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Article ; Online: Oncostatin M and its role in fibrosis.

Stawski, Lukasz / Trojanowska, Maria

2018 Volume 60, Issue 1, Page(s) 40–49

Abstract: Oncostain M, a member of the IL-6 family of cytokines, is produced by immune cells in response ...

Abstract	Oncostain M, a member of the IL-6 family of cytokines, is produced by immune cells in response to infections and tissue injury. OSM has a broad, often context-dependent effect on various cellular processes including differentiation, hematopoiesis, cell proliferation, and cell survival. OSM signaling is initiated by binding to type I (LIFRβ/gp130) or type II (OSMRβ/gp130) receptor complexes and involves activation of Janus kinase/signal transducer and activator of transcription, mitogen-activated protein kinase, and phosphatidylinositol-3-kinase. High levels of OSM have been detected in many chronic inflammatory conditions characterized by fibrosis, giving a rationale to target OSM for the treatment of these diseases. Here we discuss the current knowledge on the role of OSM in various stages of the fibrotic process including inflammation, vascular dysfunction, and activation of fibroblasts.
MeSH term(s)	Animals ; Fibrosis ; Humans ; Inflammation/pathology ; Models, Biological ; Oncostatin M/metabolism ; Signal Transduction ; Vascular System Injuries/metabolism ; Vascular System Injuries/pathology
Chemical Substances	Oncostatin M (106956-32-5)
Language	English
Publishing date	2018-07-30
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	185551-7
ISSN	1607-8438 ; 0091-1690 ; 0300-8207
ISSN (online)	1607-8438
ISSN	0091-1690 ; 0300-8207
DOI	10.1080/03008207.2018.1500558
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Article ; Online: The role of the oncostatin M/OSM receptor β axis in activating dermal microvascular endothelial cells in systemic sclerosis.

Marden, G / Wan, Q / Wilks, J / Nevin, K / Feeney, M / Wisniacki, N / Trojanowski, M / Bujor, A / Stawski, L / Trojanowska, M

Arthritis research & therapy

2020 Volume 22, Issue 1, Page(s) 179

Abstract: ... and progressive fibrosis of the skin and other organs. Oncostatin M, a member of the IL-6 family, is ...

Abstract	Background: Scleroderma (SSc) is a rare autoimmune disease characterized by vascular impairment and progressive fibrosis of the skin and other organs. Oncostatin M, a member of the IL-6 family, is elevated in SSc serum and was recognized as a significant player in various stages of fibrosis. The goal of this study was to assess the contribution of the OSM/OSMRβ pathway to endothelial cell (EC) injury and activation in SSc. Methods: IHC and IF were used to assess the distribution of OSM and OSMRβ in SSc (n = 14) and healthy control (n = 7) skin biopsies. Cell culture experiments were performed in human dermal microvascular endothelial cells (HDMECs) and included mRNA and protein analysis, and cell migration and proliferation assays. Ex vivo skin organoid culture was used to evaluate the effect of OSM on perivascular fibrosis. Results: OSMRβ protein was elevated in dermal ECs and in fibroblasts of SSc patients. Treatments of HDMECs with OSM or IL-6+sIL-6R have demonstrated that both cytokines similarly stimulated proinflammatory genes and genes related to endothelial to mesenchymal transition (EndMT). OSM was more effective than IL-6+sIL-6R in inducing cell migration, while both treatments similarly induced cell proliferation. The effects of OSM were mediated via OSMRβ and STAT3, while the LIFR did not contribute to these responses. Both OSM and IL-6+sIL-6R induced profibrotic gene expression in HDMECs, as well as expansion of the perivascular PDGFRβ Conclusions: This work provides new insights into the role of the OSM/OSMRβ axis in activation/injury of dermal ECs and supports the involvement of this pathway in SSc vascular disease.
MeSH term(s)	Endothelial Cells ; Fibrosis ; Humans ; Oncostatin M ; Oncostatin M Receptor beta Subunit/genetics ; Scleroderma, Systemic
Chemical Substances	OSM protein, human ; Oncostatin M Receptor beta Subunit ; Oncostatin M (106956-32-5)
Language	English
Publishing date	2020-07-31
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2107602-9
ISSN	1478-6362 ; 1478-6354
ISSN (online)	1478-6362
ISSN	1478-6354
DOI	10.1186/s13075-020-02266-0
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Article: Comparative studies of oncostatin M expression in the tissues of adult rodents.

