ArticleEndocrinology2011
Glucocorticoids differentially regulate the expression of CRFR1 and CRFR2α in MIN6 insulinoma cells and rodent islets.
Article in Endocrinology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- The metabolic role of corticotropin-releasing hormone receptor 2 and its UCN peptides: emerging therapeutic potential.Skeletal muscle · 2025Review
- Novel corticotropin-releasing hormone receptor genes (CRHR1 and CRHR2) linkage to and association with polycystic ovary syndrome.Journal of ovarian research · 2023Article
- Urocortin3: Local inducer of somatostatin release and bellwether of beta cell maturity.Peptides · 2022Review
- Article
- UCN2: a new candidate influencing pancreatic β-cell adaptations in pregnancy.The Journal of endocrinology · 2020Article
- Urocortins in the mammalian endocrine system.Acta veterinaria Scandinavica · 2019Review
- The Difference δ-Cells Make in Glucose Control.Physiology (Bethesda, Md.) · 2018Review
- Artemether Does Not Turn α Cells into β Cells.Cell metabolism · 2018Article
- Analysis of Purified Pancreatic Islet Beta and Alpha Cell Transcriptomes Reveals 11β-Hydroxysteroid Dehydrogenase (Hsd11b1) as a Novel Disallowed Gene.Frontiers in genetics · 2017Article
- Urocortin3 mediates somatostatin-dependent negative feedback control of insulin secretion.Nature medicine · 2015Article
- Regulation of Glucose Homeostasis by Glucocorticoids.Advances in experimental medicine and biology · 2015Review
- CRFR1 activation protects against cytokine-induced β-cell death.Journal of molecular endocrinology · 2014Article
- Reversal of β cell de-differentiation by a small molecule inhibitor of the TGFβ pathway.eLife · 2014Article
- Maturation of stem cell-derived beta-cells guided by the expression of urocortin 3.The review of diabetic studies : RDS · 2014Review
- Corticotropin-releasing factor receptor 2 mediates sex-specific cellular stress responses.Molecular medicine (Cambridge, Mass.) · 2013Article
- Regulation of gonadotropins by corticotropin-releasing factor and urocortin.Frontiers in endocrinology · 2013Article
- Urocortin 3 marks mature human primary and embryonic stem cell-derived pancreatic alpha and beta cells.PloS one · 2012Article
- Modulation of pancreatic islets-stress axis by hypothalamic releasing hormones and 11beta-hydroxysteroid dehydrogenase.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Research on the Effects of the Chronic Treatment With Different Doses of Urocortin 2 in Heart Failure Rats.Dose-response : a publication of International Hormesis SocietyArticle
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Urocortin 3 (Ucn 3), member of the corticotropin-releasing factor (CRF) family of peptide hormones, is released from β-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 β-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 CRFR2α is expressed by MIN6 insulinoma cells and by primary mouse and human islets, with no detectable expression of CRFR2β. 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 CRFR2α, while simultaneously inhibiting the expression of CRFR1 and incretin receptors. Luciferase reporters driven by the mouse CRFR1 or CRFR2α promoter in MIN6 cells confirm these differential effects of GCs. In contrast, GCs inhibit CRFR2α promoter activity in HEK293 cells and inhibit the expression of CRFR2β in A7r5 rat aortic smooth muscle cells and differentiated C2C12 myotubes. These findings suggest that the GC-mediated increase of CRFR2α 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 CRFR2α 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 CRFR2α in the endocrine pancreas represent a mechanism to shift sensitivity from CRFR1 to CRFR2 ligands.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.