ArticleCells2020
Formation of βTC3 and MIN6 Pseudoislets Changes the Expression Pattern of Gpr40, Gpr55, and Gpr119 Receptors and Improves Lysophosphatidylcholines-Potentiated Glucose-Stimulated Insulin Secretion.
Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- 3D bioprinting of collagen-based high-resolution internally perfusable scaffolds for engineering fully biologic tissue systems.Science advances · 2025Article
- Scaffold-free endocrine tissue engineering: role of islet organization and implications in type 1 diabetes.BMC endocrine disorders · 2025Review
- Characterization and functional evaluation of goat PDX1 regulatory modules through comparative analysis of conserved interspecies homologs.Scientific reports · 2024Article
- Lysophosphatidylcholines Enriched withACS medicinal chemistry letters · 2024Article
- MRPS6 modulates glucose-stimulated insulin secretion in mouse islet cells through mitochondrial unfolded protein response.Scientific reports · 2023Article
- Spleen extracellular matrix provides a supportive microenvironment for β-cell function.Iranian journal of basic medical sciences · 2022Article
- Blood-Brain Barrier Disruption Mediated by FFA1 Receptor-Evidence Using Miniscope.International journal of molecular sciences · 2022Article
- Isoprenoid Derivatives of Lysophosphatidylcholines Enhance Insulin and GLP-1 Secretion through Lipid-Binding GPCRs.International journal of molecular sciences · 2021Article
- High-Yield Generation of Glucose-Responsive Pseudoislets From Murine Insulinoma Cells forCell transplantationArticle
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The impaired spatial arrangement and connections between cells creating islets of Langerhans as well as altered expression of G protein-coupled receptors (GPCRs) often lead to dysfunction of insulin-secreting pancreatic β cells and can significantly contribute to the development of diabetes. Differences in glucose-stimulated insulin secretion (GSIS) are noticeable not only in diabetic individuals but also in model pancreatic β cells, e.g., βTC3 and MIN6 β cell lines with impaired and normal insulin secretion, respectively. Now, we compare the ability of GPCR agonists (lysophosphatidylcholines bearing fatty acid chains of different lengths) to potentiate GSIS in βTC3 and MIN6 β cell models, cultured as adherent monolayers and in a form of pseudoislets (PIs) with pancreatic MS1 endothelial cells. Our aim was also to investigate differences in expression of the GPCRs responsive to LPCs in these experimental systems. Aggregation of β cells into islet-like structures greatly enhanced the expression of
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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.