Abstract:
:In a previous study, we found that calcitonin gene-related peptide (CGRP) could be induced by proinflammatory factor IL-1beta in A549 human type II alveolar (AEII) epithelial cells. We investigated the mechanism of IL-1beta-induced CGRP secretion and found that the PKC-p38 MAPK-NF-kappaB pathway was involved. In the present study, we found that IL-1beta stimulation induced c-Jun N-terminal kinase (JNK) activity within 15min in A549 cells. In investigating whether JNK was involved in IL-1beta-induced CGRP secretion, the JNK II inhibitor SP600125 was used and it significantly attenuated IL-1beta-induced CGRP secretion and c-Jun activity, which was elevated after IL-1beta stimulation from mRNA to protein level. EMSA results showed the activation of activator protein 1 (AP-1) after 2-h IL-1beta stimulation, and the JNK II inhibitor blocked c-Jun and AP-1 activity. Bioinformatic analysis showed five predicted AP-1 binding sites on the promoter of beta-CGRP; deletion analysis identified an AP-1 consensus site at -643bp relative to the initiation site, which mediates the beta-CGRP gene transcription in response to IL-1beta. These data suggest that besides the PKC-p38 MAPK-NF-kappaB pathway, the JNK-AP-1 pathway is involved in IL-1beta-induced CGRP secretion in A549 human type II alveolar epithelial cells, and a 643-bp site upstream of the transcription start site on the promoter of beta-CGRP is the AP-1 response element.
journal_name
Peptidesjournal_title
Peptidesauthors
Li W,Zheng S,Tang C,Zhu Y,Wang Xdoi
10.1016/j.peptides.2007.03.021subject
Has Abstractpub_date
2007-06-01 00:00:00pages
1252-9issue
6eissn
0196-9781issn
1873-5169pii
S0196-9781(07)00118-0journal_volume
28pub_type
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