ArticleDevelopmental biology2013
Smad signaling pathways regulate pancreatic endocrine development.
Article in Developmental biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 39 citations in OpenAlex.
- Overlapping and Distinct Physical and Biological Phenotypes in Pure Frailty and Obese Frailty.Bioscience reports · 2024Article
- Unraveling the interplay: exploring signaling pathways in pancreatic cancer in the context of pancreatic embryogenesis.Frontiers in cell and developmental biology · 2024Review
- Regeneration of Pancreatic Beta Cells by Modulation of Molecular Targets Using Plant-Derived Compounds: Pharmacological Mechanisms and Clinical Potential.Current issues in molecular biology · 2023Review
- Chromatin accessibility differences between alpha, beta, and delta cells identifies common and cell type-specific enhancers.BMC genomics · 2023Article
- Review
- β-cell Smad2 null mice have improved β-cell function and are protected from diet-induced hyperglycemia.The Journal of biological chemistry · 2021Article
- Good Cop, Bad Cop: The Opposing Effects of Macrophage Activation State on Maintaining or Damaging Functional β-Cell Mass.Metabolites · 2020Review
- SMAD7 enhances adult β-cell proliferation without significantly affecting β-cell function in mice.The Journal of biological chemistry · 2020Article
- Cellular signaling pathways regulating β-cell proliferation as a promising therapeutic target in the treatment of diabetes.Experimental and therapeutic medicine · 2018Review
- Regulation of TGF-β Family Signaling by Inhibitory Smads.Cold Spring Harbor perspectives in biology · 2017Review
- Forkhead Box Protein 1 (FoxO1) Inhibits Accelerated β Cell Aging in Pancreas-specific SMAD7 Mutant Mice.The Journal of biological chemistry · 2017Article
- Gene expression signature predicts human islet integrity and transplant functionality in diabetic mice.PloS one · 2017Article
- A synopsis of factors regulating beta cell development and beta cell mass.Cellular and molecular life sciences : CMLS · 2016Review
- Transient Suppression of TGFβ Receptor Signaling Facilitates Human Islet Transplantation.Endocrinology · 2016Article
- Integration of ATAC-seq and RNA-seq identifies human alpha cell and beta cell signature genes.Molecular metabolism · 2016Article
- Intraislet Pancreatic Ducts Can Give Rise to Insulin-Positive Cells.Endocrinology · 2016Article
- The role of noggin in regulation of high glucose-induced apoptosis and insulin secretion in INS-1 rat beta cells.Iranian journal of basic medical sciences · 2015Article
- Transforming growth factor β receptor signaling restrains growth of pancreatic carcinoma cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- Maintaining human fetal pancreatic stellate cell function and proliferation require β1 integrin and collagen I matrix interactions.Oncotarget · 2015Article
- TGF-β signalling prevents pancreatic beta cell death after proliferation.Cell proliferation · 2015Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
Abstract
Expansion of the pancreatic endocrine cell population occurs during both embryonic development and during post-natal pancreatic growth and regeneration. Mechanisms of the expansion of endocrine cells during embryonic development are not completely understood, and no clear mechanistic link has been established between growth of the embryonic endocrine pancreas and the islet cell replication that occurs in an adult animal. We found that transforming growth factor-beta (TGF-β) superfamily signaling, which has been implicated in many developmental processes, plays a key role in regulating pancreatic endocrine maturation and development. Specifically, the intracellular mediators of TGF-β signaling, smad2 and smad3, along with their inhibitor smad7, appear to mediate this process. Smad2, smad3 and smad7 were all broadly expressed throughout the early embryonic pancreatic epithelium. However, during later stages of development, smad2 and smad3 became strongly localized to the nuclei of the endocrine positive cells, whereas the inhibitory smad7 became absent in the endocrine component. Genetic inactivation of smad2 and smad3 led to a significant expansion of the embryonic endocrine compartment, whereas genetic inactivation of smad7 led to a significant decrease in the endocrine compartment. In vitro antisense studies further corroborated these results and supported the possibility that interplay between the inhibitory smad7 and the intracellular mediators smad2/3 is a control point for pancreatic endocrine development. These results should provide a better understanding of the key control mechanisms for β-cell development.
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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.