NDLI: Hepatocyte growth factor activator inhibitor type 2 (HAI-2) modulates hepcidin expression by inhibiting the cell surface protease matriptase-2.

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Hepatocyte growth factor activator inhibitor type 2 (HAI-2) modulates hepcidin expression by inhibiting the cell surface protease matriptase-2.

Content Provider	Semantic Scholar
Author	Maurer, Eva Gütschow, Michael Stirnberg, Marit
Copyright Year	2013
Abstract	Matriptase-2, a recently identified cell surface protease, is the key enzyme of iron homoeostasis modulating the expression of the liver peptide hormone hepcidin. HAI (hepatocyte growth factor activator inhibitor) types 1 and 2 (HAI-1 and HAI-2 respectively) have been shown to inhibit the close homologue, i.e. matriptase. By co-expressing matriptase-2 and the inhibitor HAI-2 we have identified HAI-2 displaying high inhibitory potential against matriptase-2 at the cell surface as well as in conditioned medium. Accordingly, complex formation between matriptase-2 and HAI-2 was demonstrated by isolation of the complex via immobilizing either HAI-2 or matriptase-2 from lysates and conditioned medium of co-expressing cells. Furthermore, HAI-2 indirectly influences the expression of the hepcidin-encoding gene HAMP. The inhibitor abrogates the matriptase-2-mediated suppression of HAMP expression, presumably by inhibiting the supposed potential of matriptase-2 to cleave membrane-bound HJV (haemojuvelin). Taken together, the results of the present study have characterized HAI-2 as an inhibitor of matriptase-2 that modulates the synthesis of hepcidin and provides new insights into the regulatory mechanism of iron homoeostasis, with clinical importance for a treatment of iron overload diseases.
File Format	PDF HTM / HTML
DOI	10.1042/BJ20121518
Alternate Webpage(s)	https://www.pharmchem1.uni-bonn.de/ak-guetschow/pdf/guetschow_maurer2
PubMed reference number	23293962
Alternate Webpage(s)	https://doi.org/10.1042/BJ20121518
Journal	Medline
Volume Number	450
Issue Number	3
Journal	The Biochemical journal
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article

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