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Nardilysin Is Required for Maintaining Pancreatic β-Cell Function
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DOI：10.2337/db16-0178.png)
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摘要
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Type 2 diabetes (T2D) is associated with pancreatic beta-cell dysfunction, manifested by reduced glucose-stimulated insulin secretion (GSIS). Several transcription factors enriched in beta-cells, such as MafA, control beta-cell function by organizing genes involved in GSIS. Here we demonstrate that nardilysin (N-arginine dibasic convertase; Nrd1 and NRDc) critically regulates beta-cell function through MafA. Nrd1(-/-) mice showed glucose intolerance and severely decreased GSIS. Islets isolated from Nrd1(-/-) mice exhibited reduced insulin content and impaired GSIS in vitro. Moreover, beta-cell-specific NRDc-deficient (Nrd1(del beta)) mice showed a diabetic phenotype with markedly reduced GSIS. MafA was specifically downregulated in islets from Nrd1delb mice, whereas overexpression of NRDc upregulated MafA and insulin expression in INS832/13 cells. Chromatin immunoprecipitation assay revealed that NRDc is associated with Islet-1 in the enhancer region of MafA, where NRDc controls the recruitment of Islet-1 and MafA transcription. Our findings demonstrate that NRDc controls beta-cell function via regulation of the Islet-1-MafA pathway.
Keyword:
ARGININE DIBASIC CONVERTASE
MAFA TRANSCRIPTION FACTOR
GROWTH-FACTOR
LIM DOMAIN
GLUCOSE-HOMEOSTASIS
ALPHA
METALLOENDOPEPTIDASE
PROTEIN
EXPRESSION
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期刊
IF:
7.5
论文数:
2.6W
被引数:
4.6W
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引用论文
MafA is critical for maintenance of the mature beta cell phenotype in miceMafA对于维持小鼠成熟 β 细胞表型至关重要.png)
DIABETOLOGIAOAAI
DIABETOLOGIAIF10.2
OAAI分享收藏The MafA transcription factor appears to be responsible for tissue-specific expression of insulinOAAI
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