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Hair loss syndrome created in mice

n might explain variability in human keratin diseases."

In mice that kept their hair in the absence of K17, a related molecule, keratin 16 (K16), took up the slack, the scientists found. "Mice that lost hair failed to compensate for K17; K16 didn't step in," says Coulombe, a researcher in the school's Institute for Basic Biomedical Sciences. "What triggers K16 to make up for K17 in certain mice and not in others? The answer is going to be more complex than K16 itself."

The findings raise the possibility that proposed gene therapy for keratin-related diseases, or potentially others, could be less precise in their application than expected, says Coulombe.

"People talk about gene therapy as 'molecular genomic surgery,' as going in to the genetic information and slicing out what's wrong and inserting a corrected version," he explains. "But this study shows we may not need to be so sophisticated. For K17 diseases, for instance, perhaps it would be possible to identify and increase production of a compensatory keratin, without causing negative effects, and alleviate the condition."

In the original group of mice, each a cross of strains 129/Sv and C57Bl/6, animals were born with normal hair. By 5 days of age, some of the mice lacking K17 failed to grow their first round of postnatal hair. By three weeks of age, however, when the second cycle of hair production in mice begins, even the most severely affected mice re-grew hair and appeared normal.

In subsequent experiments, the scientists discovered that pure 129/Sv mice were not affected by the loss of K17, while pure C57Bl/6 mice lost all their hair. The 129/Sv mice somehow stimulated K16 to make up for the lack of K17, they found.

The results also help reveal K17's role in hair follicles in mice. Hair loss was due primarily to two flaws caused by the lack of K17: weaker strands of hair and a propensity for a key part of the hair follicle to die. Because all mice re-grew ha
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Contact: Joanna Downer
jdowner1@jhmi.edu
410-614-5105
Johns Hopkins Medical Institutions
14-Jun-2002


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