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Secretin Regulates the Expression of the Renin‐Angiotensin System in Rat Cardiac Fibroblasts
Author(s) -
Afroze Syeda,
Nizamutdinov Damir,
Feng Hao,
Gerilechaogetu Fnu,
Jensen Kendal,
Munshi MK,
Golden Honey,
Dostal David,
Alpini Gianfranco,
Glaser Shan
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1134.10
Subject(s) - endocrinology , medicine , adenylyl cyclase , renin–angiotensin system , secretin , intracellular , angiotensin ii , fibroblast , receptor , chemistry , biology , secretion , cell culture , microbiology and biotechnology , blood pressure , genetics
Secretin (SCT) is a peptide hormone produced mainly by the S cells of the duodenum that exerts its biological effects through the G‐protein coupled secretin receptor (SCTR). Studies have indicated that SCT stimulates cardiac adenylyl cyclase activity and exerts a positive inotropic action in the heart. The expression of SCT/SCTR or the effect of SCT on cardiac fibroblasts has not been fully explored. The AIM of our study was to determine the expression of SCT and SCTR in cardiac fibroblasts and to explore the effect of SCT on cardiac fibroblast expression of the renin‐angiotensin system (RAS). Results Rat cardiac fibroblasts express SCT and SCTR by qPCR, IF and FACS. SCT (0.43 ± 0.21 ng/ml) is secreted into supernatants collected from fibroblasts after 6 h. SCT stimulates an increase in intracellular cAMP (but not IP 3 ) and induces an increase in PCNA expression (an indicator of increased cell proliferation) at 6 h. SCT decreases gene expression of the profibrogenic RAS components, AT 1a , AT 1b and ACE and upregulates expression of AT 2 . Conclusions The findings suggest that SCT may have antifibrotic properties, which are protective during cardiac dysfunction.