in hASCs and preliminarily explored changes in ERα, ERβ, β-catenin, and H19 mRNA expression during hASC differentiation. Furthermore, we concluded that H19 mRNA expression was negatively correlated with differentiation, which is seemingly related to the estrogen signaling pathway.Conclusions:hASCs revealed the potential for differentiating to EECs when cocultured with hEMCs.

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简介：在所有成年体的干细胞之中，角膜的上皮的那些在他们在定义limbal结构的独占的地点是唯一的沃格特的称为的栅。作为结果，limbal的外科的嫁接上皮的干细胞与或没有前vivo扩大长被练习了在给予limbal的病人恢复风景干细胞缺乏。与另外的干细胞例子相比，不过，相对，很少对limbalniche被知道，它被相信在调整自强和命运决定oflimbal起一个枢轴的作用上皮的干细胞。这评论总结相关文学并且提出几个关键问题由集中于limbal壁龛指导未来研究进limbal干细胞缺乏和角膜的上皮的织物工程的进一步的改进的致病的更好的理解。

简介：胸腺为T房间开发和成熟提供必要微型环境。Thymic上皮的房间(侦探)它是thymic填写了外皮的上皮的房间(cTECs)和thymic髓的上皮的房间(mTECs)，很好被记录了为这些紧调整的过程批评。侦探的普通祖先房间是否能产生cTECs和mTECs，长是争论的。大进步被取得了在最近的年里描绘普通侦探祖先房间。我们此处在胸腺新生象这些祖先房间一样关于侦探区别讨论唯一的起源范例。

简介：·AIM:ToexploretheimmunomodulatoryeffectsofcurdlanoninnateimmuneresponsesagainstAspergillusfumigatus(A.fumigatus)inculturedhumancornealepithelialcells(HCECs),andwhetherC-typelectinreceptorDectin-1mediatestheimmunomodulatoryeffectsofcurdlan.·METHODS:TheHCECswerestimulatedbycurdlanindifferentconcentrations(50,100,200,400μg/mL)forvarioustime.ThenHCECspretreatedwithorwithoutlaminarin(Dectin-1blocker,0.3mg/mL)andcurdlanwerestimulatedbyA.fumigatushyphae.ThemRNAandproteinproductionoftumornecrosisfactor-α(TNF-α)andinterleukin-6(IL-6)weredeterminedbyreal-timequantitativepolymerasechainreactionandenzyme-linkedimmunosorbentassay,respectively.TheproteinlevelofDectin-1wasmeasuredbyWesternblot.·RESULTS:CurdlanstimulatedmRNAexpressionofTNF-αandIL-6inadoseandtimedependentmannerinHCECs.CurdlanpretreatmentbeforeA.fumigatushyphaestimulationsignificantlyenhancedtheexpressionofTNF-αandIL-6atmRNAandproteinlevelscomparedwithA.fumigatushyphaestimulationgroup(P<0.05).BothcurdlanandA.fumigatushyphaeup-regulatedDectin-1proteinexpressioninHCECs,andDectin-1expressionwaselevatedto1.5-to2-foldbycurdlanpretreatmentfollowedhyphaestimulation.TheDectin-1blockerlaminarinsuppressedthemRNAexpressionandproteinproductionofTNF-αandIL-6inducedbycurdlanandhyphae(P<0.05).·CONCLUSION:ThesefindingsdemonstratedthatcurdlanpretreatmentenhancedtheinflammatoryresponseinducedbyA.fumigatushyphaeinHCECs.Dectin-1isessentialfortheimmunomodulatoryeffectsofcurdlan.Curdlanmayhavehighclinicalapplicationvaluesinfungalkeratitistreatment.

简介：客观:兔子的生物特征口头的mucosal上皮的房间(OMEC)被学习，为OMEC的文化的合适的过程被探索。方法:由不同表面消毒的有教养的OMEC由不同Dispase准备，在不同媒介，在K-SFM的不同calciumion集中中等。结果:文化能显著地与2%碘答案减少的房间的微生物引起的污染以前为口头的洞的消毒使用了房间文化。在K-SFM与Dispase消化的OMEC能快速属于文化烧瓶，在PBS与Dispase消化的OMEC稀罕属于文化烧瓶。在K-SFM媒介的0或0.09mmol/L钙集中有教养的OMEC的增长出现了不统计上重要。OMEC与浆液变得快，但是区分进像成纤维细胞的房间是容易的。结论:OMEC能成长很好并且有由在这描述了的过程的上皮的房间形态学试验的典型口头的mucosal。

