ArticleEndocrine2017
Exendin-4 promotes pancreatic β-cell proliferation via inhibiting the expression of Wnt5a.
Article in Endocrine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Effect of glucagon-like peptide-1 receptor agonist on insulin secretion index and serum Wnt5a protein in patients with new-onset type 2 diabetes mellitus.Journal of diabetes and metabolic disorders · 2023Article
- CaBiomedicines · 2023Review
- The functions of CaJournal of cell communication and signaling · 2023Review
- SEL1L-HRD1 ER-associated degradation suppresses hepatocyte hyperproliferation and liver cancer.iScience · 2022Article
- The complex role of Wnt ligands in type 2 diabetes mellitus and related complications.Journal of cellular and molecular medicine · 2021Review
- SNAPIN Regulates Cell Cycle Progression to Promote Pancreatic β Cell Growth.Frontiers in endocrinology · 2021Article
- Islet Stellate Cells Regulate Insulin Secretion via Wnt5a in Min6 Cells.International journal of endocrinology · 2020Article
- Systematic Design of Trypsin Cleavage Site Mutated Exendin4-Cysteine 1, an Orally Bioavailable Glucagon-Like Peptide-1 Receptor Agonist.International journal of molecular sciences · 2017Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Exendin-4, a glucagon-like peptide-1 receptor agonist, is currently regarded as an effective therapeutic strategy for type-2 diabetes. Previous studies indicated that exendin-4 promoted β cell proliferation. However, the underlying mechanisms remain largely unknown. Recently it was reported that exendin-4 promoted pancreatic β cell proliferation by regulating the expression level of Wnt4. The present study was designed to investigate whether other Wnt isoforms take part in accommodation of β-cell proliferation. We found that exendin-4 promotes the proliferation and suppresses the expression of Wnt5a in INS-1 cell line and C57Bl/6 mouse pancreatic β-cells. Further mechanistic study demonstrated that exendin-4 promoted INS-1 cell proliferation partly through down-regulating the expression of Wnt5a. Furthermore, Wnt5a could induce the activation of calmodulin-dependent protein kinase II in INS-1 cells, thereby decreasing the cellular stable β-catenin and its nuclear translocation, and finally reduce the expression of cyclin D1. In addition, we also found that both of the receptors (Frz-2 and Ror-2) mediated the effect of Wnt5a on β cell line INS-1 proliferation. Taken together, this study suggests that Wnt5a plays a critical role in exendin-4-induced β-cell proliferation, indicating that Wnt5a might be a novel regulator in counterbalance of β cell mass.
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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.