{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T06:26:56Z","timestamp":1791268016782,"version":"4.1.0"},"reference-count":61,"publisher":"The Endocrine Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2011,1,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Urocortin 3 (Ucn 3), member of the corticotropin-releasing factor (CRF) family of peptide hormones, is released from \u03b2-cells to potentiate insulin secretion. Ucn 3 activates the CRF type-2 receptor (CRFR2) but does not activate the type-1 receptor (CRFR1), which was recently demonstrated on \u03b2-cells. While the direct actions of Ucn 3 on insulin secretion suggest the presence of cognate receptors within the islet microenvironment, this has not been established. Here we demonstrate that CRFR2\u03b1 is expressed by MIN6 insulinoma cells and by primary mouse and human islets, with no detectable expression of CRFR2\u03b2. Furthermore, stimulation of MIN6 cells or primary mouse islets in vitro or in vivo with glucocorticoids (GCs) robustly and dose-dependently increases the expression of CRFR2\u03b1, while simultaneously inhibiting the expression of CRFR1 and incretin receptors. Luciferase reporters driven by the mouse CRFR1 or CRFR2\u03b1 promoter in MIN6 cells confirm these differential effects of GCs. In contrast, GCs inhibit CRFR2\u03b1 promoter activity in HEK293 cells and inhibit the expression of CRFR2\u03b2 in A7r5 rat aortic smooth muscle cells and differentiated C2C12 myotubes. These findings suggest that the GC-mediated increase of CRFR2\u03b1 depends on the cellular context of the islet and deviates from the GC-mediated suppression of CRFR1 and incretin receptors. Furthermore, GC-induced increases in CRFR2\u03b1 expression coincide with increased Ucn 3-dependent activation of cAMP and MAPK pathways. We postulate that differential effect of GCs on the expression of CRFR1 and CRFR2\u03b1 in the endocrine pancreas represent a mechanism to shift sensitivity from CRFR1 to CRFR2 ligands.<\/jats:p>","DOI":"10.1210\/en.2010-0791","type":"journal-article","created":{"date-parts":[[2010,11,24]],"date-time":"2010-11-24T22:40:21Z","timestamp":1290638421000},"page":"138-150","source":"Crossref","is-referenced-by-count":24,"title":["Glucocorticoids Differentially Regulate the Expression of CRFR1 and CRFR2\u03b1 in MIN6 Insulinoma Cells and Rodent Islets"],"prefix":"10.1210","volume":"152","author":[{"given":"M. O.","family":"Huising","sequence":"first","affiliation":[{"name":"The Salk Institute for Biological Studies, The Clayton Foundation Laboratories for Peptide Biology, La Jolla, California 92037"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A. P.","family":"Pilbrow","sequence":"additional","affiliation":[{"name":"The Salk Institute for Biological Studies, The Clayton Foundation Laboratories for Peptide Biology, La Jolla, California 92037"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M.","family":"Matsumoto","sequence":"additional","affiliation":[{"name":"The Salk Institute for Biological Studies, The Clayton Foundation Laboratories for Peptide Biology, La Jolla, California 92037"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T.","family":"van der Meulen","sequence":"additional","affiliation":[{"name":"The Salk Institute for Biological Studies, The Clayton Foundation Laboratories for Peptide Biology, La Jolla, California 92037"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"H.","family":"Park","sequence":"additional","affiliation":[{"name":"The Salk Institute for Biological Studies, The Clayton Foundation Laboratories for Peptide Biology, La Jolla, California 92037"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. M.","family":"Vaughan","sequence":"additional","affiliation":[{"name":"The Salk Institute for Biological Studies, The Clayton Foundation Laboratories for Peptide Biology, La Jolla, California 92037"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S.","family":"Lee","sequence":"additional","affiliation":[{"name":"The Salk Institute for Biological Studies, The Clayton Foundation Laboratories for Peptide Biology, La Jolla, California 92037"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"W. 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