| Literature DB >> 27866297 |
Jae-Won Lee1, Ji-Won Park1, Ok-Kyoung Kwon1,2, Hee Jae Lee3, Hye Gwang Jeong2, Jae-Hong Kim4, Sei-Ryang Oh5, Kyoung-Seop Ahn6.
Abstract
Mucus overproduction is a fundamental hallmark of COPD that is caused by exposure to cigarette smoke. MUC5AC is one of the main mucin genes expressed in the respiratory epithelium, and its transcriptional upregulation often correlates with increased mucus secretion. Calcium-sensing receptor (CaSR) antagonists have been reported to possess anti-inflammatory effects. The purpose of the present study was to investigate the protective role of NPS2143, a selective CaSR antagonist on cigarette smoke extract (CSE)-stimulated NCI-H292 mucoepidermoid human lung cells. Treatment of NPS2143 significantly inhibited the expression of MUC5AC in CSE-stimulated H292 cells. NPS2143 reduced the expression of MMP-9 in CSE-stimulated H292 cells. NPS2143 also decreased the release of proinflammatory cytokines such as IL-6 and TNF-α in CSE-stimulated H292 cells. Furthermore, NPS2143 attenuated the activation of MAPKs (JNK, p38, and ERK) and inhibited the nuclear translocation of NF-κB in CSE-stimulated H292 cells. These results indicate that NPS2143 had a therapeutic potential in COPD.Entities:
Keywords: MAPKs; MUC5AC; NF-κB; NPS2143; chronic obstructive pulmonary disease; cigarette smoke
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Year: 2017 PMID： 27866297 DOI： 10.1007/s10753-016-0468-2
Source DB: PubMed Journal: Inflammation ISSN： 0360-3997 Impact factor: 4.092