ArticleDiabetologia2015
Prolactin-stimulated survivin induction is required for beta cell mass expansion during pregnancy in mice.
Article in Diabetologia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 35 citations in OpenAlex.
- Drug-induced regeneration of pancreatic beta cells: An approach to cellular therapeutic targets.Cell regeneration (London, England) · 2025Review
- c-Jun regulates postpartum β-cell apoptosis and survival downstream of prolactin signaling.Molecular and cellular endocrinology · 2025Article
- Kisspeptin upregulates β-cell serotonin production during pregnancy.The Journal of endocrinology · 2024Article
- Prolactin in Polycystic Ovary Syndrome: Metabolic Effects and Therapeutic Prospects.Life (Basel, Switzerland) · 2023Review
- A Supportive Role of Mesenchymal Stem Cells on Insulin-Producing Langerhans Islets with a Specific Emphasis on The Secretome.Biomedicines · 2023Review
- The beneficial metabolic actions of prolactin.Frontiers in endocrinology · 2022Review
- Identification of direct transcriptional targets of NFATC2 that promote β cell proliferation.The Journal of clinical investigation · 2021Article
- Debates in Pancreatic Beta Cell Biology: Proliferation Versus Progenitor Differentiation and Transdifferentiation in Restoring β Cell Mass.Frontiers in endocrinology · 2021Review
- The glucose-lowering effects of α-glucosidase inhibitor require a bile acid signal in mice.Diabetologia · 2020Article
- Placental growth factor in beta cells plays an essential role in gestational beta-cell growth.BMJ open diabetes research & care · 2020Article
- Organoids from the Human Fetal and Adult Pancreas.Current diabetes reports · 2019Review
- Lrrc55 is a novel prosurvival factor in pancreatic islets.American journal of physiology. Endocrinology and metabolism · 2019Article
- Endogenous Pancreatic β Cell Regeneration: A Potential Strategy for the Recovery of β Cell Deficiency in Diabetes.Frontiers in endocrinology · 2019Review
- STAT3 activation in infection and infection-associated cancer.Molecular and cellular endocrinology · 2017Review
- Metabolic recovery of lipodystrophy, liver steatosis, and pancreatic β cell proliferation after the withdrawal of OSI-906.Scientific reports · 2017Article
- Article
- An increase in immature β-cells lacking Glut2 precedes the expansion of β-cell mass in the pregnant mouse.PloS one · 2017Article
- Targeting of heme oxygenase-1 attenuates the negative impact of Ikaros isoform 6 in adult BCR-ABL1-positive B-ALL.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
aims/hypothesisProlactin (PRL)-stimulated beta cell proliferation is critical for maternal pancreatic beta cell mass expansion during pregnancy. However, the molecular effectors of the multiple putative signalling pathways downstream of the PRL receptor (PRL-R) are still elusive. Survivin has been shown to be induced during pregnancy. The aim of the present study was to define the essential role of survivin in gestational beta cell mass expansion.
methodsExpression of survivin was assessed in mouse islets during pregnancy and in insulinoma cells (INS-1) stimulated with PRL. Pregnant mice with targeted deletion of the survivin gene (also known as Birc5) in beta cells were assessed to determine the essential function of survivin in maternal beta cell mass expansion. INS-1 cells stimulated with PRL were used to explore the role of survivin in signalling pathways downstream of the PRL-R.
resultsSurvivin was significantly upregulated in maternal islets during pregnancy. With PRL stimulation, induction of survivin expression occurred predominantly in the nucleus and was associated with cell cycle progression to S and G2/M phase. Beta cell-specific survivin-knockout pregnant mice displayed glucose intolerance, attenuated beta cell mass expansion and impaired beta cell proliferation, with significant attenuation in the increased expression of Cdk4/Ccnd1, E2f1, p53 (also known as Trp53) and p21 (also known as Cdkn1a) compared with wild-type controls during pregnancy. Targeted deletion of survivin in INS-1 cells resulted in cell cycle disturbance with an arrest in G1/S phase after PRL stimulation. Inhibitors of Akt, signal transducer and activator of transcription 5 (STAT5), PIM or extracellular signal-regulated kinase (ERK), significantly decreased the expression of survivin in PRL-stimulated INS-1 cells. CONCLUSIONS/
interpretationSurvivin directly participates in PRL-mediated beta cell proliferation via Akt, STAT5-PIM and ERK signalling pathways during pregnancy.
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