CHOP-mediated hepcidin suppression modulates hepatic iron load

• Published in: The Journal of pathology Vol. 231; no. 4; pp. 532 - 542
• Main Authors: Mueller, Katrin, Sunami, Yoshiaki, Stuetzle, Michael, Guldiken, Nurdan, Kucukoglu, Ozlem, Mueller, Sebastian, Kulaksiz, Hasan, Schwarz, Peggy, Strnad, Pavel
• Format: Journal Article
• Language: English
• Published: Chichester, UK John Wiley & Sons, Ltd 01.12.2013; Wiley Subscription Services, Inc
• Subjects: alcoholic liver disease; Animals; C/EBPα; Carbon Tetrachloride; CCAAT-Enhancer-Binding Protein-alpha - biosynthesis; CCAAT-Enhancer-Binding Protein-alpha - genetics; CHOP; Female; fibrosis; Gene Expression Regulation - drug effects; Gene Knockout Techniques; hepcidin; Hepcidins - biosynthesis; Hepcidins - genetics; Humans; Iron - metabolism; Iron Overload - etiology; Iron Overload - metabolism; Liver - metabolism; Liver Cirrhosis, Experimental - chemically induced; Liver Cirrhosis, Experimental - complications; Liver Cirrhosis, Experimental - metabolism; Liver Diseases, Alcoholic - complications; Liver Diseases, Alcoholic - metabolism; Mice; Mice, Inbred C57BL; Mice, Knockout; RNA, Messenger - genetics; Signal Transduction - drug effects; Thioacetamide; Transcription Factor CHOP - biosynthesis; Transcription Factor CHOP - deficiency; Transcription Factor CHOP - genetics; Transcription Factor CHOP - physiology; C/EBPα; CHOP; alcoholic liver disease; hepcidin; fibrosis

The liver is the central regulator of iron metabolism and accordingly, chronic liver diseases often lead to systemic iron overload due to diminished expression of the iron‐regulatory hormone hepcidin. To study the largely unknown regulation of iron metabolism in the context of hepatic disease, we us...