Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2023511 | Regulatory Peptides | 2007 | 8 Pages |
Abstract
Bone morphogenetic protein-6 (BMP-6) enhances aldosterone production by upregulating angiotensin II (Ang II)-to-MAPK pathway. Here we investigated effects of Ang II and potassium on the BMP system in human adrenocortical H295R cells. BMP-6 transcription was transiently downregulated by treatments with Ang II and potassium. Aldosterone also decreased BMP-6 expression at a high concentration. Chemical inhibitions of transcription and translation abolished the transient reduction of BMP-6, suggesting that destabilization of BMP-6 mRNA was hardly involved while new protein synthesis was possibly mediated in this mechanism. However, BMP-6 protein was stably detected during the exposures of Ang II and potassium. Notably, Ang II, potassium and aldosterone decreased mRNA levels of follistatin that extracellularly neutralizes bioactivities of activins and BMPs although the BMP-6 receptor expression was unaffected. Given the maintenance of bioavailable BMP-6 protein and the receptor expression in adrenocortical cells, endogenous BMP-6 may be a key autocrine modulator for aldosterone production.
Keywords
BMPRIIBMP type II receptoractivin type II receptorTGF-βACTHPotassium (K)ActRIIFollistatinACDCHXforskolinH295R cellERKFskMAPKadrenocorticotropinaldosteroneALKAngiotensin IIactinomycin DAng IIcycloheximideAdrenal cortexBMPBone morphogenetic proteinbone morphogenetic protein (BMP)mitogen-activated protein kinaseextracellular signal-regulated kinaseactivin receptor-like kinase
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Authors
Kenichi Inagaki, Fumio Otsuka, Jiro Suzuki, Hiroyuki Otani, Masaya Takeda, Yoshihiro Kano, Tomoko Miyoshi, Misuzu Yamashita, Toshio Ogura, Hirofumi Makino,