ArticleMolecular endocrinology (Baltimore, Md.)2008
Fibroblast growth factor receptor-1 signaling in pancreatic islet beta-cells is modulated by the extracellular matrix.
Article in Molecular endocrinology (Baltimore, Md.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 56 citations in OpenAlex.
- Secretome of Cancer-Associated Fibroblasts (CAFs) Influences Drug Sensitivity in Cancer Cells.Journal of proteome research · 2024Article
- Unlocking the post-transplant microenvironment for successful islet function and survival.Frontiers in endocrinology · 2023Review
- Laminin matrix regulates beta-cell FGFR5 expression to enhance glucose-stimulated metabolism.Scientific reports · 2022Article
- The Foundation for Engineering a Pancreatic Islet Niche.Frontiers in endocrinology · 2022Review
- Pathophysiological Implications of Imbalances in Fibroblast Growth Factor 23 in the Development of Diabetes.Journal of clinical medicine · 2021Review
- Fibroblast Growth Factor Receptors (FGFRs) and Noncanonical Partners in Cancer Signaling.Cells · 2021Review
- The Role of Vascular Cells in Pancreatic Beta-Cell Function.Frontiers in endocrinology · 2021Review
- Extracellular Matrix-Associated Factors Play Critical Roles in Regulating Pancreatic β-Cell Proliferation and Survival.Endocrinology · 2019Review
- Extracellular matrix and the maintenance and loss of peripheral immune tolerance in autoimmune insulitis.Current opinion in immunology · 2018Review
- Fibroblast growth factor receptor 5 (FGFR5) is a co-receptor for FGFR1 that is up-regulated in beta-cells by cytokine-induced inflammation.The Journal of biological chemistry · 2018Article
- β-Cell Receptor Tyrosine Kinases in Controlling Insulin Secretion and Exocytotic Machinery: c-Kit and Insulin Receptor.Endocrinology · 2018Review
- Apolipoprotein E is a pancreatic extracellular factor that maintains mature β-cell gene expression.PloS one · 2018Article
- Signals in the pancreatic islet microenvironment influence β-cell proliferation.Diabetes, obesity & metabolism · 2017Review
- Pancreatic Islet Survival and Engraftment Is Promoted by Culture on Functionalized Spider Silk Matrices.PloS one · 2015Article
- Association of JAZF1 and TSPAN8/LGR5 variants in relation to type 2 diabetes mellitus in a Saudi population.Diabetology & metabolic syndrome · 2015Article
- Current understanding of the molecular biology of pancreatic neuroendocrine tumors.Journal of the National Cancer Institute · 2013Review
- Fibroblast growth factor receptor like-1 (FGFRL1) interacts with SHP-1 phosphatase at insulin secretory granules and induces beta-cell ERK1/2 protein activation.The Journal of biological chemistry · 2013Article
- GRP78 overproduction in pancreatic beta cells protects against high-fat-diet-induced diabetes in mice.Diabetologia · 2013Article
- Article
- Autofluorescence imaging of living pancreatic islets reveals fibroblast growth factor-21 (FGF21)-induced metabolism.Biophysical journal · 2012Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Maintenance of pancreatic beta-cell mass depends on extracellular stimuli that promote survival and proliferation. In the islet, these stimuli come from the beta-cell microenvironment and include extracellular matrix deposited by associated vascular endothelial cells. Fibroblast growth factor receptor-1 (FGFR1) has recently been implicated as a signaling pathway that is important for normal beta-cell function. We would like to understand how extracellular matrix and FGFR1 signaling interact to promote beta-cell survival and proliferation. To examine beta-cell-specific receptor responses, we created lentiviral vectors with rat insulin promoter-driven expression of Venus fluorescent protein-tagged full-length (R1betav) and kinase-deficient (KDR1betav) FGFR1. Significant FGF-1-dependent activation of ERK1/2 was observed in betaTC3 cells, dispersed beta-cells, and beta-cells in intact islets. This response was enhanced by R1betav expression and reduced by KDR1betav expression. Plating-dispersed beta-cells on collagen type IV resulted in enhanced expression of endogenous FGFR1 that was associated with sustained activation of ERK1/2. Conversely, plating cells on laminin reduced expression of FGFR1, and this reduction was associated with transient activation of ERK1/2. Addition of neutralizing antibodies to inhibit beta-cell attachment to laminin via alpha(6)-integrin increased high-affinity FGF-1-binding at the plasma membrane and resulted in sustained ERK1/2 activity similar to cells plated on collagen type IV. These data show that the FGF-stimulated beta-cell response is negatively affected by alpha(6)-integrin binding to laminin and suggest regulation associated with vascular endothelial cell remodeling.
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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.