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Biased G protein-coupled receptor agonism mediates Neu1 sialidase and matrix metalloproteinase-9 crosstalk to induce transactivation of insulin receptor signaling

Haxho, Fiona, Haq, Sabah, Szewczuk, Myron R.·2018·Cellular Signalling
DOI 10.1016/j.cellsig.2017.12.006
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Abstract

G protein-coupled receptors (GPCR) can participate in a number of signaling pathways, and this property led to the concept of biased GPCR agonism. Agonists, antagonists and allosteric modulators can bind to GPCRs in different ways, creating unique conformations that differentially modulate signaling through one or more G proteins. A unique neuromedin B (NMBR) GPCR-signaling platform controlling mammalian neuraminidase-1 (Neu1) and matrix metalloproteinase-9 (MMP9) crosstalk has been reported in the activation of the insulin receptor (IR) through the modification of the IR glycosylation. Here, we propose that there exists a biased GPCR agonism as small diffusible molecules in the activation of Neu1-mediated insulin receptor signaling. GPCR agonists bombesin, bradykinin, angiotensin I and angiotensin II significantly and dose-dependently induce Neu1 sialidase activity and IR activation in human IR-expressing rat hepatoma cell lines (HTC-IR), in the absence of insulin. Furthermore, the GPCR agonist-induced Neu1 sialidase activity could be specifically blocked by the NMBR inhibitor, BIM-23127. Protein expression analyses showed that these GPCR agonists significantly induced phosphorylation of IRβ and insulin receptor substrate-1 (IRS1). Among these, angiotensin II was the most potent GPCR agonist capable of promoting IRβ phosphorylation in HTC-IR cells. Interestingly, treatment with BIM-23127 and Neu1 inhibitor oseltamivir phosphate were able to block GPCR agonist-induced IR acti…

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Metadata

Authors
Haxho, F., Haq, S., & Szewczuk, M. R.
Venue
Cellular Signalling
Publisher
Elsevier BV
Published
2018-03
Volume
43
Pages
71-84
ISSN
0898-6568
DOI
10.1016/j.cellsig.2017.12.006
Cited by
42
References
1
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Funders
Natural Sciences and Engineering Research Council of Canada (RGPIN-2015-05301)

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