ArticleDiabetes2015
Augmented Stat5 Signaling Bypasses Multiple Impediments to Lactogen-Mediated Proliferation in Human β-Cells.
Article in Diabetes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
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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
42 citing papers in PubMed, 58 citations in OpenAlex.
- CBX4 stabilizes NEUROD1 through SUMO-ubiquitin crosstalk to delay β-cell senescence.Nature communications · 2026Article
- Harnessing beta-cell replication: advancing molecular insights to regenerative therapies in diabetes.Frontiers in endocrinology · 2025Review
- Article
- Identification of inflammatory biomarkers in IgA nephropathy using the NanoString technology: a validation study in Caucasians.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- Beta-cell compensation and gestational diabetes.The Journal of biological chemistry · 2023Review
- Hormonal Determinants of Growth and Weight Gain in the Human Fetus and Preterm Infant.Nutrients · 2023Review
- The gut signals to AGRP-expressing cells of the pituitary to control glucose homeostasis.The Journal of clinical investigation · 2023Article
- Pregnancy induces pancreatic insulin secretion in women with long-standing type 1 diabetes.BMJ open diabetes research & care · 2022Article
- The Essential Role of Pancreatic α-Cells in Maternal Metabolic Adaptation to Pregnancy.Diabetes · 2022Article
- Dysregulation of β-Cell Proliferation in Diabetes: Possibilities of Combination Therapy in the Development of a Comprehensive Treatment.Biomedicines · 2022Review
- Exogenous Lactogenic Signaling Stimulates Beta Cell Replication In Vivo and In Vitro.Biomolecules · 2022Article
- The Human Islet: Mini-Organ With Mega-Impact.Endocrine reviews · 2021Review
- New Aspects of Diabetes Research and Therapeutic Development.Pharmacological reviews · 2021Review
- Dynamic Regulation of JAK-STAT Signaling Through the Prolactin Receptor Predicted by Computational Modeling.Cellular and molecular bioengineering · 2021Article
- Debates in Pancreatic Beta Cell Biology: Proliferation Versus Progenitor Differentiation and Transdifferentiation in Restoring β Cell Mass.Frontiers in endocrinology · 2021Review
- Prolactin-Induced Adaptation in Glucose Homeostasis in Mouse Pregnancy Is Mediated by the Pancreas and Not in the Forebrain.Frontiers in endocrinology · 2021Article
- Adiponectin Promotes Maternal β-Cell Expansion Through Placental Lactogen Expression.Diabetes · 2021Article
- Lactogens Reduce Endoplasmic Reticulum Stress-Induced Rodent and Human β-Cell Death and Diabetes Incidence in Akita Mice.Diabetes · 2020Article
- Placental Lactogen as a Marker of Maternal Obesity, Diabetes, and Fetal Growth Abnormalities: Current Knowledge and Clinical Perspectives.Journal of clinical medicine · 2020Review
- Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 1 country.
Funding
Abstract
Pregnancy in rodents is associated with a two- to threefold increase in β-cell mass, which is attributable to large increases in β-cell proliferation, complimented by increases in β-cell size, survival, and function and mediated mainly by the lactogenic hormones prolactin (PRL) and placental lactogens. In humans, however, β-cell mass does not increase as dramatically during pregnancy, and PRL fails to activate proliferation in human islets in vitro. To determine why, we explored the human PRL-prolactin receptor (hPRLR)-Janus kinase 2 (JAK2)-signal transducer and activator of transcription 5 (STAT5)-cyclin-cdk signaling cascade in human β-cells. Surprisingly, adult human β-cells express little or no PRLR. As expected, restoration of the hPRLR in human β-cells rescued JAK2-STAT5 signaling in response to PRL. However, rescuing hPRLR-STAT5 signaling nevertheless failed to confer proliferative ability on adult human β-cells in response to PRL. Surprisingly, mouse (but not human) Stat5a overexpression led to upregulation of cyclins D1-3 and cdk4, as well as their nuclear translocation, all of which are associated with β-cell cycle entry. Collectively, the findings show that human β-cells fail to proliferate in response to PRL for multiple reasons, one of which is a paucity of functional PRL receptors, and that murine Stat5 overexpression is able to bypass these impediments.
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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.