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Biology 2019, 8(1), 19; https://doi.org/10.3390/biology8010019

Oncostatin M Mediates Adipocyte Expression and Secretion of Stromal-Derived Factor 1

1
Adipocyte Biology Laboratory, Pennington Biomedical Research Center, Baton Rouge, LA, 70808, USA
2
Matrix Biology Laboratory, Pennington Biomedical Research Center, Baton Rouge, LA, 70808, USA
*
Author to whom correspondence should be addressed.
Received: 25 February 2019 / Revised: 15 March 2019 / Accepted: 18 March 2019 / Published: 23 March 2019
(This article belongs to the Special Issue New Players in Adipocyte Biology)
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Abstract

Adipose tissue homeostasis depends on interactions between stromal cells, adipocytes, and the cytokines and chemokines they produce. The gp130 cytokine, oncostatin M (OSM), plays a role in adipose tissue homeostasis. Mice, lacking the OSM receptor (OSMR) in adipocytes (OsmrFKO mice), exhibit derangements in adipose tissue, insulin sensitivity, and immune cell balance. Here, we describe a possible role for the chemokine stromal-derived factor 1 (SDF-1) in these alterations. We treated 3T3-L1 adipocytes with OSM and observed a suppression of SDF-1 gene expression and protein secretion, an effect which was partially blunted by OSMR knockdown. However, OsmrFKO mice also exhibited decreased SDF-1 gene and protein expression in adipose tissue. These contrasting results suggest that the loss of adipocyte OSM–OSMR signaling in vivo may be indirectly affecting adipokine production and secretion by altering OSM target genes to ultimately decrease SDF-1 expression in the OsmrFKO mouse. We conclude that adipocyte OSM–OSMR signaling plays a role in adipose tissue SDF-1 production and may mitigate its effects on adipose tissue homeostasis. View Full-Text
Keywords: oncostatin M; adipose tissue; stromal-derived factor 1; adipocyte; inflammation oncostatin M; adipose tissue; stromal-derived factor 1; adipocyte; inflammation
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Hang, H.; Bailey, J.L.; Elks, C.M. Oncostatin M Mediates Adipocyte Expression and Secretion of Stromal-Derived Factor 1. Biology 2019, 8, 19.

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