简介：AbstractBackground:Estrogen is involved in the pathophysiological process of benign prostatic hyperplasia (BPH), in which epithelial-mesenchymal transition (EMT) plays an important role. Upregulation of aquaporin (AQP) 5, which is directly activated by estrogen, has been reported to promote EMT in multiple cells. This study aimed to examine the effects of AQP5 on estrogen-induced EMT in the prostate.Methods:Normal prostate (NP) tissue samples without any histopathological changes and BPH tissue samples with pathologically confirmed hyperplasia were obtained. An EMT cell model was subsequently established by adding estradiol (E2) to RWPE-1 cells, after which AQP5 knockdown was performed. Tissue morphological and immunohistochemical features were examined using hematoxylin-eosin and immunohistochemical staining. Western blot analysis was performed to determine the expression of AQPs, estrogen receptors, and EMT-related proteins. Cell proliferation was assessed and supernatants were collected for enzyme-linked immunosorbent assay to determine transforming growth factor-β1 (TGF-β1) concentrations. Immunofluorescence staining was performed to assess protein expressions in RWPE-1 cells.Results:BPH tissues exhibited greater EMT (TGF-β1: 1.362 ± 0.196 vs. 0.107 ± 0.067, P = 0.003; vimentin: 1.581 ± 0.508 vs. 0.221 ± 0.047, P < 0.001; E-cadherin: 0.197 ± 0.188 vs. 1.344 ± 0.088, P < 0.001), higher AQP5 (1.268 ± 0.136 vs. 0.227 ± 0.055, P < 0.001) and estrogen receptor (ER) α (1.250 ± 0.117 vs. 0.329 ± 0.134, P < 0.001) expression but lower ERβ (0.271 ± 0.184 vs. 1.564 ± 0.130, P < 0.001) expression than NP tissues. E2-stimulated cells had higher AQP5 expression (1.298 ± 0.058 vs. 1.085 ± 0.104, P = 0.049), increased cell proliferation (1.510 ± 0.089 vs.1.000 ± 0.038, P < 0.001), and EMT (TGF-β1 concentration: 0.352 ± 0.021 ng/mL vs. 0.125 ± 0.014 ng/mL, P < 0.001; vimentin: 1.641 ± 0.120 vs. 0.188 ± 0.020, P = 0.002; E-cadherin: 0.075 ± 0.030 vs. 0.843 ± 0.046, P < 0.001) than controls. E2-stimulated cells with AQP5 knockdown exhibited decreased EMT (TGF-β1 concentration: 0.223 ± 0.041 ng/mL vs. 0.352 ± 0.021 ng/mL, P= 0.016; vimentin: 0.675 ± 0.056 vs. 1.641 ± 0.120, P = 0.001; E-cadherin: 0.159 ± 0.037 vs. 0.075 ± 0.030, P = 0.040) than E2-stimulated cells with non-related small interfering RNA (siRNA).Conclusion:Our findings suggest that estrogen induces BPH possibly by promoting AQP5 expression. Hence, AQP5 might be a novel target for modulating EMT in prostate epithelial cells.

简介：Peroxisome激活proliferator的受体鲸鱼群妈(PPARγ)coactivator-1高山哈(PGC-1α)coactivates多重抄写因素并且调整几个代谢过程。Thecurrent学习在人的上皮的卵巢的癌症房间在apoptosis的正式就职调查了PGC-1α的角色。在人的卵巢和人的卵巢的上皮的肿瘤之间的PGC-1α信使rna水平被量的RT-PCR检验。更少的PGC-1α表示与正常卵巢相比在恶意的肿瘤的表面上皮被发现。在人的上皮的卵巢的癌症房间线Ho-8910的PGC-1α的Overexpression通过Bcl-2和Bax表示的协调规定导致了房间apoptosis。Microarray分析证实PGC-1α戏剧性地在Ho-8910房间影响了apoptosis相关的基因。Mitochondrial功能的试金证明apoptosis的正式就职通过由细胞色素c.Furthermore的版本的终端阶段，导致的apoptosis部分是，然而并非完全，由PPARγantagonist(GW9662)堵住了的PGC-1α-，并且由siRNA的PPARγ表示的抑制也在Ho-8910房间禁止了PGC-1α-inducedapoptosis。这些数据建议PGC-1α通过aPPARγ-依赖者小径施加了它的效果。我们的调查结果显示PGC-1α涉及apoptoticsignaltransduction小径，PGC-1α的down规定可以是在支持上皮的卵巢的癌症生长和前进的一个关键点。

