Diesel exhaust particulate-induced activation of Stat3 requires activities of EGFR and Src in airway epithelial cells
2007
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 are a family of cytoplasmic transcription factors that are key transducers of signaling 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 1 h following stimulation and that phosphorylated Stat3 translocates into the nucleus. Inhibition of epidermal growth factor receptor (EGFR) and Src activities by the inhibitors PD-153035 and PP2, respectively, abolished the activation of Stat3 by DEP, suggesting that Stat3 activation by DEP requires EGFR and Src kinase activation. The present study suggests that oxidativ...
Keywords:
- Transcription factor
- Cell biology
- Proto-oncogene tyrosine-protein kinase Src
- STAT3
- stat
- Growth factor
- Chemokine
- Epidermal growth factor receptor
- Biology
- Cytokine
- Biochemistry
- Endocrinology
- Internal medicine
- Respiratory tract
- Diesel exhaust
- Diesel Exhaust Particulate
- In vivo
- Cancer research
- Immunology
- Reactive oxygen species
- Epithelium
- Correction
- Source
- Cite
- Save
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