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Evidence for, and characterization of, a lipopolysaccharide‐inducible adenosine A2 receptor in human tracheal gland serous cells
Author(s) -
Merten M.D.,
Kammouni W.,
Figarella C.
Publication year - 1995
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(95)00748-x
Subject(s) - adenosine , purinergic signalling , adenosine a2b receptor , adenosine receptor , medicine , endocrinology , purinergic receptor , adenosine a1 receptor , adenylyl cyclase , secretion , stimulation , adenosine a3 receptor , biology , chemistry , receptor , microbiology and biotechnology , agonist
Human tracheal glands are considered as the principle secretory structures in the bronchotracheal tree. In earlier studies, we successfully performed primary cultures of human tracheal gland (HTG) serous cells and noted that these cells were responsive to many secretagogues including purinergic agonists but not to the inflammatory mediator adenosine. In this study, we demonstrate that adenosine was capable of inducing stimulation of protein secretion by HTG serous cells which had previously been cultured in pro‐inflammatory conditions (induced by lipopolysaccharide (LPS)). This stimulation was inhibited by 8‐phenyltheophylline but not by dipyridamole, which is indicative of a P1 purinoceptor. This inducible receptor is of the adenosine A2 subtype [rank potency order: 5′‐( N ‐ethyl)‐carboxamidoadenosine (NECA) > adenosine > N 6 ‐(phenylisopropyl)‐adenosine (PIA); and stimulation of adenylyl cyclase]. The adenosine‐induced protein secretion was concentration‐dependent, however, increased intracellular cyclic adenosine monophosphate (cAMP) was not dependent on the concentration of adenosine. The adenosine‐induced secretion and the ATP‐induced secretion were shown to be additive. This study concludes that there is evidence of a LPS‐inducible adenosine A2 receptor in human tracheal gland serous cells.