The differential effects of IL-1 and TNF-? on proinflammatory cytokine and matrix metalloproteinase expression in human chondrosarcoma cells

Shi, Jishu; Schmitt-Talbot, E.; DiMattia, Debra A.; Dullea, Robert

doi:10.1007/s00011-004-1271-3

Cited by 68 publications

(56 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We and others recently reported that the pro-inflammatory cytokines interleukin-1␤ and TNF-␣ induce BMP-2 expression in adult articular chondrocytes and a chondrosarcoma cell line (12,30). Similar BMP-2 induction by those cytokines is also observed in synovial cells (14,31) and could be a widespread event in arthritic joints.…”

supporting

confidence: 60%

Pro-inflammatory Cytokine Tumor Necrosis Factor-α Induces Bone Morphogenetic Protein-2 in Chondrocytes via mRNA Stabilization and Transcriptional Up-regulation

Fukui

Ikeda

Ohnuki

et al. 2006

Journal of Biological Chemistry

View full text Add to dashboard Cite

In articular chondrocytes, the inflammatory cytokine tumor necrosis factor-␣ (TNF-␣) induces the expression of bone morphogenetic protein-2 (BMP-2), a growth factor known to be involved in the induction of cartilage and bone. A study was performed to clarify the mechanism(s) underlying the induction of BMP-2 in chondrogenic ATDC5 cells and primary cultured adult human articular chondrocytes. In ATDC5 cells, the endogenous BMP-2 expression was consistently low throughout the process of chondrogenic differentiation, and TNF-␣ induced BMP-2 expression only after the cells acquired the chondrogenic phenotype. The results of nuclear run-off assay and cycloheximide treatment consistently indicated that ATDC5 cells acquire the capacity to synthesize BMP-2 mRNA in the nuclei during the differentiation process. In an attempt to explain the discrepancy between the active nuclear mRNA synthesis and the observed low expression level in differentiated ATDC5 cells, the stability of BMP-2 mRNA was evaluated, and the cells were found to regulate the expression of BMP-2 at the post-transcriptional level. Human chondrocytes were confirmed to have a similar post-transcriptional regulation. The result of 3-rapid amplification of cDNA end revealed that both human and mouse BMP-2 mRNAs contain multiple pentameric AUUUA motifs in a conserved manner in the 3-untranslated regions, and transient transfection experiments demonstrated that TNF-␣ increases the stability of BMP-2 mRNA through the pentameric motifs. Further experiments revealed that TNF-␣ modulates mRNA stability via p38 signal transduction pathway, whereas the cytokine also augmented the expression of BMP-2 through transcriptional up-regulation via the transcriptional factor NF-B.

show abstract

supporting

confidence: 60%

Pro-inflammatory Cytokine Tumor Necrosis Factor-α Induces Bone Morphogenetic Protein-2 in Chondrocytes via mRNA Stabilization and Transcriptional Up-regulation

Fukui

Ikeda

Ohnuki

et al. 2006

Journal of Biological Chemistry

View full text Add to dashboard Cite

show abstract

“…39 Studies by Wei et al 40 examining the effects of IL-1␤ and IFN-␥ on organ-cultured skin biopsies reported a greater degree of overlap between these two cytokines than that observed here. However, only seven proteins were analyzed by semiquantitative immunohistochemistry in the former study, with lower thresholds required for significance.…”

Section: Discussionmentioning

confidence: 43%

The Psoriatic Transcriptome Closely Resembles That Induced by Interleukin-1 in Cultured Keratinocytes

Mee

Johnson

Morar

et al. 2007

The American Journal of Pathology

View full text Add to dashboard Cite

Psoriasis has been considered an autoimmune, T cellmediated disorder in which adaptive immune responses predominate over those of non-antigen-specific innate immunity. To test this hypothesis, we profiled the transcriptome of psoriatic tissue and compared the data with that from cultured human keratinocytes exposed to the proinflammatory cytokine interleukin (IL)-1␣ and the Th1 cytokine interferon-␥. When compared with patient-matched, nonlesional skin biopsies, psoriatic samples exhibited regulation of 90 transcripts including several members of the epidermal differentiation complex, molecules with antimicrobial activity, and hyperproliferation-associated keratins. Stimulation of keratinocytes with interferon-␥ resulted in regulation of 252 transcripts, with particularly strong expression of the CXCR3-binding ligands CXCL9, -10, and -11 and class II major histocompatibility complex genes, primarily those of the HLA-DR and -DP families. In contrast, the transcriptome resulting from exposure of keratinocytes to IL-1␣ elicited differences in just 19 transcripts, particularly genes within the epidermal differentiation complex and antimicrobial molecules, including PI3 and DEFB4. Major differences between the two keratinocyte transcriptomes were exhibited with only five induced IL-1␣ transcripts also regulated in the interferon-␥ set. Unexpectedly, there was a high correlation between psoriatic lesional tissue and the IL-1␣ transcriptome. These findings suggest that the inflammatory milieu in the epidermal microenvironment in psoriasis is more likely dependent on evolutionarily ancient cytokines such as IL-1, rather than those of the adaptive immune response. (Am J

