Muscle wasting and interleukin-6-induced atrogin-I expression in the cachectic Apc ( Min/+ ) mouse.

Muscle wasting and interleukin-6-induced atrogin-I expression in the cachectic Apc ( Min/+ ) mouse.
复制标题

DOI:
10.1007/s00424-008-0574-6
复制
发表时间:
2009-03
影响因子:
4.5
通讯作者:
Carson, James A.
Carson, James A.
中科院分区:
医学3区
文献类型:
--
作者:
Baltgalvis, Kristen A.;Berger, Franklin G.;Pena, Maria Marjorette O.;Davis, J. Mark;White, James P.;Carson, James A.

文献摘要

参考文献

被引文献

相似文献

Interleukin-6 (IL-6) is necessary for cachexia in ApcMin/+ 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 ApcMin/+ mouse and to determine IL-6 regulated mechanisms contributing to muscle loss. Gastrocnemius type IIB mean fiber cross-sectional area (CSA) from ApcMin/+ mice decreased 32% between 13- and 22-wks of age. ApcMin/+ mice lacking IL-6 did not have type IIB fiber atrophy, while over-expression of circulating IL-6 exacerbated the loss of type IIB fiber CSA in ApcMin/+ mice. Muscle Atrogin-I mRNA expression was induced at least 9-fold at 18- and 22-wks of age compared to 13-wk-old mice. Atrogin-I gene expression was also induced by over-expression of circulating IL-6. These data suggest that high circulating IL-6 levels induce type IIB fiber CSA loss in ApcMin/+ mice, and circulating IL-6 is sufficient to regulate Atrogin-I gene expression in cachectic mice.
DOI: 10.1172/jci200420174
发表时间: 2004-08-01
影响因子: 15.9
作者:
Acharyya, S;Ladner, KJ;Guttridge, DC
通讯作者: Guttridge, DC
DOI: 10.1097/01.mco.0000078983.18774.cc
发表时间: 2003-07-01
影响因子: 3.1
作者:
Argilés, JM;Busquets, S;López-Soriano, FJ
通讯作者: López-Soriano, FJ
DOI: 10.1152/ajpcell.2001.280.3.c637
发表时间: 2001-03-01
影响因子: 5.5
作者:
Allen, DL;Harrison, BC;Leinwand, LA
通讯作者: Leinwand, LA
DOI: 10.1002/jgm.652
发表时间: 2005-02-01
影响因子: 3.5
作者:
Fattori, E;Cappelletti, M;La Monica, N
通讯作者: La Monica, N
DOI: 10.1158/0008-5472.can-04-2102
发表时间: 2004-11-15
期刊: CANCER RESEARCH
影响因子: 11.2
作者:
Kwak, KS;Zhou, XL;Han, HQ
通讯作者: Han, HQ