Abstract:
: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 hyperosmotic 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.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Tilly BC,Gaestel M,Engel K,Edixhoven MJ,de Jonge HRdoi
10.1016/0014-5793(96)01028-9subject
Has Abstractpub_date
1996-10-21 00:00:00pages
133-6issue
2-3eissn
0014-5793issn
1873-3468pii
0014-5793(96)01028-9journal_volume
395pub_type
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