show abstract

“…AR has been shown to be an autocrine factor in keratinocytes, so it is possible that AR-stimulated EGFR is driving this IL-1/NF-nB feedback loop in the same way as we show in SUM149 breast cancer cells (66). Sustained increases in IL-1 and NF-nB have the ability to alter matrix metalloproteinase activity and the production of other proangiogenic and invasion-inducing factors like IL-6 and IL-8 (40,52,67). Accordingly, an active autocrine loop involving IL-1, EGFR, and NF-nB would have the power to induce the rapid growth, invasion, and angiogenesis seen in aggressive breast cancer.…”

Section: Discussionsupporting

confidence: 55%

PARK2, a Large Common Fragile Site Gene, is Part of a Stress Response Network in Normal Cells that is Disrupted During the Development of Ovarian Cancer

Smith¹,

Zhu²

2008

View full text Add to dashboard Cite

Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Department of Defense, Washington Headquarters Services, Directorate for Information Operations and Reports (0704-0188), 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302. Respondents should be aware that notwithstanding any other provision of law, no person shall be subject to any penalty for failing to comply with a collection of information if it does not display a currently valid OMB control number. PLEASE DO NOT RETURN YOUR FORM TO THE ABOVE ADDRESS. REPORT DATE 01-03-2008 REPORT TYPE Annual Summary DATES COVERED PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES) 8. PERFORMING ORGANIZATION REPORT NUMBERWayne State University Detroit, MI 48201 SPONSORING / MONITORING AGENCY NAME(S) AND ADDRESS(ES) 10. SPONSOR/MONITOR'S ACRONYM(S) U.S. Army Medical Research and Materiel Command Fort Detrick, Maryland 21702-5012 SPONSOR/MONITOR'S REPORT NUMBER(S) DISTRIBUTION / AVAILABILITY STATEMENTApproved for Public Release; Distribution Unlimited SUPPLEMENTARY NOTESOriginal contains colored plates: ALL DTIC reproductions will be in black and white.14. ABSTRACT We have previously shown that an AR/EGFR autocrine loop is required for SUM149 human breast cancer cell proliferation, motility and invasion. In the present studies, we demonstrate that SUM149 cells and human mammary epithelial MCF10A cells that over express AR (MCF10A AR) or are cultured in the presence of exogenous AR, express higher levels of EGFR protein compared with MCF10A cells cultured in EGF. We show that EGFR protein remains stable in the presence of AR yet is degraded in the presence of EGF. Consistent with this observation, tyrosine 1045 on the EGFR, the c-cbl binding site, exhibited decreased phosphorylation in the presence of AR compared with EGF. Ubiquitination of EGFR was also dramatically decreased when AR was the ligand. Following AR binding, EGFR remained on the cell surface instead of being rapidly internalized as observed when EGF was present. Immunofluorescence demonstrated that MCF10A cells cultured in EGF exhibited a predominantly intracellular, punctate localization of EGFR. In stark contrast, SUM149 cells and MCF10A cells growing in the presence of AR expressed EGFR predominantly on the membrane and at cell-cell junctions. Therefore, AR alters EGFR internalization and degradation in a way that favors accumulation of EGFR at the cell surface and ultimately leads to changes in EGFR signaling. In addition, we found that AR, but not EGF upregulates NFkB activity and IL-1 production suggesting that AR may play a unique role in breast cancer progression. SUBJECT TERMS Introduction:The epidermal growt...

show abstract

The differential effects of IL-1 and TNF-? on proinflammatory cytokine and matrix metalloproteinase expression in human chondrosarcoma cells

Cited by 68 publications

References 46 publications

Pro-inflammatory Cytokine Tumor Necrosis Factor-α Induces Bone Morphogenetic Protein-2 in Chondrocytes via mRNA Stabilization and Transcriptional Up-regulation

Pro-inflammatory Cytokine Tumor Necrosis Factor-α Induces Bone Morphogenetic Protein-2 in Chondrocytes via mRNA Stabilization and Transcriptional Up-regulation

The Psoriatic Transcriptome Closely Resembles That Induced by Interleukin-1 in Cultured Keratinocytes

PARK2, a Large Common Fragile Site Gene, is Part of a Stress Response Network in Normal Cells that is Disrupted During the Development of Ovarian Cancer

Contact Info

Product

Resources

About