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(American Journal of Pathology. 2004;164:1773-1782.)
© 2004 American Society for Investigative Pathology

Cloning of cDNA Encoding a Regeneration-Associated Muscle Protease Whose Expression Is Attenuated in Cell Lines Derived from Duchenne Muscular Dystrophy Patients

Yuki Nakayama*, Noriko Nara*, Yukiko Kawakita{dagger}, Yasuhiro Takeshima{ddagger}, Masayuki Arakawa§, Masaki Katoh, Sumiyo Morita||, Ken Iwatsuki*, Kiyoko Tanaka*, Shiki Okamoto*, Toshio Kitamura||, Naohiko Seki, Ryoichi Matsuda§, Masafumi Matsuo{ddagger}, Kayoko Saito{dagger} and Takahiko Hara*

From the Department of Tumor Biochemistry,* The Tokyo Metropolitan Institute of Medical Science, Tokyo Metropolitan Organization for Medical Research, Tokyo; the Department of Pediatrics,{dagger} Tokyo Women’s Medical University, Tokyo; the Department of Pediatrics,{ddagger} Kobe University Graduate School of Medicine, Kobe; the Department of Life Sciences,§ The University of Tokyo, Tokyo; the Department of Functional Genomics, Chiba University Graduate School of Medicine, Chiba; and the Division of Cellular Therapy,|| Advanced Clinical Research Center, Institute of Medical Science, University of Tokyo, Tokyo, Japan

In the dystrophin-mutant mdx mouse, an animal model for Duchenne muscular dystrophy (DMD), damaged skeletal muscles are efficiently regenerated and thus the animals thrive. The phenotypic differences between DMD patients and the mdx mice suggest the existence of factors that modulate the muscle wasting in the mdx mice. To identify these factors, we searched for mRNAs affected by the mdx mutation by using cDNA microarrays with newly established skeletal muscle cell lines from mdx and normal mice. We found that in the mdx muscle cell line, 12 genes, including L-arginine:glycine amidinotransferase and thymosin ß4, are up-regulated, whereas 7 genes, including selenoprotein P and a novel regeneration-associated muscle protease (RAMP), are down-regulated. Northern blot analysis and in situ hybridization revealed that RAMP mRNA is predominantly expressed in normal skeletal muscle and brain, and its production is enhanced in the regenerating area of injured skeletal muscle in mice. RAMP expression was much lower in individual muscle cell lines derived from biopsies of six DMD patients compared to a normal muscle cell line. These results suggest that RAMP may play a role in the regeneration of skeletal muscle and that its down-regulation could be involved in the progression of DMD in humans.




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