Znoyko, Iya / Sohara, Naondo / Spicer, Samuel S / Trojanowska, Maria / Reuben, Adrian

The anatomical record. Part A, Discoveries in molecular, cellular, and evolutionary biology

2005 Volume 283, Issue 1, Page(s) 182–186

Abstract: Oncostatin M (OSM), a member of the interleukin-6 family of cytokines, is thought to be expressed ...

Abstract	Oncostatin M (OSM), a member of the interleukin-6 family of cytokines, is thought to be expressed mostly by activated T-lymphocytes and monocytes in adult animals. However, here we report specific constitutive tissue expression of OSM in the pancreas, kidney, testes, spleen, stomach, and brain, but not liver or lung, of three adult rodent species.
MeSH term(s)	Animals ; Cytokines/metabolism ; Female ; Gerbillinae ; Gestational Age ; Immunoenzyme Techniques ; Male ; Mice ; Oncostatin M ; Peptides/metabolism ; Rats ; Rats, Wistar ; Rodentia/metabolism ; Species Specificity
Chemical Substances	Cytokines ; Osm protein, mouse ; Peptides ; Oncostatin M (106956-32-5)
Language	English
Publishing date	2005-03
Publishing country	United States
Document type	Comparative Study ; Journal Article
ZDB-ID	2103089-3
ISSN	1552-4884 ; 0003-276X
ISSN	1552-4884 ; 0003-276X
DOI	10.1002/ar.a.20159
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Article: Expression of oncostatin M and its receptors in normal and cirrhotic human liver.

Znoyko, Iya / Sohara, Naondo / Spicer, Samuel S / Trojanowska, Maria / Reuben, Adrian

Journal of hepatology

2005 Volume 43, Issue 5, Page(s) 893–900

Abstract: ... oncostatin M (OSM) is up-regulated, but its cellular origin is unknown. Therefore, we investigated ...

Abstract	Background/aims: In the cirrhotic liver, gene expression of the multifunctional cytokine oncostatin M (OSM) is up-regulated, but its cellular origin is unknown. Therefore, we investigated the expression of OSM protein and its specific receptor subunits, OSMRbeta and LIFRbeta in normal and cirrhotic human liver using immunohistochemical and Western blot analysis. Results: OSM protein was expressed in Kupffer cells, variably in normal liver but consistently in cirrhosis. OSMRbeta was expressed at low level in hepatocytes of all normal livers examined, but in no cirrhotic sample. In contrast, LIFRbeta receptor was expressed weakly in normal livers, but much more intensely in cirrhosis, in reactive ductules, bile duct epithelial cells and perisinusoidal areas. Double immunostaining showed co-localization of LIFRbeta with cytokeratin 7, proliferating cell nuclear antigen (PCNA) and leukemia inhibitory factor (LIF), in bile duct epithelial cells, but not with alpha-smooth muscle actin, a myofibroblast marker. Conclusions: In human liver, OSM protein is expressed in Kupffer cells, variably in normals but universally in cirrhosis. The differential expression pattern of OSM and its receptors could allow for differential OSM signaling by alternative utilization of receptors to promote hepatocyte proliferation in acute injury and, with its homologue LIF, for the bile ductular reaction in cirrhosis.
MeSH term(s)	Animals ; Antineoplastic Agents/metabolism ; Gene Expression ; Growth Inhibitors/metabolism ; Hepatocytes/cytology ; Hepatocytes/metabolism ; Humans ; Inflammation Mediators/metabolism ; Keratin-7 ; Keratins/metabolism ; Leukemia Inhibitory Factor Receptor alpha Subunit ; Liver/cytology ; Liver/metabolism ; Liver Cirrhosis/metabolism ; Liver Cirrhosis/pathology ; Oncostatin M ; Peptides/metabolism ; Protein Subunits/metabolism ; Receptors, Cytokine/metabolism ; Receptors, OSM-LIF ; Receptors, Oncostatin M
Chemical Substances	Antineoplastic Agents ; Growth Inhibitors ; Inflammation Mediators ; KRT7 protein, human ; Keratin-7 ; LIFR protein, human ; Leukemia Inhibitory Factor Receptor alpha Subunit ; OSM protein, human ; Peptides ; Protein Subunits ; Receptors, Cytokine ; Receptors, OSM-LIF ; Receptors, Oncostatin M ; Oncostatin M (106956-32-5) ; Keratins (68238-35-7)
Language	English
Publishing date	2005-11
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	605953-3
ISSN	1600-0641 ; 0168-8278
ISSN (online)	1600-0641
ISSN	0168-8278
DOI	10.1016/j.jhep.2005.04.020
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Article: Climate Change Mitigation and Preservation of the Cultural Heritage—A Story of the Municipal Park in Rumia, Poland

