Regulation of kinin receptors in airway epithelial cells by inflammatory cytokines and dexamethasone
UNSPECIFIED (2002) Regulation of kinin receptors in airway epithelial cells by inflammatory cytokines and dexamethasone. EUROPEAN JOURNAL OF PHARMACOLOGY, 441 (3). pp. 193-202. ISSN 0014-2999Full text not available from this repository.
The two kinin receptors, B-1 and B-2, are upregulated in inflammation and may play a role in diseases such as asthma. In pulmonary A549 cells, TNF-alpha or interleukin-1beta dramatically increased bradykinin B-1 and B-2 receptor mRNA expression and this response was prevented by dexamethasone. In primary human bronchial epithelial cells, bradykinin B-1 receptor mRNA expression showed a similar trend, whereas bradykinin B-2 receptor showed almost constitutive expression. Radioligand-binding studies revealed significant increases in bradykinin B-1 receptor protein expression following both interleukin-1beta and TNF-alpha treatment of A549 cells; however, no evidence was found for bradykinin B-1 receptor. Functionally, the bradykinin B-2 receptor ligand, bradykinin, but not the B-1 ligand, des-Arg(10)-kallidin, produced a marked increase in prostaglandin E-2 release when administered following interleukin-1beta treatment. Arachidonic acid release in response to bradykinin was markedly enhanced by prior incubation with interleukin-1beta and this was prevented by the prior addition of dexamethasone. (C) 2002 Elsevier Science B.V. All rights reserved.
|Item Type:||Journal Article|
|Subjects:||R Medicine > RS Pharmacy and materia medica|
|Journal or Publication Title:||EUROPEAN JOURNAL OF PHARMACOLOGY|
|Publisher:||ELSEVIER SCIENCE BV|
|Date:||26 April 2002|
|Number of Pages:||10|
|Page Range:||pp. 193-202|
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