title: Intrarenal expression of microRNAs in patients with IgA nephropathy.
abstract: MicroRNAs (miRNAs) are noncoding, single-stranded RNA molecules that have important roles in a number of physiological and pathological processes. Previous studies have proved that miRNAs targeting ZEB1 and ZEB2 may repress epithelial-to-mesenchymal transition. In this work, we studied the intrarenal expression of miR-200 family, miR-205 and miR-192 in patients with immunoglobulin A (IgA) nephropathy. We studied 43 patients with biopsy-proven IgA nephropathy (IgA group). The intrarenal expression of miRNAs was quantified and compared with that of 15 patients with noninflammatory glomerulosclerosis (GS group) and 20 patients with nephrectomy for kidney cancer as controls (CTL group). The level of intrarenal miR-200c was downregulated, whereas the levels of intrarenal miR-141, miR-205 and miR-192 were upregulated in IgA but not GS group. Proteinuria significantly correlated with the intrarenal expression of miR-200c (r=-0.324, P=0.011) and glomerular filtration rate (GFR) significantly correlated with the intrarenal expression of miR-205 (r=-0.280, P=0.030). The degree of tubulointerstitial scarring correlated with miR-205 expression (r=0.389, P=0.021), whereas glomerulosclerosis correlated with miR-192 expression (r=-0.311, P=0.045). The rate of GFR decline significantly correlated with the intrarenal expression of miR-192 (r=0.373, P=0.015). The intrarenal expression of E-cadherin significantly correlated with the intrarenal expression of miR-200c (r=0.392, P=0.002). The results show that intrarenal expression of miR-200c, miR-141, miR-205 and miR-192 was diversely regulated and correlated with disease severity and progression in patients with IgA nephropathy. These miRNA species may be important in the pathogenesis and progression of IgA nephropathy.
authors.affiliation: Department of Medicine and Therapeutics, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China.
authors.forename: Gang
authors.initials: G
authors.lastname: Wang
authors.forename: Bonnie C-H
authors.initials: BC
authors.lastname: Kwan
authors.forename: Fernand M-M
authors.initials: FM
authors.lastname: Lai
authors.forename: Paul C-L
authors.initials: PC
authors.lastname: Choi
authors.forename: Kai-Ming
authors.initials: KM
authors.lastname: Chow
authors.forename: Philip K-T
authors.initials: PK
authors.lastname: Li
authors.forename: Cheuk-Chun
authors.initials: CC
authors.lastname: Szeto
mesh_terms: D000328:Adult; D000368:Aged; D015536:Down-Regulation; D005260:Female; D005786:Gene Expression Regulation; D005919:Glomerular Filtration Rate; D005922:Glomerulonephritis, IGA / Q000235:genetics* / Q000503:physiopathology; D006801:Humans; D007668:Kidney / Q000378:metabolism* / Q000503:physiopathology; D007674:Kidney Diseases / Q000235:genetics / Q000473:pathology / Q000503:physiopathology; D007678:Kidney Glomerulus / Q000473:pathology; D007680:Kidney Neoplasms / Q000235:genetics / Q000601:surgery; D008297:Male; D035683:MicroRNAs / Q000378:metabolism*; D008875:Middle Aged; D009392:Nephrectomy; D012598:Sclerosis; D012720:Severity of Illness Index; D015854:Up-Regulation
chemical_list: D035683:MicroRNAs; C533895:MIRN141 microRNA, human; C546783:MIRN192 microRNA, human; C533896:MIRN200 microRNA, human; C534425:MIR205, human