Oncostatin M stimulates expression of stromal-derived factor-1 in human mesenchymal stem cells

Lee, Mi‐Jeong; Song, Hae Young; Kim, Mi Ra; Sung, Sang-Min; Jung, Jin Sup; Kim, Jae Ho

doi:10.1016/j.biocel.2006.11.003

Cited by 23 publications

(21 citation statements)

References 37 publications

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“…MSCs and endothelial cells are essential components of medullar HSC niches (63-66) and play a major role in HSC maintenance by secreting key cytokines, such as CXCL12 (67). In that respect, it is interesting to note that CXCL12 levels are increased in NHO patient plasma (Supplemental Figure 6) and that CXCL12's expression has been reported to be stimulated by OSM in MSCs (68). Beside their capacity for AOC differentiation, human NHO-MSCs exhibit similar molecular and functional characteristics to BM-MSCs in terms of long-term human hematopoiesis support and SP functionality induction in vitro (48).…”

Section: Discussionmentioning

confidence: 99%

Macrophage-derived oncostatin M contributes to human and mouse neurogenic heterotopic ossifications

Torossian¹,

Guerton²,

Anginot³

et al. 2017

JCI Insight

157

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Section: Discussionmentioning

confidence: 99%

Macrophage-derived oncostatin M contributes to human and mouse neurogenic heterotopic ossifications

Torossian¹,

Guerton²,

Anginot³

et al. 2017

JCI Insight

157

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“…A preliminary study of signaling pathways identified the MEK-p38-STAT3 axis as likely mediating the effect of OSM on CXCL12 expression. Upon an accurate literature review, it appeared that OSM was already known to be induced in classically activated M1 macrophages (30), able to stimulate CXCL12 production by MSCs (31), and possibly involved in SC retention within the BM (32). In addition, gp130 ligands have been shown to be upregulated in the BM of long-standing murine diabetes, whereas genetic deletion of gp130 reverses some pathologic hematopoietic features associated with diabetes (33).…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2015

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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. Depletion of BMMF restored SC mobilization in diabetic mice. We found that CD169 labels M1 macrophages and that conditioned medium (CM) from M1 macrophages, but not from M0 and M2 macrophages, induced chemokine (C-X-C motif) ligand 12 (CXCL12) expression by mesenchymal stem/stromal cells. In silico data mining and in vitro validation identified oncostatin M (OSM) as the soluble mediator contained in M1 CM that induces CXCL12 expression via a mitogenactivated protein kinase kinase-p38-signal transducer and activator of a transcription 3-dependent pathway. In diabetic mice, OSM neutralization prevented CXCL12 induction and improved granulocyte-colony stimulating factor and ischemia-induced mobilization, SC homing to ischemic muscles, and vascular recovery. In patients with diabetes, BM plasma OSM levels were higher and correlated with the BM-to-PB SC ratio. In conclusion, BMMF prevent SC mobilization by OSM secretion, and OSM antagonism is a strategy to restore BM function in diabetes, which can translate into protection mediated by BMSCs.

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“…In many cell types, OSM stimulation has also been reported to activate the MAPK ERK1/2 and the stress-activated protein kinases p38 and JNK (20 -22). These kinases have been implicated in the regulation of OSM-mediated chemokine expression in previous studies, i.e., eotaxin expression in fibroblasts, stromal-derived factor-1 in mesenchymal stem cells and CCL21 in microvascular endothelial cells (23)(24)(25).…”

mentioning

confidence: 94%

Oncostatin M-Induced and Constitutive Activation of the JAK2/STAT5/CIS Pathway Suppresses CCL1, but Not CCL7 and CCL8, Chemokine Expression

Hintzen

Haan

Tuckermann

et al. 2008

The Journal of Immunology

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The recruitment of leukocytes to injured tissue is crucial for the initiation of inflammatory responses as well as for immune surveillance to fight tumor progression. In this study, we show that oncostatin M, a member of the IL-6-type cytokine family and potent proinflammatory cytokine stimulates the expression of the chemokines CCL1, CCL7, and CCL8 in primary human dermal fibroblasts at a faster kinetic than IL-1␤ or TNF-␣. The production of CCL1 and CCL8 is important for migration of monocytes, while specific Abs against CCL1 additionally inhibit the migration of T lymphocytes. We identify the mitogen-activated protein kinases ERK1/2 and p38 as crucial factors for the enhanced expression of CCL1 and CCL8. T he appropriate immune response relies on the interaction of various cell types orchestrated by direct cell contact or soluble factors. As an initial step, recruitment of leukocytes to sites of tissue damage or invaded pathogens occurs. This process is mainly controlled by members of the chemokine superfamily, in particular by the inducible "inflammatory" chemokines (1-3). This subfamily comprises the majority of the so far known 50 chemokines in humans and is distinguished from the constitutively expressed "homeostatic" chemokines. Apart from their function, chemokines can be sorted according to their structure into four groups, designated C, CX 3 C, CXC, and CC depending on the number and spacing of conserved cysteines (1-3). The family of monocyte-chemoattractant proteins (CCL2/MCP-1, CCL7/ MCP-3, CCL8/MCP-2, and CCL13/MCP-4) has mainly proinflammatory activities and exerts its biologic effects through binding to the G-protein coupled receptors CCR1 and CCR2, which are present on the cell surface of a variety of cell types (1, 3). CCL1/ I-309 has been originally identified as a gene expressed in activated T cell lines (4) and specifically binds to CCR8, which is expressed on the cell surface of polarized Th2 cells and regulatory T cells as well as macrophages (5-8).CCL1 as well as the MCP family members CCL7 and CCL8 are considered to play an important role in the recruitment of monocytes and T lymphocytes to sites of inflammation (9 -11). Their enhanced expression during inflammatory processes is stimulated by different cytokines in various cell types, i.e., by IL-1, TNF-␣, and IFN-␥ in human airway smooth-muscle cells (12), by IL-1 and IFN-␥ in both fibroblasts and epithelial cells (13) and by endogenous IL-1 in monocytes (14).In this study, we describe the regulation of CCL1, CCL7, and CCL8 by the IL-6-type cytokine oncostatin M (OSM) 3 in primary human dermal fibroblasts. OSM is a known proinflammatory cytokine, which is secreted by activated monocytes, neutrophils, and T lymphocytes (15). The human cytokine can signal through two receptor complexes: the type I receptor complex consisting of gp130, the common receptor subunit of all IL-6-type cytokines, and the LIF receptor or the type II receptor complex composed of gp130 and the OSM receptor ␤ subunit (16). In contrast, murine OSM only signals throu...

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Oncostatin M stimulates expression of stromal-derived factor-1 in human mesenchymal stem cells

Cited by 23 publications

References 37 publications

Macrophage-derived oncostatin M contributes to human and mouse neurogenic heterotopic ossifications

Macrophage-derived oncostatin M contributes to human and mouse neurogenic heterotopic ossifications

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

Oncostatin M-Induced and Constitutive Activation of the JAK2/STAT5/CIS Pathway Suppresses CCL1, but Not CCL7 and CCL8, Chemokine Expression

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