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Altered Renal Pathology in an Autoimmune Disease Mouse Model After Induction of Diabetes Mellitus

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Title: Altered Renal Pathology in an Autoimmune Disease Mouse Model After Induction of Diabetes Mellitus
Authors: Hiramatsu, Shiori Browse this author
Ichii, Osamu Browse this author →KAKEN DB
Namba, Takashi Browse this author
Otani, Yuki Browse this author
Nakamura, Teppei Browse this author →KAKEN DB
Masum, Md Abdul Browse this author
Elewa, Yaser Hosny Ali Browse this author →ORCID
Kon, Yasuhiro Browse this author →KAKEN DB
Keywords: autoimmune disease
diabetes mellitus
diabetic kidney disease
Issue Date: Aug-2021
Publisher: Cambridge University Press
Journal Title: Microscopy and microanalysis
Volume: 27
Issue: 4
Start Page: 897
End Page: 909
Publisher DOI: 10.1017/S143192762100057X
Abstract: Diabetes mellitus (DM) is a predisposing factor for renal disorder progression and is referred to as diabetic kidney disease (DKD). However, there are no reports of DKD with an underlying autoimmune disorder. In this study, we compared the pathophysiological changes caused by DM induction after streptozotocin (STZ) injection in comparison with that in a control group receiving citrate buffer (CB) in the autoimmune disease model mice "BXSB/MpJ-Yaa" (Yaa) and the wild-type strain BXSB/MpJ. Both strains showed hyperglycemia after 12 weeks of STZ injection. Interestingly, the Yaa group developed membranous and proliferative glomerulonephritis, which tended to be milder glomerular lesions in the STZ group than in the CB group, as indicated by a decreased mesangial area and ameliorated albuminuria. Statistically, the indices for hyperglycemia and autoimmune abnormalities were negatively and positively correlated with the histopathological parameters for mesangial matrix production and glomerular proliferative lesions, respectively. STZ treatment induced renal tubular anisonucleosis and dilations in both strains, and they were more severe in Yaa. Significantly decreased cellular infiltration was observed in the Yaa group compared to the CB group. Thus, in DKD related to autoimmune nephritis, hyperglycemia modifies its pathology by decreasing the mesangial area and interstitial inflammation and aggravating renal tubular injury.
Rights: This article has been published in a revised form in [Microscopy Society of America] []. This version is published under a Creative Commons CC-BY-NC-ND. No commercial re-distribution or re-use allowed. Derivative works cannot be distributed. ©[ The Author(s)].
Type: article (author version)
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: 市居 修

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