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Please use this identifier to cite or link to this item: http://hdl.handle.net/2241/103879

Title: MafA-deficient and beta cell-specific MafK-overexpressing hybrid transgenic mice develop human-like severe diabetic nephropathy
Authors: Shimohata, Homare
Yoh, Keigyou
Fujita, Akiko
Morito, Naoki
Ojima, Masami
Tanaka, Hiromi
Hirayama, Kouichi
Kobayashi, Masaki
Kudo, Takashi
Yamagata, Kunihiro
Takahashi, Satoru
楊, 景堯
森戸, 直記
工藤, 崇
山縣, 邦弘
高橋, 智
Issue Date: Nov-2009
Publisher: Elsevier Inc.
Journal Title: Biochemical and biophysical research communications
Volume: 389
Issue: 2
Start Page: 235
End Page: 240
DOI: 10.1016/j.bbrc.2009.08.124
PMID: 19715672
Abstract: Transcription factor MafA is a key molecule in insulin secretion and the development of pancreatic islets. Previously, we demonstrated that some of theMafA-deficient mice develop overt diabetes mellitus, and the phenotype of these mice seems to be mild probably because of redundant functions of other Maf proteins. In this study, we generated hybrid transgenic mice that were MafA-deficient and also over-expressed MafK specifically in beta cells (MafA −/−MafK+). MafA−/−MafK+ mice developed severe overt diabetes mellitus within 5 weeks old, and showed higher levels of proteinuria and serum creatinine. Histological analysis revealed that embryonic development ofbeta cells in the MafA −/−MafK+ mice was significantly suppressed and the reduced number of beta cells was responsible for the early onset of diabetes. Furthermore, after uninephrectomy, these mice demonstrated three characteristics of human diabetic nephropathy: diffuse, nodular, and exudative lesions. MafA−/−MafK+ mice might be a useful model for the analysis of human diabetic nephropathy.
URI: http://hdl.handle.net/2241/103879
Rights: © 2009 Elsevier Inc.
Text Version: author
Appears in Collections:Biochemical and biophysical research communications
高橋 智 (Takahashi Satoru)
山縣 邦弘 (Yamagata Kunihiro)
工藤 崇 (Kudo Takashi)
森戸 直記 (Morito Naoki)
楊 景堯 (Yoh Keigyou)

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