当前位置： SCI文献检索 > CELLULAR SIGNALLING期刊下所有文献 > ERK1/2 and p38-MAPK signalling pathways, through MSK1, are involved in NF-kappaB transactivation during oxidative stress in skeletal myoblasts.

ERK1/2 and p38-MAPK signalling pathways, through MSK1, are involved in NF-kappaB transactivation during oxidative stress in skeletal myoblasts.

Abstract：

:Skeletal muscle is highly adapted to respond to oxidative imbalances, since it is continuously subjected to an increased production of reactive oxygen species (ROS) during exercise. Oxidative stress, however, has been associated with skeletal muscle atrophy and damage in many diseases. In this study, we examined whether MAPK and NF-kappaB pathways participate in the response of skeletal myoblasts to oxidative stress, and whether there is a cross talk between these pathways. H(2)O(2) induced a strong activation of ERKs, JNKs and p38-MAPK in a time- and dose-dependent profile. ERK and JNK activation by H(2)O(2), but not that of p38-MAPK, was mediated by Src kinase and, at least in part, by EGFR. H(2)O(2) also stimulated a mild translocation of NF-kappaB to the nucleus, as well as a moderate phosphorylation of its endogenous cytoplasmic inhibitor IkappaB (at Ser32/36), without any significant decrease in IkappaB total levels. Moreover, oxidative stress induced a strong phosphorylation of NF-kappaB p65 subunit at Ser536 and Ser276. Inhibition of MAPK pathways by selective inhibitors did not appear to affect H(2)O(2)-induced nuclear translocation of NF-kappaB or the phosphorylation of IkappaB. In contrast, phosphorylation of p65 at Ser276 was found to be mediated by MSK1, a substrate of both ERKs and p38-MAPK. In conclusion, it seems that, during oxidative stress, NF-kappaB translocation to the nucleus is most likely not related with the MAPK activation, while p65 phosphorylations are in part mediated by MAPKs pathways, probably modifying signal specificity.

journal_name

Cell Signal

journal_title

Cellular signalling

authors

Kefaloyianni E,Gaitanaki C,Beis I

doi

10.1016/j.cellsig.2006.05.004

subject

Has Abstract

pub_date

2006-12-01 00:00:00

pages

2238-51

issue

12

eissn

0898-6568

issn

1873-3913

pii

S0898-6568(06)00110-0

journal_volume

18

pub_type

杂志文章

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