These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Up-regulation of bradykinin receptors in a murine in-vitro model of chronic airway inflammation.
    Author: Zhang Y, Adner M, Cardell LO.
    Journal: Eur J Pharmacol; 2004 Apr 05; 489(1-2):117-26. PubMed ID: 15063163.
    Abstract:
    Tumour necrosis factor-alpha (TNF-alpha) is a mediator with a likely role in chronic airway inflammation and airway hyperresponsiveness. In the present study, mouse tracheal segments were cultured for 1, 4 or 8 days in the absence and presence of TNF-alpha. Contractile response of cultured segments to des-Arg9-bradykinin and bradykinin was assessed in myographs and mRNA for bradykinin B1 and B2 receptors was quantified by real-time polymerase chain reaction. Both contraction to des-Arg9-bradykinin and bradykinin, mediated via bradykinin B1 and B2 receptors, respectively, and mRNA levels for these receptors were up-regulated following culture. These responses were markedly increased in segments treated with TNF-alpha. Experiments with SP600125 (anthrax(1,9-cd)pyrazol-6(2H)-one) and PD98059 (2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one) demonstrated that both intracellular c-Jun N-terminal kinase and extracellular signal-regulated kinase 1/2 pathways were implicated in this process. Thus, TNF-alpha causes an increase of bradykinin contractility in mouse trachea, which at least partly is due to a transcriptional increase of bradykinin receptors.
    [Abstract] [Full Text] [Related] [New Search]