Trojanowska, Monika

Land. 2022 Jan. 02, v. 11, no. 1

2022

Abstract: Climate change may affect cultural heritage in at least two ways: direct physical effects on the site, building, or structure and effects on social structures. Creating urban parks with therapeutic landscapes can mitigate some of these detrimental ... ...

Abstract	Climate change may affect cultural heritage in at least two ways: direct physical effects on the site, building, or structure and effects on social structures. Creating urban parks with therapeutic landscapes can mitigate some of these detrimental effects. This paper presents the revitalization of the former water forge, located in the center of Rumia, near the Tri-City agglomeration. The study focused on the history of the site and the historic manor house called “Dwór pod Lipami” and the preservation efforts. The social engagement, which led to the development of the landscape park and the construction of a talent playground, was an essential factor in the renewal process. The second part of the work presents an assessment of the therapeutic and recreational values of the new urban park using the Universal Standard for Health-Promoting Places, Community Park Audit Tool (CPAT), and mapping the users’ preferences. This operation of urban renewal resulted in creating a popular park that helps promote the health and well-being of the local community.
Keywords	climate change ; cultural heritage ; health promotion ; land ; landscapes ; therapeutics ; urban development ; urban parks ; Poland
Language	English
Dates of publication	2022-0102
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2682955-1
ISSN	2073-445X
ISSN	2073-445X
DOI	10.3390/land11010065
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Article ; Online: Comparison of 1.0 M gadobutrol and 0.5 M gadopentate dimeglumine-enhanced MRI in 471 patients with known or suspected renal lesions: results of a multicenter, single-blind, interindividual, randomized clinical phase III trial.

Tombach, Bernd / Bohndorf, Klaus / Brodtrager, Wolfgang / Claussen, Claus D / Düber, Christoph / Galanski, Michael / Grabbe, Eckhardt / Gortenuti, Giacomo / Kuhn, Michael / Gross-Fengels, Walter / Hammerstingl, Renate / Happel, Brigitte / Heinz-Peer, Gertraud / Jung, Gregor / Kittner, Thomas / Lagalla, Roberto / Lengsfeld, Philipp / Loose, Reinhard / Oyen, Raymond H G /

Pavlica, Pietro / Pering, Christiane / Pozzi-Mucelli, Roberto / Persigehl, Thorsten / Reimer, Peter / Renken, Nomdo S / Richter, Götz M / Rummeny, Ernst J / Schäfer, Fritz / Szczerbo-Trojanowska, Malgorzata / Urbanik, Andrzej / Vogl, Thomas J / Hajek, Paul

European radiology

2008 Volume 18, Issue 11, Page(s) 2610–2619

Abstract: ... contrast agents, 1.0 M gadobutrol and 0.5 M gadopentate dimeglumine, for magnetic resonance imaging (MRI ... documents evidence for the noninferiority of a single i.v. bolus injection of 1.0 M gadobutrol compared with 0.5 M ...

