Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.5.4.4 (
adenosine deaminase
)
5,136
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The aim of the present study was to investigate the mechanisms regulating
endothelin-1
(
ET-1
) secretion in rat thyroid FRTL-5 cells.
ET-1
was found to be secreted after stimulation with adenosine and ATP. The release of
ET-1
was sensitive to pertussis toxin, indicating a role of G-proteins in the stimulus-secretion coupling. The stimulation evoked by ATP or adenosine was inhibited by the P1-receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), and in the presence of
adenosine deaminase
the adenosine- and ATP-mediated
ET-1
secretion was abolished. These evidences suggest a role of a P1-adenosine receptor in the secretion of
ET-1
. Increasing cyclic AMP with forskolin decreased the adenosine-mediated secretion. In addition, the intracellular calcium chelator BAPTA or inhibition of calcium entry with Ni2+ prevented the response. Protein kinase C (PKC) is also partly involved in
ET-1
secretion in FRTL-5 cells. Activation of PKC with the phorbol ester phorbol 12-myristate 13-acetate (PMA) stimulated the secretion of
ET-1
in a time- and dose-dependent manner. Furthermore, downregulation of PKC decreased the secretion of
ET-1
stimulated by adenosine. In conclusion,
ET-1
secretion in FRTL-5 cells is stimulated via a pertussis toxin-sensitive P1-receptor pathway which is modulated by several signal transduction mechanisms including cAMP, Ca2+, and PKC.
...
PMID:Purinergic agonists stimulate the secretion of endothelin-1 in rat thyroid FRTL-5 cells. 895 3
