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Differential display analysis of murine collagen‐induced arthritis: cloning of the cDNA‐encoding murine ATPase inhibitor
Author(s) -
YAMADA E.,
ISHIGURO N.,
MIYAISHI O.,
TAKEUCHI A.,
NAKASHIMA I.,
IWATA H.,
ISOBE K.
Publication year - 1997
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.1997.00370.x
Subject(s) - arthritis , atpase , complementary dna , biology , gene , gene expression , cloning (programming) , microbiology and biotechnology , northern blot , inflammation , biochemistry , enzyme , immunology , computer science , programming language
We used the differential display technique in order to detect a new gene involved in murine type II collagen‐induced arthritis (CIA). In this study, we have identified a novel gene, IF 1 , whose expression level is increased during the natural course of CIA. Northern blot analyses suggest that IF 1 is involved in the natural course of CIA but is not involved as a trigger of CIA. IF 1 is considered to be the murine ATPase inhibitor gene for several reasons. First, IF 1 shows an extremely high homology to the rat ATPase inhibitor; the highly conserved region between rat and bovine amino acid residues 22–45, which is the minimum sequence showing ATPase inhibitory activities, is also highly conserved in IF 1 . Second, IF 1 possesses a histidine‐rich region in the same area, which is thought to be important for regulation of mammalian inhibitors. Third, the tissue distribution of IF 1 is very suggestive. The expression of IF 1 was very strong in energetic organs such as the heart, brain and kidney, and the development of arthritis requires great amounts of ATP. As arthritis develops rapidly, the cellular ATP pool may be decreased. Before the ATP pool is exhausted, the ATPase inhibitor may serve as a brake for ATP hydrolysis. If the supply of free energy can be reduced, the inflammation of arthritis may in turn be restored. Our hypothesis is that the ATPase inhibitor is involved in regulating the inflammatory responses.