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cyclophilins A and B oppositely regulate renal tubular epithelial cell phenotype

Journal of Molecular Cell Biology 2020年第7期12卷 499-514页

作者： Eduard Sarró Mónica Durán Ana Rico Diana Bou-Teen Vanesa Fernández-Majada Anthony J.Croatt Karl A.Nath Maria Teresa Salcedo Justin H.Gundelach Daniel Batlle Richard J.Bram Anna Meseguer Renal Physiopathology Group CIBBIM-NanomedicineVall d’Hebron Research Institute08035 BarcelonaSpain Cardiovascular Diseases Group Vall d’Hebron Research Institute08035 BarcelonaSpain Biomimetic Systems for Cell Engineering Laboratory Institute for Bioengineering of Catalonia(IBEC)The Barcelona Institute of Science and Technology(BIST)08028 BarcelonaSpain Division of Nephrology and Hypertension and Department of Medicine Mayo ClinicRochesterMN 55905USA Department of Pathology Hospital Universitari Vall d’Hebron08035 BarcelonaSpain Department of Pediatric and Adolescent Medicine College of MedicineMayo ClinicRochesterMN 55905USA Department of Biochemistry and Molecular Biology College of MedicineMayo ClinicRochesterMN 55905USA Division of Nephrology and Hypertension Northwestern University Feinberg School of MedicineChicagoIL 60611USA Department of Immunology College of MedicineMayo ClinicRochesterMN 55905USA Departament de Bioquímica i Biologia Molecular Unitat de Bioquímica de MedicinaUniversitat Autònoma de Barcelona08193 BellaterraSpain Red de Investigación Renal(REDINREN) Instituto de Salud Carlos III-FEDER28040 MadridSpain

Restoration of kidney tubular epithelium following sublethal injury sequentially involves partial epithelial–mesenchymal transition(pEMT),proliferation,and further redifferentiation into specialized tubule epithelial cells(TECs).Because the immunosuppressant cyclosporine-A produces pEMT in TECs and inhibits the peptidyl-prolyl isomerase(PPIase)activity of cyclophilin(Cyp)proteins,we hypothesized that cyclophilins could regulate TEC *** we demonstrate that in cultured TECs,CypA silencing triggers loss of epithelial features and enhances transforming growth factorβ(TGFβ)-induced EMT in association with upregulation of epithelial repressors Slug and *** pro-epithelial action of CypA relies on its PPIase *** contrast,CypB emerges as an epithelial repressor,because CypB silencing promotes epithelial differentiation,prevents TGFβ-induced EMT,and induces tubular structures in 3D *** addition,in the kidneys of CypB knockout mice subjected to unilateral ureteral obstruction,inflammatory and pro-fibrotic events were *** silencing/knockout leads to Slug,but not Snail,*** support of Slug expression depends on its endoplasmic reticulum location,where it interacts with calreticulin,a calcium-buffering chaperone related to Slug *** CypB silencing reduces ionomycin-induced calcium release and Slug upregulation,we suggest that Slug expression may rely on CypB modulation of calreticulin-dependent calcium *** conclusion,this work uncovers new roles for CypA and CypB in modulating TEC plasticity and identifies CypB as a druggable target potentially relevant in promoting kidney repair.

关键词： cyclophilins epithelial phenotype Slug TGFβ UUO fibrosis

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