Authors: Kristen A Baltgalvis Franklin G Berger Maria Marjorette O Peña J Mark Davis James P White James A Carson
Publish Date: 2008/08/19
Volume: 457, Issue: 5, Pages: 989-1001
Abstract
Interleukin6 IL6 is necessary for cachexia in Apc Min/+ mice but the mechanisms inducing this myofiber wasting have not been established The purpose of this study was to examine gastrocnemius muscle wasting in the Apc Min/+ mouse and to determine IL6 regulated mechanisms contributing to muscle loss Gastrocnemius type IIB mean fiber crosssectional area CSA from Apc Min/+ mice decreased 32 between 13 and 22 weeks of age Apc Min/+ mice lacking IL6 did not have type IIB fiber atrophy while overexpression of circulating IL6 exacerbated the loss of type IIB fiber CSA in Apc Min/+ mice Muscle AtroginI mRNA expression was induced at least ninefold at 18 and 22 weeks of age compared to 13weekold mice AtroginI gene expression was also induced by overexpression of circulating IL6 These data suggest that high circulating IL6 levels induce type IIB fiber CSA loss in Apc Min/+ mice and circulating IL6 is sufficient to regulate AtroginI gene expression in cachectic miceThe authors would like to thank Tia Davis Joseph McClung and April Wilson for technical assistance The research described in this report was supported by the National Institutes of Health NIH Grant P20 RR017698 from the National Center for Research Resources Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the NIH
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