Abstract	The purpose of this phase III clinical trial was to compare two different extracellular contrast agents, 1.0 M gadobutrol and 0.5 M gadopentate dimeglumine, for magnetic resonance imaging (MRI) in patients with known or suspected focal renal lesions. Using a multicenter, single-blind, interindividual, randomized study design, both contrast agents were compared in a total of 471 patients regarding their diagnostic accuracy, sensitivity, and specificity to correctly classify focal lesions of the kidney. To test for noninferiority the diagnostic accuracy rates for both contrast agents were compared with CT results based on a blinded reading. The average diagnostic accuracy across the three blinded readers ('average reader') was 83.7% for gadobutrol and 87.3% for gadopentate dimeglumine. The increase in accuracy from precontrast to combined precontrast and postcontrast MRI was 8.0% for gadobutrol and 6.9% for gadopentate dimeglumine. Sensitivity of the average reader was 85.2% for gadobutrol and 88.7% for gadopentate dimeglumine. Specificity of the average reader was 82.1% for gadobutrol and 86.1% for gadopentate dimeglumine. In conclusion, this study documents evidence for the noninferiority of a single i.v. bolus injection of 1.0 M gadobutrol compared with 0.5 M gadopentate dimeglumine in the diagnostic assessment of renal lesions with CE-MRI.
MeSH term(s)	Contrast Media ; Europe/epidemiology ; Female ; Gadolinium DTPA/administration & dosage ; Humans ; Image Enhancement/methods ; Kidney Neoplasms/diagnosis ; Kidney Neoplasms/epidemiology ; Magnetic Resonance Imaging/methods ; Male ; Middle Aged ; Organometallic Compounds/administration & dosage ; Reproducibility of Results ; Sensitivity and Specificity ; Single-Blind Method
Chemical Substances	Contrast Media ; Organometallic Compounds ; gadobutrol (1BJ477IO2L) ; Gadolinium DTPA (K2I13DR72L)
Language	English
Publishing date	2008-07-08
Publishing country	Germany
Document type	Clinical Trial, Phase III ; Journal Article ; Multicenter Study ; Randomized Controlled Trial
ZDB-ID	1085366-2
ISSN	1432-1084 ; 0938-7994 ; 1613-3749
ISSN (online)	1432-1084
ISSN	0938-7994 ; 1613-3749
DOI	10.1007/s00330-008-1054-2
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Article: Oncostatin M stimulates tissue inhibitor of metalloproteinase-1 via a MEK-sensitive mechanism in human myofibroblasts.

Sohara, Naondo / Trojanowska, Maria / Reuben, Adrian

Journal of hepatology

2002 Volume 36, Issue 2, Page(s) 191–199

Abstract: Background/aims: We previously showed that in cultured human myofibroblasts (hMFBs), Oncostatin M ...

Abstract	Background/aims: We previously showed that in cultured human myofibroblasts (hMFBs), Oncostatin M (OSM)-stimulated collagen accumulation is associated with increased tissue inhibitor of metalloproteinase (TIMP)1 message. However, the mechanism is unknown. Methods: hMFBs were isolated by outgrowth from cirrhotic liver explants and cultured. Using OSM (10 ng/ml) stimulation, with and without PD98059 (PD, a specific mitogen-activated protein kinase/extracellular signal-related kinase (MEK) inhibitor), we measured: TIMP-1 protein in culture medium by Western blot, TIMP-1 mRNA levels and stability by Northern analysis, TIMP-1 promoter activity (including transcription site mutation analysis), DNA binding activity to nuclear proteins by electrophoretic mobility shift assay (EMSA), and total and phosphorylated MAP kinase in hMFB extracts by Western blot. Results: OSM stimulation of hMFBs increased TIMP-1 protein production 1.69-fold, TIMP-1 mRNA levels 2.36-fold, promoter activity 2.22-fold, TIMP-1 message stability, and phosphorylation of mitogen-activated protein kinase (MAPK). PD inhibited OSM-mediated stimulation of TIMP-1 protein, mRNA, promoter activity, phosphorylation of MAPK, and TIMP-1 message stability. An SP-1 transcription site of the TIMP-1 promoter is essential for OSM induction of TIMP-1 promoter activity. EMSA demonstrates that this site binds to transcriptional factors SP-1 and SP-3. Conclusions: OSM stimulates the TIMP-1 axis in hMFBs in vitro via a MEK-MAP kinase cascade.
MeSH term(s)	Cells, Cultured ; Enzyme Inhibitors/pharmacology ; Fibroblasts/cytology ; Fibroblasts/enzymology ; Flavonoids/pharmacology ; Gene Expression/drug effects ; Growth Inhibitors/pharmacology ; Humans ; Liver/cytology ; MAP Kinase Kinase Kinase 1 ; MAP Kinase Signaling System/drug effects ; MAP Kinase Signaling System/physiology ; Oncostatin M ; Peptides/pharmacology ; Phosphorylation ; Promoter Regions, Genetic/drug effects ; Promoter Regions, Genetic/genetics ; Protein-Serine-Threonine Kinases/metabolism ; RNA, Messenger/analysis ; Tissue Inhibitor of Metalloproteinase-1/genetics
Chemical Substances	Enzyme Inhibitors ; Flavonoids ; Growth Inhibitors ; OSM protein, human ; Peptides ; RNA, Messenger ; Tissue Inhibitor of Metalloproteinase-1 ; Oncostatin M (106956-32-5) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; MAP Kinase Kinase Kinase 1 (EC 2.7.11.25) ; MAP3K1 protein, human (EC 2.7.11.25) ; 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one (SJE1IO5E3I)
Language	English
Publishing date	2002-01-30
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	605953-3
ISSN	1600-0641 ; 0168-8278
ISSN (online)	1600-0641
ISSN	0168-8278
DOI	10.1016/s0168-8278(01)00265-3
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Article: Oncostatin M: a cytokine upregulated in human cirrhosis, increases collagen production by human hepatic stellate cells.

