| First Author | Zhang W | Year | 2019 |
| Journal | Biochem Biophys Res Commun | Volume | 516 |
| Issue | 2 | Pages | 571-577 |
| PubMed ID | 31235256 | Mgi Jnum | J:291236 |
| Mgi Id | MGI:6443200 | Doi | 10.1016/j.bbrc.2019.06.072 |
| Citation | Zhang W, et al. (2019) Rho-kinase inhibitor attenuates airway mucus hypersecretion and inflammation partly by downregulation of IL-13 and the JNK1/2-AP1 signaling pathway. Biochem Biophys Res Commun 516(2):571-577 |
| abstractText | We measured the effect of Rho-kinase on inflammation and mucus hypersecretion in the airways of mouse models of asthma. Additionally, we aimed to determine if these effects were the result of JNK 1/2-AP1 pathway inhibition.We sensitized and challenged female C57BL/6 mice using house dust mites (HDM) followed by treatment with an inhibitor of Rho-kinase. Lung tissue was harvested to evaluate inflammation and mucus secretion in the airways of asthma mice. Cytokine expression in broncho-alveolar lavage fluid (BALF) was established by ELISA and airway responsiveness, and was determined by the invasive lung function test. JNK1/2, p-JNK1/2, AP-1, and p-AP-1 protein expression was determined by Western blot analysis. Asthma model mice that were treated with Rho-kinase inhibitor showed a significantly decrease in inflammation score, inflammatory cells, and airway responsiveness. Additionally, we found that IL-13 expressions in BALF and mucus secretion were decreased in HDM-challenged mice treated with Rho-kinase inhibitor. Furthermore, Rho-kinase inhibitor treatment decreased the expression of JNK1/2 and AP-1 phosphorylation. Our findings indicated that the Rho-kinase inhibitor decreased HDM-induced mucus secretion as well as airway inflammation in asthma mice through regulation of the JNK1/2-AP-1 pathway. |
