Interleukin-13-induced activation of signal transducer and activator of transcription 6 is mediated by an activation of Janus kinase 1 in cultured human bronchial smooth muscle cells

• Published in: Pharmacological reports 2012, Vol.64 (2), p.454-458
• Main Authors: Yoshihiko, Chiba, Kumiko, Goto, Miwa, Misawa
• Format: Article
• Language: English
• Subjects: Bronchi - cytology; Bronchi - drug effects; Bronchi - immunology; Bronchi - metabolism; Bronchial Hyperreactivity - immunology; Bronchial Hyperreactivity - metabolism; bronchial smooth muscle cells; Cells, Cultured; Drug Safety and Pharmacovigilance; Enzyme Activation; Humans; interleukin-13 (IL-13); Interleukin-13 - pharmacology; Interleukin-13 - physiology; Janus kinase (JAK); Janus Kinase 1 - antagonists & inhibitors; Janus Kinase 1 - metabolism; Muscle, Smooth - cytology; Muscle, Smooth - drug effects; Muscle, Smooth - immunology; Muscle, Smooth - metabolism; Pharmacotherapy; Pharmacy; Phosphorylation; Protein Kinase Inhibitors - pharmacology; Short Communication; signal transducer and activator of transcription 6 (STAT6); STAT6 Transcription Factor - metabolism
• ISSN: 1734-1140; 2299-5684
• DOI: 10.1016/S1734-1140(12)70788-0

The current study was carried out to identify the JAK molecule(s) that is involved in the IL-13-induced activation of STAT6 in cultured human bronchial smooth muscle cells (hBSMCs). Cultured hBSMCs were stimulated with IL-13 in the absence and presence of JAK inhibitor-I (a nonspecific JAKs inhibitor), tyrphostin-AG490 (a specific JAK2 inhibitor), WHI-P131 (a specific JAK3 inhibitor), or tyrphostin-AG9 (a specific Tyk2 inhibitor), and levels of phosphorylated STAT6 were measured by immunoblot analyses. The IL-13-induced phosphorylation of STAT6 was abolished by JAK inhibitor-I, whereas the other inhibitors had no significant effect. These findings indicate that the STAT6 phosphorylation/activation induced by IL-13 is mediated by an activation of JAK1 in cultured hBSMCs.