2015
DOI: 10.2337/db14-1473
|View full text |Cite
|
Sign up to set email alerts
|

Bone Marrow Macrophages Contribute to Diabetic Stem Cell Mobilopathy by Producing Oncostatin M

Abstract: Diabetes affects bone marrow (BM) structure and impairs mobilization of stem cells (SCs) into peripheral blood (PB). This amplifies multiorgan complications because BMSCs promote vascular repair. Because diabetes skews macrophage phenotypes and BM macrophages (BMMF) prevent SC mobilization, we hypothesized that excess BMMF contribute to diabetic SC mobilopathy. We show that patients with diabetes have increased M1 macrophages, whereas diabetic mice have increased CD169+ BMMF with SC-retaining activity. Depleti… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1
1
1

Citation Types

2
71
1

Year Published

2015
2015
2023
2023

Publication Types

Select...
10

Relationship

1
9

Authors

Journals

citations
Cited by 91 publications
(74 citation statements)
references
References 37 publications
2
71
1
Order By: Relevance
“…Interestingly, in diabetic mice OSM neutralization prevented SDF-1/CXCL12 induction and improved G-CSF-as well as ischemia-induced mobilization. Furthermore, in diabetic patients increased levels of OSM correlated with a substantially higher number of CD34 + HSC in the BM than in peripheral blood [103].…”
Section: Role Of Osm In Hematopoiesis Adipogenesis and Osteogenesismentioning
confidence: 88%
“…Interestingly, in diabetic mice OSM neutralization prevented SDF-1/CXCL12 induction and improved G-CSF-as well as ischemia-induced mobilization. Furthermore, in diabetic patients increased levels of OSM correlated with a substantially higher number of CD34 + HSC in the BM than in peripheral blood [103].…”
Section: Role Of Osm In Hematopoiesis Adipogenesis and Osteogenesismentioning
confidence: 88%
“…However, the inactivation of all protease activity does not prevent efficient mobilization suggesting that protease activity is dispensable. Macrophages appear to play a critical role in retaining HSCs in the BM by promoting the synthesis of retention factors by the niche (Chow et al, 2011; Christopher et al, 2011; Winkler et al, 2010), possibly via the secretion of Oncostatin M (Albiero et al, 2015). G-CSF signaling in macrophage suppresses the retention influence of macrophage on the niche, thereby enhancing an opposing influence of the SNS to reduce CXCL12 synthesis and promote HSC release (Mendez-Ferrer et al, 2008).…”
Section: Discussionmentioning
confidence: 99%
“…54 Recent studies have suggested that this factor was oncostatin M. 177 Thus, macrophages and sympathetic nerves exert the opposite action to the niche, forming a regulatory loop. 54 HSC retention in the BM and the spleen relies at least partially on a ligand for VCAM-1, integrin VLA-4, 178180 which is expressed by macrophages.…”
Section: Heterogeneity Of Cells Of the Nichementioning
confidence: 99%