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Close Relations between Podocyte Injuries and Membranous Proliferative Glomerulonephritis in Autoimmune Murine Models

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Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/53122

Title: Close Relations between Podocyte Injuries and Membranous Proliferative Glomerulonephritis in Autoimmune Murine Models
Authors: Kimura, Junpei Browse this author
Ichii, Osamu Browse this author →KAKEN DB
Otsuka, Saori Browse this author →KAKEN DB
Sasaki, Hayato Browse this author
Hashimoto, Yoshiharu Browse this author →KAKEN DB
Kon, Yasuhiro Browse this author →KAKEN DB
Keywords: Autoimmune disease
B6.MRL-(D1Mit202-D1Mit403)
BXSB/MpJ
Membranous proliferative glomerulonephritis
Podocyte
Systemic lupus erythematosus
Issue Date: Jul-2013
Publisher: Karger
Journal Title: American Journal Of Nephrology
Volume: 38
Issue: 1
Start Page: 27
End Page: 38
Publisher DOI: 10.1159/000353093
PMID: 23817053
Abstract: Background: Membranous proliferative glomerulonephritis (MPGN) is a major primary cause of chronic kidney disease (CKD). Podocyte injury is crucial in the pathogenesis of glomerular disease with proteinuria, leading to CKD. To assess podocyte injuries in MPGN, the pathological features of spontaneous murine models were analyzed. Methods: The autoimmune-prone mice strains BXSB/MpJ-Yaa and B6.MRL-(D1Mit202-D1Mit403) were used as the MPGN models, and BXSB/MpJ-Yaa(+) and C57BL/6 were used as the respective controls. In addition to clinical parameters and glomerular histopathology, the protein and mRNA levels of podocyte functional markers were evaluated as indices for podocyte injuries. The relation between MPGN pathology and podocyte injuries was analyzed by statistical correlation. Results: Both models developed MPGN with albuminuria and elevated serum anti-double-strand DNA (dsDNA) antibody levels. BXSB/MpJ-Yaa and B6.MRL showed severe proliferative lesions with T and B cell infiltrations and membranous lesions with T cell infiltrations, respectively. Foot process effacement and microvillus-like structure formation were observed ultrastructurally in the podocytes of both MPGN models. Furthermore, both MPGN models showed a decrease in immune-positive areas of nephrin, podocin and synaptopodin in the glomerulus, and in the mRNA expression of Nphs1, Nphs2, Synpo, Actn4, Cd2ap, and Podxl in the isolated glomerulus. Significant negative correlations were detected between serum anti-dsDNA antibody levels and glomerular Nphs1 expression, and between urinary albumin-to-creatinine ratio and glomerular expression of Nphs1, Synpo, Actn4, Cd2ap, or Podxl. Conclusion: MPGN models clearly developed podocyte injuries characterized by the decreased expression of podocyte functional markers with altered morphology. These data emphasized the importance of regulation of podocyte injuries in MPGN. Copyright (c) 2013 S. Karger AG, Basel
Rights: Copyright (c) 2013 S. Karger AG, Basel
Type: article (author version)
URI: http://hdl.handle.net/2115/53122
Appears in Collections:獣医学院・獣医学研究院 (Graduate School of Veterinary Medicine / Faculty of Veterinary Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 昆 泰寛

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