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

Hardy Hang; Jennifer L Bailey; Carrie M Elks

doi:10.3390/biology8010019

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

Biology (Basel). 2019 Mar 23;8(1):19. doi: 10.3390/biology8010019.

Authors

Hardy Hang¹, Jennifer L Bailey², Carrie M Elks³

Affiliations

¹ Adipocyte Biology Laboratory, Pennington Biomedical Research Center, Baton Rouge, LA, 70808, USA. hardy.hang@pbrc.edu.
² Matrix Biology Laboratory, Pennington Biomedical Research Center, Baton Rouge, LA, 70808, USA. jennifer.bailey@pbrc.edu.
³ Matrix Biology Laboratory, Pennington Biomedical Research Center, Baton Rouge, LA, 70808, USA. carrie.elks@pbrc.edu.

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 (Osmr^FKO 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, Osmr^FKO 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 Osmr^FKO 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.

Keywords: adipocyte; adipose tissue; inflammation; oncostatin M; stromal-derived factor 1.

Abstract

Grants and funding