ArticleMolecular metabolism2016
The F-actin modifier villin regulates insulin granule dynamics and exocytosis downstream of islet cell autoantigen 512.
Article in Molecular metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 29 citations in OpenAlex.
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- The changing view of insulin granule mobility: From conveyor belt to signaling hub.Frontiers in endocrinology · 2022Review
- Severe pantothenic acid deficiency induces alterations in the intestinal mucosal proteome of starter Pekin ducks.BMC genomics · 2021Article
- Overexpression of PTPRN Promotes Metastasis of Lung Adenocarcinoma and Suppresses NK Cell Cytotoxicity.Frontiers in cell and developmental biology · 2021Article
- The adaptor protein APPL2 controls glucose-stimulated insulin secretion via F-actin remodeling in pancreatic β-cells.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Vitamin-D-Binding Protein Contributes to the Maintenance of α Cell Function and Glucagon Secretion.Cell reports · 2020Article
- Upregulation of vitamin D-binding protein is associated with changes in insulin production in pancreatic beta-cells exposed to p,p'-DDT and p,p'-DDE.Scientific reports · 2019Article
- ICA512 RESP18 homology domain is a protein-condensing factor and insulin fibrillation inhibitor.The Journal of biological chemistry · 2019Article
- Statistics for real-time deformability cytometry: Clustering, dimensionality reduction, and significance testing.Biomicrofluidics · 2018Article
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Authors and funding
15 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveInsulin release from pancreatic islet β cells should be tightly controlled to avoid hypoglycemia and insulin resistance. The cortical actin cytoskeleton is a gate for regulated exocytosis of insulin secretory granules (SGs) by restricting their mobility and access to the plasma membrane. Prior studies suggest that SGs interact with F-actin through their transmembrane cargo islet cell autoantigen 512 (Ica512) (also known as islet antigen 2/Ptprn). Here we investigated how Ica512 modulates SG trafficking and exocytosis.
methodsTranscriptomic changes in Ica512 (-/-) mouse islets were analyzed. Imaging as well as biophysical and biochemical methods were used to validate if and how the Ica512-regulated gene villin modulates insulin secretion in mouse islets and insulinoma cells.
resultsThe F-actin modifier villin was consistently downregulated in Ica512 (-/-) mouse islets and in Ica512-depleted insulinoma cells. Villin was enriched at the cell cortex of β cells and dispersed villin (-/-) islet cells were less round and less deformable. Basal mobility of SGs in villin-depleted cells was enhanced. Moreover, in cells depleted either of villin or Ica512 F-actin cages restraining cortical SGs were enlarged, basal secretion was increased while glucose-stimulated insulin release was blunted. The latter changes were reverted by overexpressing villin in Ica512-depleted cells, but not vice versa.
conclusionOur findings show that villin controls the size of the F-actin cages restricting SGs and, thus, regulates their dynamics and availability for exocytosis. Evidence that villin acts downstream of Ica512 also indicates that SGs directly influence the remodeling properties of the cortical actin cytoskeleton for tight control of insulin secretion.
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