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Hypo‐osmotic cell swelling activates the p38 MAP kinase signalling cascade
Author(s) -
Tilly Ben C,
Gaestel Matthias,
Engel Katrin,
Edixhoven Marcel J,
de Jonge Hugo R
Publication year - 1996
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(96)01028-9
Subject(s) - p38 mitogen activated protein kinases , mitogen activated protein kinase , microbiology and biotechnology , osmotic shock , chemistry , kinase , protein kinase a , biophysics , biochemistry , biology , gene
Hypo‐osmotic swelling of human Intestine 407 cells leads to a significant increase of intracellular MAPKAP‐kinase 2 activity and Hsp27 phosphorylation. Pre‐treatment of the cells with the p38 MAP kinase inhibitor SB‐203580 blocks this activation, indicating that the hypotonicity‐induced activation of MAPKAP kinase 2 is, similarly to that described for hyper‐osmotic treatment, the result of an activated p38 MAP kinase cascade. The activation of MAPKAP kinase 2 proceeds with kinetics similar to that of one of the first physiological responses of hypo‐osmotic treatment, the opening of compensatory Cl − channels. However, inhibition of the p38 MAP kinase cascade does not block the osmo‐sensitive anion efflux and, vice versa, activation of p38 MAP kinase by cytokines and anisomycin does not increase the efflux. These results indicate that the p38 MAP kinase cascade is not directly involved in Cl − channel activation but instead may play a role in subsequent cellular repair processes.

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