c-Fos induction by gut hormones and extracellular ATP in osteoblastic-like cell lines

Pacheco-Pantoja, Elda Leonor, Dillon, Jane P ORCID: 0000-0002-7055-5664, Wilson, Peter JM, Fraser, William D and Gallagher, James A ORCID: 0000-0002-0852-279X (2016) c-Fos induction by gut hormones and extracellular ATP in osteoblastic-like cell lines. Purinergic Signalling, 12 (4). pp. 647-651.

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Official URL: http://dx.doi.org/10.1007/s11302-016-9526-3

Abstract

It is widely accepted that the c-Fos gene has a role in proliferation and differentiation of bone cells. ATP-induced c-Fos activation is relevant to bone homeostasis, because nucleotides that are present in the environment of bone cells can contribute to autocrine/paracrine signalling. Gut hormones have previously been shown to have an effect on bone metabolism. In this study, we used the osteoblastic Saos-2 cell line transfected with a c-Fos-driven reporter stimulated with five gut hormones: glucose inhibitory peptide (GIP), glucagon-like peptide-1 (GLP-1), glucagon-like peptide-2 (GLP-2), ghrelin and obestatin, in the presence or absence of ATP. In addition, TE-85 cells were used to determine the time course of c-Fos transcript induction following stimulation with GLP-1, and GLP-2 with or without ATP, using reverse transcription qPCR. The significant results from the experiments are as follows: higher level of c-Fos induction in presence of GIP, obestatin (p = 0.019 and p = 0.011 respectively), and GIP combined with ATP (p < 0.001) using the luciferase assay; GLP-1 and GLP-2 combined with ATP (p = 0.034 and p = 0.002, respectively) and GLP-2 alone (p < 0.001) using qPCR. In conclusion, three of the gut peptides induced c-Fos, providing a potential mechanism underlying the actions of these hormones in bone which can be directed or enhanced by the presence of ATP.

Item Type:	Article
Uncontrolled Keywords:	ATP, GIP, GLP-1, GLP-2, Osteoblasts, c-Fos
Depositing User:	Symplectic Admin
Date Deposited:	27 Oct 2016 13:02
Last Modified:	19 Jan 2023 07:29
DOI:	10.1007/s11302-016-9526-3
Related URLs:	Author Publisher
URI:	https://livrepository.liverpool.ac.uk/id/eprint/3003727