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LIF upregulates expression of NK-1R in NHBE cells.

Authors: Hu, CP  Feng, JT  Tang, YL  Zhu, JQ  Lin, MJ  Yu, ME 
Citation: Hu CP, etal., Mediators Inflamm. 2006;2006(5):84829.
Pubmed: (View Article at PubMed) PMID:17392578
DOI: Full-text: DOI:10.1155/MI/2006/84829

Leukemia inhibitory factor (LIF), a cytokine at the interface between neurobiology and immunology, is mainly mediated through JAK/STAT pathway and MAPK/ERK pathway. Evidence suggested LIF is related to the higher expression of neurokinin-1 receptor (NK-1R) in asthma. In this study, the immunohistochemistry stain showed the expressions of NK-1R, LIF, p-STAT3, and p-ERK1/2 in the lung tissues of allergic rats were increased compared with the controls, and the main positive cell type was airway epithelial cell. Normal human bronchial epithelial cells were treated with LIF in the presence or absence of AG490 (JAK2 inhibitor), PD98059 (MEK inhibitor), and the siRNA against STAT3. Western blot and RT-PCR indicated that LIF induced the expression of NK-1R, which was inhibited by the inhibitors mentioned above. No significant interaction was found between JAK/STAT pathway and MAPK/ERK pathway. In summary, bronchial epithelial cell changes in asthma are induced by LIF which promotes the expression of NK-1R, and JAK/STAT pathway and MAPK/ERK pathway may participate in this process.

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CRRD Object Information
CRRD ID: 2304339
Created: 2009-03-13
Species: All species
Last Modified: 2009-03-13
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.