MAPK in canine tracheal smooth muscle cells - PubMed (original) (raw)

Tumour necrosis factor-alpha enhances bradykinin-induced signal transduction via activation of Ras/Raf/MEK/MAPK in canine tracheal smooth muscle cells

Y M Hsu et al. Cell Signal. 2001 Sep.

Abstract

Inhalation of tumour necrosis factor-alpha (TNF-alpha) induced a bronchial hyperreactivity to contractile agonists. However, the mechanisms of TNF-alpha involved in the pathogenesis of bronchial hyperreactivity were not completely understood. Therefore, we investigated the effect of TNF-alpha on bradykinin (BK)-induced inositol phosphate (IP) accumulation and Ca(2+) mobilization, and up-regulation of BK receptor density in canine cultured tracheal smooth muscle cells (TSMCs). Pretreatment of TSMCs with TNF-alpha potentiated BK-induced IP accumulation and Ca(2+) mobilization. However, there was no effect on the IP response induced by endothelin-1 (ET-1), 5-hydroxytryptamine (5-HT), and carbachol. Pretreatment with PDGF B-chain homodimer (PDGF-BB) also enhanced BK-induced IP response. These enhancements induced by TNF-alpha and PDGF-BB might be due to an increase in BK B(2) receptor density (B(max)), since [3H]BK binding to TSMCs was inhibited by the B(2) selective agonist and antagonist, BK and Hoe 140, but not by the B(1) selective reagents. The enhancing effects of TNF-alpha and PDGF-BB were attenuated by PD98059 (an inhibitor of activation of MAPK kinase, MEK) and cycloheximide (an inhibitor of protein synthesis), suggesting that TNF-alpha may share a common signalling pathway with PDGF-BB via protein(s) synthesis in TSMCs. Furthermore, overexpression of dominant negative mutants, H-Ras-15A and Raf-N4, significantly suppressed p42/p44 mitogen-activated protein kinase (MAPK) activation induced by TNF-alpha and PDGF-BB and attenuated the effect of TNF-alpha on BK-induced IP response, indicating that Ras and Raf may be required for activation of these kinases. These results suggest that the augmentation of BK-induced responses produced by TNF-alpha might be, at least in part, mediated through activation of Ras/Raf/MEK/MAPK pathway in TSMCs.

PubMed Disclaimer

Cited by

The kinin system--bradykinin: biological effects and clinical implications. Multiple role of the kinin system--bradykinin.
Golias Ch, Charalabopoulos A, Stagikas D, Charalabopoulos K, Batistatou A. Golias Ch, et al. Hippokratia. 2007 Jul;11(3):124-8. Hippokratia. 2007. PMID: 19582206 Free PMC article.
Expression and activation of the oxytocin receptor in airway smooth muscle cells: Regulation by TNFalpha and IL-13.
Amrani Y, Syed F, Huang C, Li K, Liu V, Jain D, Keslacy S, Sims MW, Baidouri H, Cooper PR, Zhao H, Siddiqui S, Brightling CE, Griswold D, Li L, Panettieri RA Jr. Amrani Y, et al. Respir Res. 2010 Jul 29;11(1):104. doi: 10.1186/1465-9921-11-104. Respir Res. 2010. PMID: 20670427 Free PMC article.
A review on bradykinin-related peptides isolated from amphibian skin secretion.
Xi X, Li B, Chen T, Kwok HF. Xi X, et al. Toxins (Basel). 2015 Mar 18;7(3):951-70. doi: 10.3390/toxins7030951. Toxins (Basel). 2015. PMID: 25793726 Free PMC article. Review.
LINC01225 promotes occurrence and metastasis of hepatocellular carcinoma in an epidermal growth factor receptor-dependent pathway.
Wang X, Zhang W, Tang J, Huang R, Li J, Xu D, Xie Y, Jiang R, Deng L, Zhang X, Chai Y, Qin X, Sun B. Wang X, et al. Cell Death Dis. 2016 Mar 3;7(3):e2130. doi: 10.1038/cddis.2016.26. Cell Death Dis. 2016. PMID: 26938303 Free PMC article. Clinical Trial.
Airway smooth muscle in asthma: just a target for bronchodilation?
Black JL, Panettieri RA Jr, Banerjee A, Berger P. Black JL, et al. Clin Chest Med. 2012 Sep;33(3):543-58. doi: 10.1016/j.ccm.2012.05.002. Epub 2012 Jul 11. Clin Chest Med. 2012. PMID: 22929101 Free PMC article. Review.

Tumour necrosis factor-alpha enhances bradykinin-induced signal transduction via activation of Ras/Raf/MEK/MAPK in canine tracheal smooth muscle cells - PubMed (original) (raw)