Abstract:
:The present study was undertaken in an attempt to clarify the pathway by which hyperosmotic stress induces HB-EGF gene expression in rat aortic smooth muscle cells (RASMC). Hyperosmotic stress induced by a high concentration of glucose or mannitol resulted in an increase in HB-EGF mRNA level in a dose- and time-dependent manner. HB-EGF induction was blocked by curcumin, a c-jun/fos antisense oligonucleotide and a dominant-negative mutant of JNK1. Electrophoretic mobility shift assay also showed the involvement of AP-1 in HB-EGF gene expression by glucose. In addition, hyperosmotic stress induced rapid phosphorylation of Pyk2 in RASMC. TPA and calcium chelating agents (BAPTA-AM and EGTA) blocked Pyk2 phosphorylation and HB-EGF gene expression. Furthermore, HB-EGF gene expression and JNK activation by hyperosmotic stress were sensitive to PP2, an Src kinase-specific inhibitor. These findings indicate that hyperosmotic stress activates JNK via calcium-Pyk2 signaling cascades, which in turn induce HB-EGF gene expression.
journal_name
J Biochemjournal_title
Journal of biochemistryauthors
Koh YH,Che W,Higashiyama S,Takahashi M,Miyamoto Y,Suzuki K,Taniguchi Ndoi
10.1093/oxfordjournals.jbchem.a002993keywords:
subject
Has Abstractpub_date
2001-09-01 00:00:00pages
351-8issue
3eissn
0021-924Xissn
1756-2651journal_volume
130pub_type
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