WikiGenes - Osm - oncostatin M

de Hooge, A.S., Langdon, C., Holzer, R.G., Langdon, C., Richards, C.D., et al.

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Disease relevance of Osm

Overexpression of murine OSM in lungs of C57BL/6 mice using an adenovirus vector encoding murine OSM resulted in a vigorous inflammatory response by day 7 after intranasal administration, including marked extracellular matrix accumulation and eosinophil infiltration [1].
Bone resorption was also inhibited by OSM [2].
We examined the effects of OSM on the proliferation and metastatic potential of the murine mammary carcinoma cell lines M6 (adenocarcinoma) and M6c (metastatic adenocarcinoma) [3].
Previously, oncostatin M (OSM) has been shown to inhibit the proliferation of breast cancer cells in vitro [3].
Immunohistochemistry showed that macrophage-like cells infiltrating human aortic aneurysms expressed oncostatin M, so it is present during a chronic inflammatory reaction [4].

High impact information on Osm

Regulation of an extrathymic T-cell development pathway by oncostatin M [5].
Injection of the Th1 cytokine Oncostatin M but not other cytokines into Stat4-deficient mice recovers progenitor cell activity to wild-type levels [6].
In addition, OSM enhances the formation of endothelial cell clusters [7].
This protein blocked cell proliferation and chemotaxis of AIDS-KS cells in response to activated lymphocyte conditioned medium (AL-CM) and oncostatin M (OSM) [8].
Stress erythropoiesis, therefore, requires stage-specific EpoR-PY343-Stat5 signals, some of which selectively bolster SCF and oncostatin-M action [9].

Chemical compound and disease context of Osm

Oncostatin-M (OSM) is a glycoprotein interleukin-6 cytokine known to inhibit bone resorption in fetal long bone cultures [10].

Biological context of Osm

In this study, we investigated the role of OSM in regulation of VCAM-1 expression, and STAT6 tyrosine 641 phosphorylation in murine fibroblasts [11].
OSM strongly induced interleukin (IL)-6 gene expression, a known mediator of osteoclast development [12].
Collectively, these results provide good evidence that OSM regulates synovial fibroblast function differently than other IL-6-type cytokines, and can induce a proliferative invasive phenotype of synovium in vivo in mice on overexpression [13].
To elucidate the in vivo effect of OSM on bone remodeling, we injected an adenoviral vector encoding murine OSM in knee joints of mice [12].
OSM affected mesenchymal cell differentiation and promoted the hematopoietic supportive activity of marrow stromal cell lines [14].

Anatomical context of Osm

Murine oncostatin M stimulates mouse synovial fibroblasts in vitro and induces inflammation and destruction in mouse joints in vivo [13].
These data strongly support a role of OSM in lung inflammatory responses that involve eosinophil infiltration [1].
In vitro OSM enhanced the effect of bone morphogenetic protein-2 on osteoblast differentiation [12].
Adenoviral transfer of murine oncostatin M elicits periosteal bone apposition in knee joints of mice, despite synovial inflammation and up-regulated expression of interleukin-6 and receptor activator of nuclear factor-kappa B ligand [12].
Studies in human, canine, and murine models have revealed oncostatin M (OSM) expression in infiltrating leukocytes [15].

Associations of Osm with chemical compounds

LIF and OSM specifically trigger STAT1 cytoplasmic to nuclear translocation, whereas PGF2alpha fails to do so [16].
The activity of OSM was reduced by indomethacin (10(-8)-10(-6) M), whereas addition of dexamethasone (DEX) at 10(-7)-10(-5) M synergistically enhanced OSM-induced numbers of TRAP(+)MNC [17].
In wild type animals, the IL-6 family member Oncostatin M (OSM) was found to be transiently expressed in the luminal epithelium on late day 4 and then in the stroma at the attachment site on days 5-6 of pregnancy, with a similar but not identical pattern to that of Cox-2 [18].
Oncostatin M (OM) is a 28-kD glycoprotein that exhibits a panoply of biologic effects [19].
Mice deficient in the OSM receptor (OSMR(-/-)) showed impaired liver regeneration with persistent parenchymal necrosis after carbon tetrachloride (CCl(4)) exposure [20].

Regulatory relationships of Osm

STAT6 was not essential for OSM-induced VCAM-1 or eotaxin-1 as assessed in STAT6(-/-) MLF [11].
Oncostatin M regulates eotaxin expression in fibroblasts and eosinophilic inflammation in C57BL/6 mice [1].
TBR31-2 is a bipotent progenitor for adipocytes and osteoblasts, and OSM stimulated osteogenic differentiation while inhibiting adipogenic differentiation [14].
In addition, OSM induces the expression of Cox-2 mRNA, and of the 74 kDa form of Cox-2 protein [3].
Most OSM-expressing cells expressed IL-5 receptor alpha subunit, a marker for eosinophil lineage [21].

