ArticleMolecular endocrinology (Baltimore, Md.)2011
Signaling cross talk between growth hormone (GH) and insulin-like growth factor-I (IGF-I) in pancreatic islet β-cells.
Article in Molecular endocrinology (Baltimore, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- A Supportive Role of Mesenchymal Stem Cells on Insulin-Producing Langerhans Islets with a Specific Emphasis on The Secretome.Biomedicines · 2023Review
- β Cell mass expansion during puberty involves serotonin signaling and determines glucose homeostasis in adulthood.JCI insight · 2022Article
- Milk Exosomal microRNAs: Postnatal Promoters of β Cell Proliferation but Potential Inducers of β Cell De-Differentiation in Adult Life.International journal of molecular sciences · 2022Review
- Musculoskeletal Effects of Altered GH Action.Frontiers in physiology · 2022Review
- Review
- Exosome-Derived MicroRNAs of Human Milk and Their Effects on Infant Health and Development.Biomolecules · 2021Review
- Classical and novel GH receptor signaling pathways.Molecular and cellular endocrinology · 2020Review
- Growth hormone (GH) receptor (GHR)-specific inhibition of GH-Induced signaling by soluble IGF-1 receptor (sol IGF-1R).Molecular and cellular endocrinology · 2019Article
- Insulin/IGF-driven cancer cell-stroma crosstalk as a novel therapeutic target in pancreatic cancer.Molecular cancer · 2018Review
- Menin and PRMT5 suppress GLP1 receptor transcript and PKA-mediated phosphorylation of FOXO1 and CREB.American journal of physiology. Endocrinology and metabolism · 2017Article
- Prolactin and oleic acid synergistically stimulate β-cell proliferation and growth in rat islets.Islets · 2017Article
- DMP-1-mediated Ghr gene recombination compromises skeletal development and impairs skeletal response to intermittent PTH.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Beneficial effects of growth hormone-releasing hormone agonists on rat INS-1 cells and on streptozotocin-induced NOD/SCID mice.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Review
- Hyperactivation of BDNF-TrkB signaling cascades in human hypothalamic hamartoma (HH): a potential mechanism contributing to epileptogenesis.CNS neuroscience & therapeutics · 2015Article
- Human GH receptor-IGF-1 receptor interaction: implications for GH signaling.Molecular endocrinology (Baltimore, Md.) · 2014Article
- Minireview: mechanisms of growth hormone-mediated gene regulation.Molecular endocrinology (Baltimore, Md.) · 2014Review
- Functional collaboration of insulin-like growth factor-1 receptor (IGF-1R), but not insulin receptor (IR), with acute GH signaling in mouse calvarial cells.Endocrinology · 2014Article
- IGF-1R modulation of acute GH-induced STAT5 signaling: role of protein tyrosine phosphatase activity.Molecular endocrinology (Baltimore, Md.) · 2013Article
- Growth hormone potentiates 17β-estradiol-dependent breast cancer cell proliferation independently of IGF-I receptor signaling.Endocrinology · 2013Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Dysfunction and destruction of pancreatic islet β-cells is a hallmark of diabetes. Better understanding of cell signals regulating β-cell growth and antiapoptosis will allow development of therapeutic strategies for diabetes by preservation and expansion of β-cell mass. GH and IGF-I share a complicated physiological relationship and have both been implicated in β-cell function. GH and IGF-I exert their biological effects through binding to respective receptors (GHR and IGF-IR) and subsequently engaging downstream signaling pathways. However, their collaborative roles in modulation of β-cell mass and the underlying molecular mechanisms remain poorly understood. In this study, we demonstrate that cultured β-cells are appealing systems for investigating potential GH-IGF-I signaling cross talk. We uncover that GH specifically promotes formation of a protein complex containing GHR, Janus kinase 2 (a nonreceptor kinase coupled to GH/GHR signaling), and IGF-IR. More importantly, GH and IGF-I synergistically activate both signal transducer and activator of transcription 5 and Akt pathways. Concomitantly, β-cells proliferate more robustly and are better protected from serum deprivation-induced apoptosis when exposed to GH and IGF-I in combination vs. GH or IGF-I alone. The augmented proliferative effects by GH and IGF-I are confirmed in isolated islets. Taken together, our findings strongly suggest that there exists a novel signaling relationship between GH/GHR and IGF-I/IGF-IR systems in β-cells, i.e. IGF-IR may serve as a proximal component of GH/GHR signaling, contributing to enhancement of β-cell mass and function. In support of this, IGF-IR knockdown in β-cells resulted in the desensitization of acute GH-induced signal transducer and activator of transcription 5 activation.
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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.