简介：AIMTo在透镜调查Aquaporin-1(AQP-1)的角色上皮的房间(LEC)和它的潜在的目标基因。AQP-1明确地在眼睛的LEC被表示并且为透镜动态平衡和透明性维护是重要的。此处，在LEC的AQP-1表示被调查在奔流formation.METHODSLECs与它的潜在的角色联合在房间幸存上评估它的影响是有带AQP-1的lentivirus的transfected小介入RNA(siRNA)。实时聚合酶链反应(PCR)并且西方的弄污被进行从不同的组在LEC检测AQP-1表示。同时，房间数kit-8(CCK-8)试金和流动cytometry被执行测量LEC增长和apoptosis，respectively.RESULTSAQP-1表示显著地在LEC被减少，两个都在mRNA和蛋白质铺平(P<；0.05)，在siRNA处理以后。减少的房间生存能力被CCK-8试金与siRNA干扰在LEC检测，与控制房间相比(P<；0.05)。apoptosis率显著地在siRNA干扰以后在房间增加了(P<；0.05).CONCLUSIONThe减少了在规定下面的房间生存能力追随者AQP-1大部分由于它LEC的apoptosis的正式就职。AQP-1减小可能在LEC导致生理的功能的变化，它可能与奔流的出现和发展被联系。

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：AbstractBackground:The use of microRNAs in the therapy of kidney disease is hampered by the difficulties in their effective delivery. Microvesicles (MVs) are known as natural carriers of small RNAs. Our prior research has demonstrated that MVs isolated from mesenchymal stem cells (MSCs) are capable of attenuating kidney injuries induced by unilateral ureteral obstruction and 5/6 sub-total nephrectomy in mice. The present study aimed to evaluate the effects of miR-34a-5p (miR-34a)-modified MSC-MVs on transforming growth factor (TGF)-β1-induced fibrosis and apoptosis in vitro.Methods:Bone marrow MSCs were modified by lentiviruses over-expressing miR-34a, from which MVs were collected for the treatment of human Kidney-2 (HK-2) renal tubular cells exposed to TGF-β1 (6 ng/mL). The survival of HK-2 cells was determined using 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide (MTT) and Annexin V-Light 650/propidium iodide (PI) assays. The expression levels of epithelial markers (tight junction protein 1 [TJP1] and E-cadherin) and mesenchymal markers (smooth muscle actin alpha (α-SMA) and fibronectin) in HK-2 cells were measured using Western blot analysis and an immunofluorescence assay. In addition, changes in Notch-1/Jagged-1 signaling were analyzed using Western blotting. Data were analyzed using a Student’s t test or one-way analysis of variance.Results:MiR-34a expression increased three-fold in MVs generated by miR-34a-modified MSCs compared with that expressed in control MVs (P < 0.01, t= 16.55). In HK-2 cells, TJP1 and E-cadherin levels decreased to 31% and 37% after treatment with TGF-β1, respectively, and were restored to 62% and 70% by miR-34a-enriched MSC-MVs, respectively. The expression of α-SMA and fibronectin increased by 3.9- and 5.0-fold following TGF-β1 treatment, and decreased to 2.0- and 1.7-fold after treatment of HK-2 cells with miR-34a-enriched MSC-MVs. The effects of miR-34a-enriched MSC-MVs on epithelial-mesenchymal transition (EMT) markers were stronger than control MSC-MVs. The effects of miR-34a-enriched MSC-MVs on these EMT markers were stronger than control MSC-MVs. Notch-1 receptor and Jagged-1 ligand, two major molecules of Notch signaling pathway, are predicted targets of miR-34a. It was further observed that elevation of Notch-1 and Jagged-1 induced by TGF-β1 was inhibited by miR-34a-enriched MSC-MVs. In addition, TGF-β1 exposure also induced apoptosis in HK-2 cells. Although miR-34a-mofidied MSC-MVs were able to inhibit TGF-β1-triggered apoptosis in HK-2 cells, the effects were less significant than control MSC-MVs (control:TGF-β1 :miR-nc-MV:miR-34a-MV = 1.3:0.6:1.1:0.9 for MTT assay, 1.8%:23.3%:9.4%:17.4% for apoptosis assay). This phenomenon may be the result of the pro-apoptotic effects of miR-34a.Conclusions:The present study demonstrated that miR-34a-over-expressing MSC-MVs inhibit EMT induced by pro-fibrotic TGF-β1 in renal tubular epithelial cells, possibly through inhibition of the Jagged-1/Notch-1 pathway. Genetic modification of MSC-MVs with an anti-fibrotic molecule may represent a novel strategy for the treatment of renal injuries.