Other interactions of Osm

Differential regulation of macrophage differentiation in response to leukemia inhibitory factor/oncostatin-M/interleukin-6: the effect of enforced expression of the SCL transcription factor [22].
OSM was able to fully substitute for LIF; both cytokines promoted the proliferation of migratory PGC (mPGC) and enhanced the viability of postmigratory (colonizing) PGC (cPGC) when cultured on SI/SI4-m220 cells [23].
Ciliary neurotrophic factor, but not oncostatin M, had the same effect, although they both bind to the IL-6ST (gp130) receptor [24].
Mouse OSM, LIF and CT-1 strongly induced the formation of tartrate resistant acid phosphatase positive (TRAP(+)) multinucleated cells (MNC) in a dose-dependent fashion [17].
Combination of IL-4 and OSM synergistically enhanced eotaxin-1 expression in MLF [11].

Analytical, diagnostic and therapeutic context of Osm

To investigate whether OSM acts on the hematopoietic progenitors directly or indirectly, we performed BM transplantation experiments [25].
In this study, we performed in situ hybridization to examine the tissue distribution of cells expressing OSM mRNA in the developing and the adult mice [21].
We found that subcutaneous injection of oncostatin M in mice caused an acute inflammatory reaction [4].
Fetal liver development requires a paracrine action of oncostatin M through the gp130 signal transducer [26].
Interleukin (IL)-6, IL-11, leukemia inhibitory factor, and oncostatin M similarly induce osteoclast formation in cocultures of osteoblastic cells and bone marrow cells [27].

