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Modification in the von Hippel-Lindau Protein Is Involved in the Progression of Experimentally Induced Rat Glomerulonephritis
Author(s) -
Yoshihiro Kudo,
Yoshihiko Kakinuma,
Mitsuko Iguchi,
Takayuki Sato,
Tetsuro Sugiura,
Mutsuo Furihata,
Taro Shuin
Publication year - 2007
Publication title -
nephron experimental nephrology
Language(s) - English
Resource type - Journals
ISSN - 1660-2129
DOI - 10.1159/000103022
Subject(s) - pathogenesis , podocyte , thrombin , endocrinology , medicine , kidney , western blot , inducer , immunohistochemistry , glomerulonephritis , angiotensin ii , blot , cancer research , biology , receptor , proteinuria , gene , platelet , biochemistry
We previously demonstrated that angiotensin II (AII) combined with Habu snake venom (HV) induces glomerulonephritis (GN) in rats, with lesions being restricted to the glomeruli 2 days after the administration of both reagents, but the mechanisms inducing GN are unclear. We also indicated a role for hypoxia-inducible factor (HIF)-1alpha in attenuating the progression of GN. However, a role of the von Hippel-Lindau (VHL) protein in GN and mechanisms by which HV regulates the pathogenesis of GN remains unclear.

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