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- W2131104865 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." @default.
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- W2131104865 date "2001-09-01" @default.
- W2131104865 modified "2023-10-17" @default.
- W2131104865 title "Osmotic Stress Induces HB-EGF Gene Expression via Ca2+/Pyk2/JNK Signal Cascades in Rat Aortic Smooth Muscle Cells" @default.
- W2131104865 doi "https://doi.org/10.1093/oxfordjournals.jbchem.a002993" @default.
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