Levy, M T / Trojanowska, M / Reuben, A

Journal of hepatology

2000 Volume 32, Issue 2, Page(s) 218–226

Abstract: ... extracellular matrix seen in cirrhosis. The cytokine oncostatin M has been implicated in fibrogenesis in vitro ... is unknown.: Methods: To examine the effect of oncostatin M on collagen production by human ... in response to oncostation M stimulation. To explore the potential biological significance of this work ...

Abstract	Background/aims: Hepatic stellate cells are predominantly responsible for the increased extracellular matrix seen in cirrhosis. The cytokine oncostatin M has been implicated in fibrogenesis in vitro in other cell types and in vivo in other tissues, although its effect on hepatic stellate cells or in cirrhosis is unknown. Methods: To examine the effect of oncostatin M on collagen production by human hepatic stellate cells in culture, collagen protein was measured and collagen alpha2(1) mRNA was quantified by Northern analysis. Tissue inhibitor of metalloproteinase-1 (an inhibitor of collagen degradation) mRNA was measured in response to oncostation M stimulation. To explore the potential biological significance of this work to human liver disease, oncostatin M messenger RNA in normal and cirrhotic human liver was measured. Results: Oncostatin M induced in a 2-fold increase in collagen secretion. The potency of induction of collagen protein secretion was equal to that observed after transforming growth factor beta stimulation. An increase in endogenous collagen alpha2(1) mRNA could not be detected. This suggested a post-transcriptional mechanism for the increase in collagen protein. In response to oncostatin M stimulation, there was a 2-fold increase in the tissue inhibitor or metalloproteinase-1 mRNA. Oncostatin M mRNA was detected in 6/6 cirrhotic livers and 1/7 normal livers after 28 PCR cycles. Conclusion: These results suggest that oncostatin M expression is upregulated in cirrhosis where it may have a role as a profibrogenic cytokine in hepatic stellate cells.
MeSH term(s)	Cells, Cultured ; Collagen/biosynthesis ; Collagen/genetics ; Collagen/metabolism ; Collagen Type I ; Culture Media/metabolism ; Humans ; Liver/cytology ; Liver/drug effects ; Liver/metabolism ; Liver Cirrhosis/metabolism ; Oncostatin M ; Peptides/metabolism ; Peptides/pharmacology ; RNA, Messenger/metabolism ; Tissue Inhibitor of Metalloproteinase-1/genetics ; Transforming Growth Factor beta/pharmacology ; Up-Regulation
Chemical Substances	Collagen Type I ; Culture Media ; OSM protein, human ; Peptides ; RNA, Messenger ; Tissue Inhibitor of Metalloproteinase-1 ; Transforming Growth Factor beta ; Oncostatin M (106956-32-5) ; Collagen (9007-34-5)
Language	English
Publishing date	2000-02
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	605953-3
ISSN	1600-0641 ; 0168-8278
ISSN (online)	1600-0641
ISSN	0168-8278
DOI	10.1016/s0168-8278(00)80066-5
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Article ; Online: Chemical Fractionation in Environmental Studies of Potentially Toxic Particulate-Bound Elements in Urban Air: A Critical Review.

