Abstract:
:Activation of mineralocorticoid receptor (MR) is shown in resistant hypertension including diabetes mellitus. Although protein kinase C (PKC) signaling is involved in the pathogenesis of diabetic complications, an association between PKC and MR is not known. Activation of PKCα and PKCβ by TPA (12-O-Tetradecanoylphorbol 13-acetate) increased MR proteins and its transcriptional activities in HEK293-MR cells. In contrast, a high glucose condition resulted in PKCβ but not PKCα activation, which is associated with elevation of MR protein levels and MR transcriptional activities. Reduction of endogenous PKCβ by siRNA decreased those levels. Interestingly, high glucose did not affect MR mRNA levels, but rather decreased ubiquitination of MR proteins. In db/db mice kidneys, levels of phosphorylated PKCβ2, MR and Sgk-1 proteins were elevated, and the administration of PKC inhibitor reversed these changes compared to db/+ mice. These data suggest that high glucose stimulates PKCβ signaling, which leads to MR stabilization and its transcriptional activities.
journal_name
Int Heart Jjournal_title
International heart journalauthors
Hayashi T,Shibata H,Kurihara I,Yokota K,Mitsuishi Y,Ohashi K,Murai-Takeda A,Jo R,Ohyama T,Sakamoto M,Tojo K,Tajima N,Utsunomiya K,Itoh Hdoi
10.1536/ihj.16-649subject
Has Abstractpub_date
2017-10-21 00:00:00pages
794-802issue
5eissn
1349-2365issn
1349-3299journal_volume
58pub_type
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