Downregulation of miR-205 Modulates Cell Susceptibility to Oxidative and Endoplasmic Reticulum Stresses in Renal Tubular Cells 英文参考文献.docVIP

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Downregulation of miR-205 Modulates Cell Susceptibility to Oxidative and Endoplasmic Reticulum Stresses in Renal Tubular Cells 英文参考文献.doc

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Downregulation of miR-205 Modulates Cell Susceptibility to Oxidative and Endoplasmic Reticulum Stresses in Renal Tubular Cells 英文参考文献

DownregulationofmiR-205ModulatesCellSusceptibility toOxidativeandEndoplasmicReticulumStressesin RenalTubularCells ShiyoMuratsu-Ikeda,MasaomiNangaku*,YoichiroIkeda,TetsuhiroTanaka,TakehikoWada, ReikoInagi* DivisionofNephrologyandEndocrinology,UniversityofTokyoSchoolofMedicine,Tokyo,Japan Abstract Background: Oxidative stress and endoplasmic reticulum (ER) stress play a crucial role in tubular damage in both acute kidneyinjury(AKI)andchronickidneydisease(CKD).WhilethepathophysiologicalcontributionofmicroRNAs(miRNA)to renaldamagehasalsobeenhighlighted,theeffectofmiRNAonrenaldamageunderoxidativeandERstressesconditions remainselusive. Methods: We assessed changes in miRNA expression in the cultured renal tubular cell line HK-2 under hypoxia- reoxygenation-induced oxidative stress or ER stress using miRNA microarray assay and real-time RT-PCR. The pathophysiological effect of miRNA was evaluated by cell survival rate, intracellular reactive oxygen species (ROS) level, andanti-oxidantenzymeexpressioninmiRNA-inhibitedHK-2ormiRNA-overexpressedHK-2underthesestressconditions. ThetargetgeneofmiRNAwasidentifiedby39-UTR-luciferaseassay. Results: We identified 8 and 10 miRNAs whose expression was significantly altered by oxidative and ER stresses, respectively. Among these, expression of miR-205 was markedly decreased in both stress conditions. Functional analysis revealedthatdecreasedmiR-205ledtoanincreaseincellsusceptibilitytooxidativeandERstresses,andthatthisincrease wasassociatedwiththeinductionofintracellularROSandsuppressionofanti-oxidantenzymes.WhileincreasedmiR-205by itself made no change in cell growth or morphology, cell viability under oxidative or ER stress conditions was partially restored. Further, miR-205 bound to the 39-UTR of the prolyl hydroxylase 1 (PHD1/EGLN2) gene and suppressed the transcriptionlevelofEGLN2,whichmodulatesbothintracellularROSlevelandERstressstate. Conclusions: miR-205 serves a protective role against both oxidative and ER stresses via the