Świetlik, Ryszard / Trojanowska, Marzena

Toxics

2022 Volume 10, Issue 3

Abstract: In recent years, studies of heavy metal air pollution have increasingly gone beyond determining total concentrations of individual toxic metals. Chemical fractionation of potentially toxic elements in airborne particles is becoming an important part of ... ...

Abstract	In recent years, studies of heavy metal air pollution have increasingly gone beyond determining total concentrations of individual toxic metals. Chemical fractionation of potentially toxic elements in airborne particles is becoming an important part of these studies. This review covers the articles that have been published over the last three decades. Attention was paid to the issue of atmospheric aerosol sampling, sample pretreatment, sequential extraction schemes and conditions of individual extractions. Geochemical forms of metals occurring in the air in urban areas were considered in detail. Based on the data sets from chemical fractionation of particulate matter samples by three sequential extraction procedures (SEPs)-Fernández Espinosa, BCR and Chester's-the compilation of the chemical distribution patterns of As, Cd, Co, Cr, Cu, Fe, Mn, Ni, Pb and Zn was prepared. The human health risk posed by these toxic and/or carcinogenic elements via inhalation of atmospheric particles was estimated for two categories of polluted urban areas: the commonly encountered pollution level and the high pollution level.
Language	English
Publishing date	2022-03-04
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2733883-6
ISSN	2305-6304 ; 2305-6304
ISSN (online)	2305-6304
ISSN	2305-6304
DOI	10.3390/toxics10030124
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Article: Oncostatin M stimulates transcription of the human alpha2(I) collagen gene via the Sp1/Sp3-binding site.

Ihn, H / LeRoy, E C / Trojanowska, M

The Journal of biological chemistry

1997 Volume 272, Issue 39, Page(s) 24666–24672

Abstract: Oncostatin M (OSM), a member of the hematopoietic cytokine family, has been implicated in excessive ...

Abstract	Oncostatin M (OSM), a member of the hematopoietic cytokine family, has been implicated in excessive bone growth and in the process of fibrosis. As part of an ongoing study of the molecular mechanisms of fibrosis, we have investigated the transcriptional regulation of the alpha2(I) collagen gene by OSM in human fibroblasts. An OSM response element was mapped by deletional analysis between base pairs (bp) -148 and -108 in the alpha2(I) collagen promoter. Further functional analysis of the alpha2(I) collagen promoter containing various substitution mutations revealed that both the basal activity and OSM stimulation of this promoter are mediated by a TCCTCC motif located between bp -128 and -123. Furthermore, three copies of the 12-bp synthetic alpha2(I) collagen promoter fragment containing the "TCC" motif conferred OSM inducibility to the otherwise unresponsive thymidine kinase promoter. Electrophoretic mobility shift assays demonstrated that the TCCTCC motif constitutes a novel binding site for the transcription factors Sp1 and Sp3. No differences have been observed in in vitro gel shift binding assays between unstimulated and OSM-stimulated fibroblasts. However, subtle conformational changes were detected in the region of the promoter surrounding TCC repeats after OSM stimulation using in vivo footprint analysis. In conclusion, this study characterized a dual-function response element that mediates the basal activity and OSM stimulation of the human alpha2(I) collagen promoter.
MeSH term(s)	Binding Sites ; Collagen/genetics ; Collagen/metabolism ; Cytokines/metabolism ; Cytokines/physiology ; DNA-Binding Proteins/metabolism ; Humans ; Nuclear Proteins/metabolism ; Oncostatin M ; Peptides/metabolism ; Peptides/physiology ; Promoter Regions, Genetic ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Sp1 Transcription Factor/metabolism ; Sp3 Transcription Factor ; Transcription Factors/metabolism ; Transcription, Genetic/physiology ; Up-Regulation
Chemical Substances	Cytokines ; DNA-Binding Proteins ; Nuclear Proteins ; OSM protein, human ; Peptides ; RNA, Messenger ; SP3 protein, human ; Sp1 Transcription Factor ; Transcription Factors ; Oncostatin M (106956-32-5) ; Sp3 Transcription Factor (148710-94-5) ; Collagen (9007-34-5)
Language	English
Publishing date	1997-09-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.272.39.24666
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