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Immune-associated renal disease found in caspase 3-deficient mice

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Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/80362

Title: Immune-associated renal disease found in caspase 3-deficient mice
Authors: Suzuki, Takashi Browse this author
Ichii, Osamu Browse this author →KAKEN DB
Nakamura, Teppei Browse this author
Horino, Taro Browse this author
Elewa, Yaser Hosny Ali Browse this author →ORCID
Kon, Yasuhiro Browse this author →KAKEN DB
Keywords: Kidney
Glomerulus
Caspase 3
Knockout
Immunity
Issue Date: Feb-2020
Publisher: Springer
Journal Title: Cell and tissue research
Volume: 379
Issue: 2
Start Page: 323
End Page: 335
Publisher DOI: 10.1007/s00441-019-03084-w
Abstract: Caspase (CASP) 3 is known as a representative effector CASP of apoptosis and recently as a mediator in inflammatory cell death called pyroptosis. Interestingly, homozygotes of Casp3 knockout (KO) mice with 129-background show complete embryonic lethality; however, some of those with C57BL/6 (B6)-background (B6.129S1-Casp3(tm1Flv)/J) survived at a lower rate (KO, 11%; WT, 22%), developing immune abnormality-associated renal phenotypes. Homozygotes of Casp3 KO mice with B6-background that survived for 8-12 months showed abnormality in the kidney and spleen but not in other organs. Briefly, these Casp3 KO kidneys showed proliferative glomerular lesions characterized by increased cells, matrices, immune complex depositions containing IgA and complement 3 in the mesangial area, podocyte injuries and inflammatory cell infiltrations in the tubulointerstitium. However, severe membranous lesion or renal dysfunction was not observed. Increased expression of inflammation-associated gene sets and inflammatory Casps, including Casp12, was observed in these Casp3 KO kidneys. Moreover, these Casp3 KO mice showed mild splenomegaly compared with WT mice. Thus, the long-surviving Casp3 KO mice with B6-background developed renal lesions with altered immune conditions. CASP3 deficiency and aging factors could affect this phenotype by altering the function and/or development of each cell in the kidney and immune organs.
Rights: This is a post-peer-review, pre-copyedit version of an article published in Cell and tissue research. The final authenticated version is available online at: http://dx.doi.org/10.1007/s00441-019-03084-w
Type: article (author version)
URI: http://hdl.handle.net/2115/80362
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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