简介：瞄准：为了学习不同Helicobacterpylori(Hpylori)的效果，文化在胃的上皮细胞的生长上过滤。方法：肉汤文化Hpylori过滤被准备。胃的上皮细胞与filtrates被对待，并且房间生长被生长曲线和流动血细胞计数决定。胃的上皮细胞的DNA损坏被单个房间的微胶化电气泳动测量。结果：当由CagA-gene-positive对待时，胃的上皮细胞活跃地增殖了肉汤文化过滤，并且到达的菌落形成40%。在S阶段的房间的数字与控制相比增加了。彗星试金在对待与的GES-1房间显示出41.2%彗星房间CagA积极过滤(P<0.05)。结论：CagA积极过滤在形态学和人的胃的上皮细胞瘤细胞的生长特征提高变化。也许，涉及生长的机制之一改变的DNA损坏。

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简介：HumanprimaryepithelialcellsofrenalpelviswasestablishedtoinvestigatetheadherenceofuropathogenicEscherichiacoli(UPEC)tothiscellline,inwhichtheprimarycellculturewasperformedbyusingcultivationofthenormalepitheliumofrenalpelvisinkeratinocyteserumfreemedium(K-SFM)withepidermalgrowthfactor(EGF)andbovinepituitaryextract(BPE).BothUPEC132obtainedfromurinespecimenofpatientswithpyelonephritisandthepilus-freerepresentativestrainE.coliK-12p678-54wereusedtostudytheadherenceofthesestrainsonhumanprimaryepithelialcellsofrenalpelvis.TheUPECadherencewasperformedwithobservationonthemorphologicalchangesoftheadheredcells,whiletheadhesionratesandindiceswerecalculatedindifferenttimesofexperiment.Inaddition,thevirulencegeneshlyandcnf1ofUPEC132weredetectedbymultiplexPCRassay.Inthisstudy,thehumanprimaryepithelialcellsofrenalpelviswasfoundtoexhibitthecharacterofthetransitionalepithelialcells.Comparedwiththecontrolgroup,theadhesionratesandindicesbegantoincreasefrom15minoftheexperimenttimeandreacheditspeakin120min.TheadhesionrateandindexofUPEC132tohumanprimaryepithelialcellsofrenalpelviswere74.4%and34.0respectively.ManymicroscopicchangesintheprimarycellsadheredwithUPEC132couldbedetected,suchasroundingorirregularityinshape,unevennessinstainingandthecytoplasmicandnuclearchanges.ItsuggeststhathumanprimaryepithelialcellsofrenalpelviscanbeusedfortheexperimentonUPECadhesion,thusprovidingabasisforthefurtherstudyonthepathogenesisofUPEC.

简介：AIMTo学习discoidin象我一样domaincontaining蛋白质3的效果(EDIL3)在人的透镜的增长和上皮间充质的转变(EMT)上的弄空上皮的房间(LEC).METHODSRNA干扰被用来在vitro在人的LEC禁止EDIL3的表示。房间的形态学用一台转换显微镜被观察。房间增长用EdU工具包被估计。房间移植用Transwell房间被调查，LEC的EMT用共焦的显微镜并且西方的弄污被估计。转变生长因素(TGF)小径用数据显示出的西方的blotting.RESULTSThe被调查那个silencingEDIL3表达式改变了LEC形态学并且压制了LEC增长(P<0.05)并且移植(P<0.01)。而且，西方的弄污的结果证明那EDIL3弄空减少了光滑的肌肉肌动朊的表示(-SMA)(P<0.001)并且vimentin(P<0.01)，当增加时E-cadherin的表示(P<0.001)。EDIL3弄空能压制Smad2的phosphorylation(P<0.01)并且Smad3(P<0.01)并且exracellular信号的激活调整了kinase(英皇家空军之阶级最低之兵)(P<0.05).CONCLUSIONThe调查结果显示EDIL3可能经由TGF小径在LEC参予增长和EMT并且可以是为以后的囊opacification的处理的一个潜在的治疗学的目标。