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'Mighty Mice' Made Mightier

Date:
August 29, 2007
Source:
Johns Hopkins Medical Institutions
Summary:
The scientist who first showed that the absence of the protein myostatin leads to oversized muscles in mice and men has now found a second protein, follistatin, whose overproduction in mice lacking myostatin doubles the muscle-building effect. Results of the new study show that while mice that lack the gene that makes myostatin have roughly twice the amount of body muscle as normal, mice without myostatin that also overproduce follistatin have about four times as much muscle as normal mice.

Comparison of body and muscle size between normal mice (left) and double mutant mice lacking myostatin and overproducing follistatin (right.
Credit: Image courtesy of Johns Hopkins Medical Institutions

The Johns Hopkins scientist who first showed that the absence of the protein myostatin leads to oversized muscles in mice and men has now found a second protein, follistatin, whose overproduction in mice lacking myostatin doubles the muscle-building effect.

Results of the new study by Se-Jin Lee, M.D., Ph.D., in PloS One, show that while mice that lack the gene that makes myostatin have roughly twice the amount of body muscle as normal, mice without myostatin that also overproduce follistatin have about four times as much muscle as normal mice.

Lee, a professor of molecular biology and genetics, says this added muscle increase could significantly boost research efforts to “beef up” livestock or promote muscle growth in patients with muscular dystrophy and other wasting diseases.

Specifically, Lee first discovered that follistatin was capable of blocking myostatin activity in muscle cells grown under lab conditions. When he gave it to normal mice, the rodents bulked up, just as would happen if the myostatin gene in these animals was turned off.

He then genetically engineered a mouse that both lacked myostatin and made extra follistatin. If follistatin was increasing muscle growth solely by blocking myostatin, then Lee surmised that follistatin would have no added effect in the absence of myostatin.

“To my surprise and delight, there was an additive effect,” said Lee, who notes that these muscular mice averaged a 117 percent increase in muscle fiber size and a 73 percent increase in total muscle fibers compared to normal mice.

“These findings show that the capacity for increasing muscle growth by targeting these pathways is much more extensive than we have appreciated,” adds Lee. “Now we’ll search for other players that cooperate with myostatin so we can tap the full potential for enhancing muscle growth for clinical applications.”

Lee adds that this issue is of particular significance, as most agents targeting this pathway, including one drug being currently tested in a muscular dystrophy clinical trial, have been designed to block only myostatin and not other related proteins.

The research was funded by grants from the NIH and the Muscular Dystrophy Association and by a gift from Merck Research Laboratories.


Story Source:

The above story is based on materials provided by Johns Hopkins Medical Institutions. Note: Materials may be edited for content and length.


Cite This Page:

Johns Hopkins Medical Institutions. "'Mighty Mice' Made Mightier." ScienceDaily. ScienceDaily, 29 August 2007. <www.sciencedaily.com/releases/2007/08/070828215611.htm>.
Johns Hopkins Medical Institutions. (2007, August 29). 'Mighty Mice' Made Mightier. ScienceDaily. Retrieved October 21, 2014 from www.sciencedaily.com/releases/2007/08/070828215611.htm
Johns Hopkins Medical Institutions. "'Mighty Mice' Made Mightier." ScienceDaily. www.sciencedaily.com/releases/2007/08/070828215611.htm (accessed October 21, 2014).

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