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Protective induction of Hsp70 in heat‐stressed primary myoblasts: Involvement of MAPKs
Author(s) -
Bironaite Daiva,
Brunk Ulf,
Venalis Algirdas
Publication year - 2013
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.24550
Subject(s) - p38 mitogen activated protein kinases , hsp70 , kinase , microbiology and biotechnology , heat shock , mitogen activated protein kinase , chemistry , myocyte , heat shock protein , stem cell , stem cell factor , protein kinase a , biology , biochemistry , progenitor cell , gene
The involvement of extracellular signal‐regulated kinases 1 and 2 (ERK1,2), stress kinase p38 and c‐Jun NH 2 ‐terminal kinases 1 and 2 (JNK1,2) on Hsp70‐upregulation following mild heat shock, and resulting cell protection, was studied on rabbit primary myoblasts. Cells subjected to heat stress (42°C; 60 min) showed a significantly enhanced amount of heat‐shock‐induced protein 70 (Hsp70), correlating with sustained phosphorylation of MAP kinases ERK1,2, inhibition of p38 and JNK1,2 activation. Induced Hsp70 did not autocrinally suppress activation of transcription factor c‐Jun, suggesting involvement of the latter in the protection of myoblasts following heat shock. The inhibition of stress kinases p38, JNK1,2, and MEK1,2 by SP600125, SB203580, and UO126, respectively, established the involvement of JNK1,2 and p38 as upstream, and ERK1,2 as downstream targets of Hsp70 induction. Moreover, the effect of the MEK1,2 inhibitor UO126 revealed a new pathway of c‐Jun activation by ERK1,2 in myogenic heat‐stressed stem cells. The presented data show that transient activation of JNK1, JNK2, and p38 is necessary for Hsp70 induction and ensuing cell protection. In conclusion, affecting myogenic stem cell protective mechanisms might be a useful strategy in improving stem cell survival and their expanded application in therapy. J. Cell. Biochem. 114: 2024–2031, 2013. © 2013 Wiley Periodicals, Inc.