3/6/98
CELLS FROM BONE MARROW CAN MAKE NEW MUSCLE
By Margaret Wahl, MDA Science Writer
Primitive cells that originate in bone marrow and circulate in blood can travel to damaged muscle and repair it, say scientists in Italy who published their findings in the March 6 issue of the journal Science. Their work is based in part on findings by Arnold Caplan of Case Western Reserve University in Cleveland. In 1996, Caplan, with MDA funding, identified bone-marrow-derived stem cells that are apparently capable of forming muscle.
The findings of the Italian group have at least three possible therapeutic implications, according to Caplan, who is a professor of biology and director of the Skeletal Research Center at Case Western Reserve. First, he says, people with muscular dystrophy might benefit from receiving donated bone marrow cells from close relatives who don't have any muscle disorder. Such cells would carry a full complement of muscle protein genes, including those lacking in muscular dystrophy patients. This type of strategy is already being tried in children with a genetic bone disorder, Caplan notes.
Caplan says another possibility to pursue is using a patient's own bone marrow cells, engineered to carry a new gene, to treat muscular dystrophy, in which an abnormal muscle protein gene leads to muscle loss. For example, children with Duchenne muscular dystrophy could have bone marrow cells extracted (normally done from the hip bone, using a large needle), engineered to carry a dystrophin gene in the laboratory, and then reinserted. Bone marrow cells can be reinserted by injecting them into the bloodstream; they don't have to be reinjected into bone.
A third possibility, and perhaps the most practical for the near future, would be to increase production of bone marrow cells that can lead to muscle without changing their genetic makeup. Since boys with Duchenne dystrophy generally walk until they're at least 7 or 8 years old, many researchers have speculated that, until this age, muscle regeneration outpaces degeneration despite the presence of an abnormal dystrophin gene. (A similar process probably occurs in other forms of muscular dystrophy, where the onset of severe weakness sometimes arrives after childhood, despite an abnormal gene's presence since birth.)
If it were possible to increase muscle regeneration, even if the genetic defect remained in place, you might significantly tip the balance toward muscle preservation and strength preservation, instead of muscle destruction and weakness, Caplan said.
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