B-cell translocation gene 2 promotes hepatic hepcidin production via induction of Yin Yang 1

Title
B-cell translocation gene 2 promotes hepatic hepcidin production via induction of Yin Yang 1
Author(s)
장현욱이성은[이성은]황승락장원구[장원구]김용득[김용득]
Keywords
THERAPEUTIC IMPLICATIONS; IRON HOMEOSTASIS; RECEPTOR; GLUCONEOGENESIS; MICE
Issue Date
201505
Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
Citation
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.460, no.4, pp.996 - 1001
Abstract
Hepcidin is a peptide hormone secreted in the liver and plays a key role in maintaining iron homeostasis. Here, we demonstrate that B-cell translocation gene 2 (BTG2) is a key player in hepatic hepcidin regulation via induction of Yin Yang I (YY1). Hepatic hepcidin gene expression significantly enhanced by fasting states and glucagon exposure led to induction of gluconeogenic gene expression, and elevated serum hepcidin production in mice. Notably, overexpression of BTG2 using adenoviral system (Ad-BTG2) significantly elevated serum hepcidin levels via a significant induction of YY1 gene transcription. Immunoprecipitation studies demonstrated that BTG2 physically interacted with YY1 and recruited on the hepcidin gene promoter. Finally, ablation of hepatic BTG2 gene by gene silencing markedly attenuated the elevation of serum hepcidin production along with YY1 and hepcidin mRNA expression in fasting state. Likewise, forskolin (FSK)-stimulated hepcidin promoter activity was dramatically disrupted by endogenous BTG2 knockdown. Overall, our current study provides a novel molecular mechanism of BTG2-mediated induction of hepcidin gene expression, thereby contributing to a better understanding of the hepatic hepcidin production involved in iron homeostasis. (C) 2015 Elsevier Inc. All rights reserved.
URI
http://hdl.handle.net/YU.REPOSITORY/32262http://dx.doi.org/10.1016/j.bbrc.2015.03.140
ISSN
0006-291X
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약학대학 > 약학부 > Articles
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