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Induction of interleukin‐8 by ozone is mediated by tyrosine kinase and protein kinase A, but not by protein kinase C
Author(s) -
Jaspers Ilona,
Chen Lung Chi,
Flescher Eliezer
Publication year - 1998
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/(sici)1097-4652(199811)177:2<313::aid-jcp13>3.0.co;2-a
Subject(s) - cyclin dependent kinase 2 , mitogen activated protein kinase kinase , cyclin dependent kinase 9 , map2k7 , protein kinase a , ask1 , tyrosine kinase , map kinase kinase kinase , chemistry , protein kinase r , c raf , kinase , microbiology and biotechnology , biochemistry , biology , signal transduction
Ozone is one of the most common air pollutants humans routinely inhale. We have previously shown that in vitro ozone exposure induces the DNA‐binding activities of NF‐ κ B and NF‐IL6 as well as the expression of interleukin 8 in respiratory epithelial cells. In this study, we investigated intracellular signaling steps mediating ozone‐induced inflammatory mediator release. A549 cells, a type II like alveolar epithelial cell line, were exposed in vitro to air or 0.1 ppm of ozone in the presence of several kinase inhibitors. Exposure to ozone increased interleukin 8 expression and transcription factor activities in a protein tyrosine kinase (PTK)‐dependent and protein kinase A (PKA)‐dependent, yet protein kinase C (PKC)‐independent, manner. Furthermore, ozone‐induced PTK and PKA activities but failed to induce PKC activity. In addition, our results suggest that ozone‐induced PTK and PKA activities were reactive oxygen intermediate dependent and occurred in parallel, because specific inhibitors for PTK and PKA failed to block the other kinase's activity. These results indicate that PTK and PKA activities are early events in the signal transduction cascade mediating the ozone‐induced activation of NF‐ κ B and NF‐IL6 as well as the release of interleukin 8. J. Cell. Physiol. 177:313–323, 1998. © 1998 Wiley‐Liss, Inc.