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New 'mighty mice' research brings muscle growth closer to reality

The Johns Hopkins scientists who first created "mighty mice" by genetically engineering animals with a missing growth regulator called myostatin have now created a second group of mice whose genetic makeup shows it's possible to get the same effect by blocking the gene for myostatin, rather than entirely knocking it out.

Reporting in the July 16 issue of the Proceedings of the National Academy of Sciences, the researchers say they have identified several proteins (follastatin, mutant activin type II receptors, and myostatin propetide) that can block the activity of myostatin. Moreover, they have engineered mice with normal myostatin, but various levels of these blockers.

"By expressing high levels of these proteins in mice, we have been able to increase muscle mass to levels comparable to those seen in mice completely lacking myostatin," says Se-Jin Lee, M.D., Ph.D., lead author of the Hopkins study. "Although more study is needed to prove that these mice are good models for humans and to find other myostatin signaling components, our work suggests that these kinds of myostatin antagonists may be effective muscle-enhancing agents for both human and agricultural applications."

The 1997 report from Lee and his colleagues focused on the muscle-building capability of knocking out, or deleting the myostatin gene, to allow the buildup of skeletal muscle in the animals.

"Until now, it's been purely theoretical that we could block the gene and obtain the same muscle-building effect as deleting the gene," Lee continues.

The researchers discovered that while mice that were engineered to produce large amounts of follistatin exhibited the most herculean muscles, the other two groups, one with excess mutant activin II receptors and one with myostatin peptide, also showed increased muscle growth.

Scientists are hopeful that the finding will provide new opportunities to treat many muscle-wasting diseases like muscular dystroph
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Contact: Joanna Downer
jdowner1@jhmi.edu
410-614-5105
Johns Hopkins Medical Institutions
16-Jul-2001


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