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Papers In Press, published online ahead of print May 22, 2002
Department of Biochemistry II, Nagoya University School of Medicine, Nagoya 466-0065
Corresponding Author: koichi{at}med.nagoya-u.ac.jp
We established a double knock-out mice of GM2/GD2 synthase gene and GD3 synthase gene by mating single gene mutants, and analyzed the abnormal phenotypes of the mutant mice expressing only GM3 ganglioside. We observed a refractory skin lesion which took place mainly on the face of the mutant mice at 25 weeks or later after birth. Frequent scratching movement toward the wound sites was observed in the mutant mice with the skin injury, suggesting it is a triggering factor to exacerbate the injury. This was confirmed by accommodating mice into special cages for metabolic study, in which the skin injury developed more rapidly. Characteristic proliferation of nerve fibers was found in epidermis and sub-epidermis of the mutants at injured sites, probably as a result of continuous skin injury. Peripheral nerve degeneration was observed in young mutant mice, suggesting that reduced sensory function induced over-scratching and the skin lesion. The facts that the sensory function to mechanical stimuli reduced, while that to hot stimuli rather increased in the mutant mice supported the interpretation. Thus, only GM3-expressing mice showed important roles of gangliosides in maintaining skin integrity via the regulation of the peripheral nerves.
J. Biol. Chem, 10.1074/jbc.M201631200
Submitted on February 18, 2002
Revised on May 14, 2002
Accepted on May 21, 2002
Refractory skin injury in the complex knock-out mice expressing only GM3 ganglioside
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