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Single-cell Transcriptomic Analyses of Mouse Pancreatic Endocrine Cells
Published on: September 30, 2018
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Bromodomain and Extra Terminal Protein Inhibitors Promote Pancreatic Endocrine Cell Fate.
Lukas Huijbregts1, Maja Borup Kjær Petersen2, Claire Berthault1
1INSERM U1016, Institut Cochin, Université Paris Descartes, Paris, France.
Diabetes
|January 19, 2019
Summary
Bromodomain and extraterminal (BET) proteins regulate pancreatic development. Inhibiting BET proteins enhances endocrine progenitor formation but differentially affects gene expression in mouse and human models.
Area of Science:
- Developmental Biology
- Epigenetics
- Endocrinology
Background:
- Bromodomain and extraterminal (BET) proteins are epigenetic readers involved in gene regulation.
- Their role in cancer progression is established, but their function in embryonic pancreatic development is unknown.
Purpose of the Study:
- To investigate the role of BET proteins in embryonic pancreatic development using mouse and human cell models.
- To determine the effects of BET protein inhibition on pancreatic progenitor and endocrine cell differentiation.
Main Methods:
- Utilized mouse embryonic pancreatic explants and human induced pluripotent stem cells (hiPSCs).
- Administered BET inhibitors (I-BET151, JQ1) during differentiation protocols.
- Analyzed gene expression of pancreatic and endocrine cell markers (NEUROG3, Ins1, Cpa1, CelA, Amy, C-peptide, glucagon, UCN3, MAFA, ghrelin).
Main Results:
- BET inhibition increased neurogenin3 (NEUROG3) positive endocrine progenitors in both models.
- Mouse explants showed increased beta-cell and acinar markers but repressed Ins1 and Amy.
- hiPSC differentiation showed repressed C-peptide and glucagon but increased ghrelin.
- Pulsed inhibition followed by chase enhanced beta-cell maturation markers in mouse explants but not in hiPSCs.
Conclusions:
- BET proteins play a significant role in regulating multiple facets of pancreatic development.
- BET inhibition presents differential effects on pancreatic cell differentiation depending on the model system.
- Further research is warranted to understand the precise mechanisms and therapeutic potential of targeting BET proteins in pancreatic development and disease.
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