You are here:
DIESEL EXHAUST PARTICULATE (DEP)-INDUCED ACTIV ATION OF STAT3 REQUIRES ACTIVITIES OF EGFR AND SRC IN AIRWAY EPITHELIAL CELLS
Citation:
CAO, D., T. TAL, L. M. GRAVES, IAN I. GILMOUR, W. P. LINAK, W. REED, P. BROMBERG, AND J. M. SAMET. DIESEL EXHAUST PARTICULATE (DEP)-INDUCED ACTIV ATION OF STAT3 REQUIRES ACTIVITIES OF EGFR AND SRC IN AIRWAY EPITHELIAL CELLS. American Journal of Physiology - Lung Cellular and Molecular Physiology. American Physiological Society, Bethesda, MD, 292(2):L422-L429, (2007).
Description:
In vivo exposure to diesel exhaust particles (DEP) elicits acute inflammatory responses in the lung characterized by inflammatory cell influx and elevated expression of mediators such as cytokines, and chemokines. Signal transducers and activators of transcription (STAT) proteins provide signals in response to cytokine and growth factor stimulation. One member of the STAT family, Stat3, has been implicated as a regulator of inflammation, but has not been studied in regard to DEP exposure. The results of this study show that DEP induces Stat3 phosphorylation as early as one hour following stimulation, and that phosphorylated Stat3 translocated into the nucleus. Inhibition of epidermal growth factor receptor (EFGR) and Src activities by inhibitors PD153035 and PP2 abolished the activation of Stat3 by DEP, suggesting that Stat3 activation by DEP requires EGFR and SRC kinase activation.