2014 Fiscal Year Final Research Report
The role of Mafb in secondary hyperparathyroidism.
Project/Area Number |
24591223
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Kidney internal medicine
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Research Institution | University of Tsukuba |
Principal Investigator |
MORITO Naoki 筑波大学, 医学医療系, 講師 (70463825)
|
Co-Investigator(Kenkyū-buntansha) |
YOH Keigyou 筑波大学, 医学医療系, 准教授 (90323302)
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Project Period (FY) |
2012-04-01 – 2015-03-31
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Keywords | 2次性副甲状腺機能亢進症 |
Outline of Final Research Achievements |
Secondary hyperparathyroidism (HPT) is a common disorder in patients with chronic kidney disease (CKD). Recently, it was reported that the transcription factor Mafb is essential for differentiation of parathyroid gland. However, the role of Mafb in secondary hyperparathyroidism is not well known. Six-week-old WT (wild-type) and Mafb+/- mice were fed with adenine containing or normal diet. After 6 weeks of feeding, secondary hyperparathyroidism was assessed. Interestingly, secondary HPT was prevented in Mafb+/- mice. Mafb+/- mice had lower serum PTH levels and smaller parathyroid gland areas compared to their WT littermates after adenine feeding. Moreover, we found lower PTH and cyclinD2 expression in Mafb+/- parathyroid glands. These facts suggest that Mafb directly regulates the PTH and cyclinD2 expression in parathyroid glands.Mafb might play an important role in secondary HPT through PTH and cyclinD2 transcription.
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Free Research Field |
腎臓内科
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