简介：Anovertphenotypeofaquaporin-1knockout(AQP1ko)miceisgrowthretardation,suggestingpossibledefectsinbonedevelopmentandmetabolism.Inthepresentstudy,weanalyzedthebonemineraldensity(BMD),bonecalciumandphosphoruscontents,andbonemetabolisminanAQP1komousemodel.TheBMDoffemursinAQP1komicewassignificantlylowerthanthatoflitter-matchedwildtypemiceasmeasuredbydualenergyX-rayabsorptiometry.Consistently,thecontentsofbonetotalcalciumandphosphoruswerealsosignificantlylowerinAQP1komice.ThereducedBMDcausedbyAQP1deficiencymainlyaffectmalemice.Bonemetabolicactivity,asindicatedby99mTc-MDPabsorptionmeasurements,wasremarkablyreducedinAQP1komice.TheseresultsprovidethefirstevidencethatAQP1playanimportantroleinbonestructureandmetabolism.

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：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。