title: Plasma gelsolin levels are decreased and correlate with fibrosis in IgA nephropathy.
abstract: IgA nephropathy (IgAN) is an immune complex glomerulonephritis that is characterized by recurrent hematuria as the main clinical manifestation. In this study, we used the IgAN mouse model which was previously established to investigate the possible mechanism by which IgAN fibrosis correlates with decreased plasma gelsolin (pGSN) levels. We investigated the levels of pGSN, transforming growth factor β1 (TGFβ1), and oxidative stress markers including superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and malondialdehyde (MDA) in the serum and renal tissues of different groups. The between-group differences and correlations in the results for the IgAN group were analyzed with statistical methods. The pathological and urinalysis results obtained from the IgAN mouse model showed that this model conforms to the basic lesion characteristics observed in human IgAN. The serum pGSN levels and SOD, CAT, GSH levels in renal tissues were decreased in the IgAN group (P < 0.01), and pGSN, TGFβ1, MDA levels in renal tissues of the IgAN group were increased which compared with those in the other groups (P < 0.01). The correlation analysis for serum pGSN levels in the IgAN group showed a significant correlation with different test results (P < 0.01). The possible mechanism by which IgAN fibrosis correlates with decreased pGSN levels involves the regulation of TGFβ1 and oxidative stress.
authors.affiliation: Department of Pathology, Harbin Medical University, Harbin 150081 The People's Republic of China.
authors.forename: Changsong
authors.initials: C
authors.lastname: Han
authors.forename: Lei
authors.initials: L
authors.lastname: Zhang
authors.forename: Xiaoling
authors.initials: X
authors.lastname: Zhu
authors.forename: Jing
authors.initials: J
authors.lastname: Tang
authors.forename: Xiaoming
authors.initials: X
authors.lastname: Jin
mesh_terms: D000818:Animals; D002374:Catalase / Q000097:blood / Q000378:metabolism; D004195:Disease Models, Animal; D018450:Disease Progression; D005355:Fibrosis / Q000097:blood* / Q000473:pathology; D018260:Gelsolin / Q000097:blood* / Q000378:metabolism; D005922:Glomerulonephritis, IGA / Q000097:blood* / Q000473:pathology; D005978:Glutathione / Q000097:blood / Q000378:metabolism; D007668:Kidney / Q000378:metabolism; D008315:Malondialdehyde / Q000097:blood / Q000378:metabolism; D051379:Mice; D018384:Oxidative Stress; D013482:Superoxide Dismutase / Q000097:blood / Q000378:metabolism; D053773:Transforming Growth Factor beta1 / Q000097:blood / Q000378:metabolism
chemical_list: D018260:Gelsolin; D053773:Transforming Growth Factor beta1; D008315:Malondialdehyde; D002374:Catalase; D013482:Superoxide Dismutase; D005978:Glutathione
keywords: IgA nephropathy; Plasma gelsolin; TGFβ1; mouse IgA nephropathy model; oxidative stress