Massachusetts General Hospital researchers report that thecytoskeletal protein gelsolin directly affects cell movement andmay have a role in wound healing.
Dr. C. Casey Cunningham and his co-workers, writing in Sciencemagazine on Friday, showed that introducing a human gelsolingene into mouse fibroblasts enhanced the ability of these cellsto migrate and to close a wound made in a cell culture model.
Cunningham told BioWorld that understanding how gelsolinbreaks down and rebuilds actin polymers in a cell'scytoskeleton may lead to methods to improve wound healingand to prevent the spread of cancer cells. However, hecautioned that the research will only have practicalimplications if scientists can determine how to turn gelsolinexpression on and off.
He sees this research as beginning to answer the question ofhow cells migrate to carry out wound healing or to spreadcancer. Such knowledge will enable researchers to intelligentlymanipulate the system and to avoid the pitfalls of just adding aprotein to effect a cure.
Many companies, including Amgen Inc., CaliforniaBiotechnology Inc., Celtrix Laboratories Inc., Chiron Corp.,Creative Biomolecules Inc. (CBM) and Synergen, are developingwound-healing therapeutics.
Gelsolin may provide another way for researchers to study howdrugs or growth factors affect cell growth and migration, saidCBM President Charlie Cohen.
SCIENTISTS HOME IN ON FRAGILE X DEFECT
Researchers are zeroing in on the gene responsible for fragile Xsyndrome, which causes the most common inherited form ofmental retardation.
Fragile X syndrome, which affects one in every 1,500 males,causes X chromosomes to break easily. The breakage causesmental retardation in most affected individuals.
A team of French, Italian and American scientists reported inFriday's issue of Science the identification of a site on the Xchromosome that may pinpoint the gene(s) causing the disease.If they are right, DNA probes from this region may be used todiagnose the disease.
Thirteen labs currently test for fragile X syndrome, usingrestriction fragment length polymorphism assays. But suchassays are often not sensitive enough to distinguish betweenaffected and normal individuals, said Dr. Ray Fenwick at BaylorCollege of Medicine. He added that a number of labs are in therace to identify the fragile X gene. -- CTV
-- Carol Talkington Verser, Ph.D. Special to BioWorld
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