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Wnt4 antagonises Wnt3a mediated increases in growth and glucose stimulated insulin secretion in the pancreatic beta-cell line, INS-1.
- Source :
-
Biochemical and biophysical research communications [Biochem Biophys Res Commun] 2016 Oct 28; Vol. 479 (4), pp. 793-799. Date of Electronic Publication: 2016 Sep 28. - Publication Year :
- 2016
-
Abstract
- The Wnt signalling pathway in beta-cells has been linked to the development of type 2 diabetes. Investigating the impact of a non-canonical Wnt ligand, Wnt4, on beta-cell function we found that in INS-1 cells, Wnt4 was able to completely block Wnt3a stimulated cell growth and insulin secretion. However, despite high levels of Wnt4 protein being detected in INS-1 cells, reducing the expression of Wnt4 had no impact on cell growth or Wnt3a signalling. As such, the role of the endogenously expressed Wnt4 in beta-cells is unclear, but the data showing that Wnt4 can act as a negative regulator of canonical Wnt signalling in beta-cells suggests that this pathway could be a potential target for modulating beta-cell function.<br /> (Copyright © 2016 Elsevier Inc. All rights reserved.)
- Subjects :
- Animals
Cell Line
Cell Proliferation
Glucose metabolism
Glucose pharmacology
Humans
Immunohistochemistry
Insulin metabolism
Insulin Secretion
Insulin-Secreting Cells cytology
Insulin-Secreting Cells drug effects
Islets of Langerhans cytology
Islets of Langerhans metabolism
RNA, Messenger genetics
RNA, Messenger metabolism
RNA, Small Interfering genetics
Rats
Wnt Signaling Pathway
Wnt3A Protein antagonists & inhibitors
Wnt3A Protein pharmacology
Wnt4 Protein genetics
Wnt4 Protein pharmacology
beta Catenin genetics
beta Catenin metabolism
Insulin-Secreting Cells metabolism
Wnt3A Protein metabolism
Wnt4 Protein metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1090-2104
- Volume :
- 479
- Issue :
- 4
- Database :
- MEDLINE
- Journal :
- Biochemical and biophysical research communications
- Publication Type :
- Academic Journal
- Accession number :
- 27687546
- Full Text :
- https://doi.org/10.1016/j.bbrc.2016.09.130