N to SP600125 endosomes and on release into the cell cytoplasm hen the production of reactive oxygen species by direct interaction with mitochondria obtained. Previous studies have suggested that intracellular Ang II exercise Re effects by binding to its receptors in various cytoplasmic organelles such as the nucleus. In fact, Ang is shown II to the intracellular Re calcium mobilization in renal proximal tubule cells and cell proliferation in the respiratory ChineseAs cause important eukaryocyte, k Closely can Ras / MEK / ERK cascade and JAK / STAT signaling cascade be used. In many cell types in culture, sustained expression of activated Ras effector or downstream can cause cell cycle arrest and differentiation, and some researchers have found that were the biological effects of the Ras / Raf / MEK / ERK is activated by a LIF / JAK / STAT pathway.
In LIF/gp130 induced cardiac BMS 794833 hypertrophy, AG490 and PD98059 were applied to compare the significance of ERK cascade and JAK / STAT cascade, and it has been shown that LIF-induced expression of Fos and other C was ma Decisively by PD98059 suppressed and m suppressed by pure AG490, but STAT3 activation was not suppressed by PD98059 and ERK1 / 2 activation was not suppressed by AG490. It was suggested that there The two canals from each independent le ngig are. In this study, the airway tissues of asthmatic rats by immunohistochemistry for LIF linked substance tested. Compared with the contr On it was observed for LIF-and NK-1R expression in rats with asthma increased ht Browsing, and Ver were similar Changes for p and p STAT3 ERK1 / 2.
The most important cell type was positive airway epithelial cells, and others were such as lymphocytes and structural observed. These results were comparable to data provided by Knight et al and Bai et al. Combining these results with the data mentioned above HNT, it is assumed that LIF NK verst 1R expression RKT in the airways of asthma models, and the improvement may be linked to the JAK STAT or the MAPK pathway. In addition, airway epithelial cells, the main cell type in the tats Be chlichen process. To test the hypothesis that cells cultured with LIF NHBE treated inhibitors of JAK / STAT and MAPK / ERK-cars and the activator showed the protein kinase C. This study suggests that the expression of LIF-induced NK 1R in NHBE cells by RT PCR and immunocytochemistry was determined.
In this process, Similar NK 1 R, the expressions of STAT3 and p ERK1 / 2 in NHBE cells treated with LIF all increased Ht. Expression of total STAT3 and ERK1 / 2 between LIF-treated cells and cells controlled They were not significantly different. AG490 and PD98059 abolished the LIF-induced expression of NK-1R. AG490 inhibited the LIF-induced phosphorylation of STAT3, w While PD98059 showed no inhibition on the contrary, PD98059 significantly inhibited the LIF-induced phosphorylation of ERK1 / 2, w While AG490 showed no inhibition. PMA, a potent activator of protein kinase C, will have as a strong effect of the activation of ERK1 / 2, and dependent Ngig Levels of related substances are still down in the team of ERK. Our study showed that compared to controls, increases the expression of PMA ht p ERK1 / 2 and NK-1R in NHBE cells, but there was no significant difference in input