References

Oncostatin M regulates eotaxin expression in fibroblasts and eosinophilic inflammation in C57BL/6 mice. Langdon, C., Kerr, C., Tong, L., Richards, C.D. J. Immunol. (2003)
Oncostatin-M: a new bone active cytokine that activates osteoblasts and inhibits bone resorption. Jay, P.R., Centrella, M., Lorenzo, J., Bruce, A.G., Horowitz, M.C. Endocrinology (1996)
Oncostatin M stimulates the detachment of a reservoir of invasive mammary carcinoma cells: role of cyclooxygenase-2. Holzer, R.G., Ryan, R.E., Tommack, M., Schlekeway, E., Jorcyk, C.L. Clin. Exp. Metastasis (2004)
Oncostatin M is a proinflammatory mediator. In vivo effects correlate with endothelial cell expression of inflammatory cytokines and adhesion molecules. Modur, V., Feldhaus, M.J., Weyrich, A.S., Jicha, D.L., Prescott, S.M., Zimmerman, G.A., McIntyre, T.M. J. Clin. Invest. (1997)
Regulation of an extrathymic T-cell development pathway by oncostatin M. Clegg, C.H., Rulffes, J.T., Wallace, P.M., Haugen, H.S. Nature (1996)
Th1 cells regulate hematopoietic progenitor cell homeostasis by production of oncostatin M. Broxmeyer, H.E., Bruns, H.A., Zhang, S., Cooper, S., Hangoc, G., McKenzie, A.N., Dent, A.L., Schindler, U., Naeger, L.K., Hoey, T., Kaplan, M.H. Immunity (2002)
In vitro expansion of murine multipotential hematopoietic progenitors from the embryonic aorta-gonad-mesonephros region. Mukouyama, Y., Hara, T., Xu, M., Tamura, K., Donovan, P.J., Kim, H., Kogo, H., Tsuji, K., Nakahata, T., Miyajima, A. Immunity (1998)
Apolipoprotein E (ApoE), a novel heparin-binding protein inhibits the development of Kaposi's sarcoma-like lesions in BALB/c nu/nu mice. Browning, P.J., Roberts, D.D., Zabrenetzky, V., Bryant, J., Kaplan, M., Washington, R.H., Panet, A., Gallo, R.C., Vogel, T. J. Exp. Med. (1994)
Signals for stress erythropoiesis are integrated via an erythropoietin receptor-phosphotyrosine-343-Stat5 axis. Menon, M.P., Karur, V., Bogacheva, O., Bogachev, O., Cuetara, B., Wojchowski, D.M. J. Clin. Invest. (2006)
Effect of oncostatin-M on proliferation and activity in osteoblastic MC3T3-E1 cells. Shih, C., Yen, C.C. Zhonghua Yi Xue Za Zhi (Taipei) (1999)
Oncostatin-M up-regulates VCAM-1 and synergizes with IL-4 in eotaxin expression: involvement of STAT6. Fritz, D.K., Kerr, C., Tong, L., Smyth, D., Richards, C.D. J. Immunol. (2006)
Adenoviral transfer of murine oncostatin M elicits periosteal bone apposition in knee joints of mice, despite synovial inflammation and up-regulated expression of interleukin-6 and receptor activator of nuclear factor-kappa B ligand. de Hooge, A.S., van de Loo, F.A., Bennink, M.B., de Jong, D.S., Arntz, O.J., Lubberts, E., Richards, C.D., vandDen Berg, W.B. Am. J. Pathol. (2002)
Murine oncostatin M stimulates mouse synovial fibroblasts in vitro and induces inflammation and destruction in mouse joints in vivo. Langdon, C., Kerr, C., Hassen, M., Hara, T., Arsenault, A.L., Richards, C.D. Am. J. Pathol. (2000)
Oncostatin m regulates mesenchymal cell differentiation and enhances hematopoietic supportive activity of bone marrow stromal cell lines. Yanai, N., Obinata, M. In Vitro Cell. Dev. Biol. Anim. (2001)
Oncostatin M differentially regulates CXC chemokines in mouse cardiac fibroblasts. Lafontant, P.J., Burns, A.R., Donnachie, E., Haudek, S.B., Smith, C.W., Entman, M.L. Am. J. Physiol., Cell Physiol. (2006)
Leukemia inhibitory factor induces DNA synthesis in Swiss mouse 3T3 cells independently of cyclin D1 expression through a mechanism involving MEK/ERK1/2 activation. Dekanty, A., Sauane, M., Cadenas, B., Coluccio, F., Barrio, M., Casala, J., Paciencia, M., Rogers, F., Coso, O.A., Piwien-Pilipuk, G., Rudland, P.S., de Asúa, L.J. J. Biol. Chem. (2006)
Stimulation of osteoclast differentiation in vitro by mouse oncostatin M, leukaemia inhibitory factor, cardiotrophin-1 and interleukin 6: synergy with dexamethasone. Richards, C.D., Langdon, C., Deschamps, P., Pennica, D., Shaughnessy, S.G. Cytokine (2000)
Characterization of the uterine phenotype during the peri-implantation period for LIF-null, MF1 strain mice. Fouladi-Nashta, A.A., Jones, C.J., Nijjar, N., Mohamet, L., Smith, A., Chambers, I., Kimber, S.J. Dev. Biol. (2005)
Thrombocytopoietic properties of oncostatin M. Wallace, P.M., MacMaster, J.F., Rillema, J.R., Peng, J., Burstein, S.A., Shoyab, M. Blood (1995)
Hepatocyte proliferation and tissue remodeling is impaired after liver injury in oncostatin M receptor knockout mice. Nakamura, K., Nonaka, H., Saito, H., Tanaka, M., Miyajima, A. Hepatology (2004)
Expression of oncostatin M in hematopoietic organs. Tamura, S., Morikawa, Y., Miyajima, A., Senba, E. Dev. Dyn. (2002)
Differential regulation of macrophage differentiation in response to leukemia inhibitory factor/oncostatin-M/interleukin-6: the effect of enforced expression of the SCL transcription factor. Tanigawa, T., Nicola, N., McArthur, G.A., Strasser, A., Begley, C.G. Blood (1995)
Functional requirement of gp130-mediated signaling for growth and survival of mouse primordial germ cells in vitro and derivation of embryonic germ (EG) cells. Koshimizu, U., Taga, T., Watanabe, M., Saito, M., Shirayoshi, Y., Kishimoto, T., Nakatsuji, N. Development (1996)
Leukemia inhibitory factor enhances formation of germ cell colonies in neonatal mouse testis culture. Kanatsu-Shinohara, M., Inoue, K., Ogonuki, N., Miki, H., Yoshida, S., Toyokuni, S., Lee, J., Ogura, A., Shinohara, T. Biol. Reprod. (2007)
Targeted disruption of oncostatin M receptor results in altered hematopoiesis. Tanaka, M., Hirabayashi, Y., Sekiguchi, T., Inoue, T., Katsuki, M., Miyajima, A. Blood (2003)
Fetal liver development requires a paracrine action of oncostatin M through the gp130 signal transducer. Kamiya, A., Kinoshita, T., Ito, Y., Matsui, T., Morikawa, Y., Senba, E., Nakashima, K., Taga, T., Yoshida, K., Kishimoto, T., Miyajima, A. EMBO J. (1999)
Osteoclasts are present in gp130-deficient mice. Kawasaki, K., Gao, Y.H., Yokose, S., Kaji, Y., Nakamura, T., Suda, T., Yoshida, K., Taga, T., Kishimoto, T., Kataoka, H., Yuasa, T., Norimatsu, H., Yamaguchi, A. Endocrinology (1997)