Detection of Macrophage Migration Inhibitory Factor (MIF) in Human Cholesteatomas and Functional Implications of Correlations to Recurrence Status and to Expression of Matrix Metalloproteinases‐3/9, Retinoic Acid Receptor‐β, and Anti‐apoptotic Galectin‐3

Choufani, Georges; Ghanooni, Rose; Decaestecker, Christine; Delbrouck, Karine; Simon, Patricia; Schüring, Max-Peter; Zick, Yehiel; Hassid, Sergio; Gabius, Hans‐Joachim; Kiss, Róbert

doi:10.1097/00005537-200109000-00031

Cited by 26 publications

(23 citation statements)

References 39 publications

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“…Transfection of murine colon carcinoma cells with an antisense MIF plasmid was associated with significant decreases in cell proliferation (28). Recently, MIF detection in human cholesteatomas was found to correlate strongly with levels of the antiapoptotic protein galectin and to reflect the biologic aggressiveness of these lesions (29). The current study provides evidence that recombinant MIF can prevent apoptosis in human synoviocytes and that endogenous MIF has an antiapoptotic effect.…”

Section: Discussionmentioning

confidence: 55%

Regulation of p53 by macrophage migration inhibitory factor in inflammatory arthritis

Leech

Lacey

Xue

et al. 2003

Arthritis & Rheumatism

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Objective. To study the capacity of macrophage migration inhibitory factor (MIF) to regulate proliferation, apoptosis, and p53 in an animal model of rheumatoid arthritis (RA) and in fibroblast-like synoviocytes (FLS) from humans with RA.Methods. Antigen-induced arthritis (AIA) was induced in MIF -/-mice and littermate controls. FLS were obtained from patients with RA. Western blotting and immunohistochemistry were used to measure p53 in cells and tissues. Apoptosis was detected in cells by flow cytometry using TUNEL and annexin V/propidium iodide labeling. Apoptosis in tissue was detected using TUNEL. Proliferation was assessed in cultured cells and tissue by 3 H-thymidine incorporation and Ki-67 immunostaining, respectively.Results. MIF inhibited p53 expression in human RA FLS. Levels of p53 were correspondingly increased in MIF -/-mouse tissues and cells. Spontaneous and sodium nitroprusside-induced apoptosis were significantly increased in MIF -/-cells. In vitro exposure of FLS to MIF reduced apoptosis and significantly induced FLS proliferation. Synoviocyte proliferation in MIF -/-mice was correspondingly reduced. A decrease in the severity of AIA in MIF -/-mice was associated with an increase in p53 and apoptosis in synovium. Evidence of in situ proliferation was scant in this model, and no difference in in situ proliferation was detectable in MIF -/-mice compared with wild-type mice.Conclusion. These results indicate a role for MIF in the regulation of p53 expression and p53-mediated events in the inflamed synovium and support the hypothesis that MIF is of critical importance in the pathogenesis of RA.

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Section: Discussionmentioning

confidence: 55%

Regulation of p53 by macrophage migration inhibitory factor in inflammatory arthritis

Leech

Lacey

Xue

et al. 2003

Arthritis & Rheumatism

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“…A primary target of Gal-8 could be the sugar chains on members of the integrin family, which are abundantly expressed on the surface of leukocytes. [46][47][48][49][50] Gal-9 is able to induce decreased levels of pro-inflammatory cytokines such as IL-17, IL-12 and IFNc. Gal-9 decreases numbers of CD4(+) TIM-3(+) T cells in peripheral blood.…”

Section: Role Of Galectins In Trophoblast Invasionmentioning

confidence: 99%

REVIEW ARTICLE: Governing the Invasive Trophoblast: Current Aspects on Intra‐ and Extracellular Regulation

Fitzgerald

Germeyer

Huppertz

et al. 2010

American J Rep Immunol

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Citation Fitzgerald JS, Germeyer A, Huppertz B, Jeschke U, Knöfler M, Moser G, Scholz C, Sonderegger S, Toth B, Markert UR. Governing the invasive trophoblast: current aspects on intra‐ and extracellular regulation. Am J Reprod Immunol 2010This review summarizes several aspects especially of regulating factors governing trophoblast invasion. Those include the composition of the extracellular matrix containing a variety of matrix metalloproeinases and their inhibitors, but also intracellular signals. Furthermore, a newly described trophoblast subtype, the endoglandular trophoblast, is presented. Its presence may provide a possible mechanism for opening and connecting uterine glands into the intervillous space. Amongst others, two intracellular signalling pathways are crucial for regulation of trophoblast functions and development: Wnt‐ and signal transducer and activator of transcription (STAT)3 signalling. Wnt signalling promotes implantation, placentation and trophoblast differentiation. Several Wnt‐dependent cascades and regulatory mechanisms display different functions in trophoblast cells. The STAT3 signalling system is fundamental for induction and regulation of invasiveness in physiological trophoblastic cells, but also in tumours. The role of galectins (Gal) in trophoblast regulation and placenta development comes increasingly into focus. The Gal‐ 1–4, 7–10 and 12–14 have been detected in humans. Detailed information is only available for Gal‐1, ‐2, ‐3, ‐4, ‐9 and ‐12 in endometrium and decidua. Gal‐1, ‐3 and ‐13 (‐14) have been detected and studied in trophoblast cells.

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“…All the histochemical procedures were carried out as detailed previously (34,41). Briefly, 5 m-thick sections were taken from each of the 99 clinical samples (i.e., 20 normal cases, 69 colorectal tumors and 10 hepatic metastases).…”

Section: Mif and Galectin-3 Immunohistochemistrymentioning

confidence: 99%

“…While the Labeling Index (LI) refers to the percentage of tissue area specifically stained by a given histochemical marker, the Mean Optical Density (MOD) denotes the mean staining intensity computed in immunopositive cells only. The way in which we used the computer-assisted system to quantify the histochemical staining is detailed elsewhere, as are all the standardization procedures dealing with the manner in which we used the computer-assisted microscopy and ensuring measure reproducibility (34,41,43). A negative histological control slide (from which either the primary anti-MIF or the anti-galectin-3 antibody was omitted, as mentioned above) was analyzed for each case under study.…”

Section: Computer-assisted Microscopymentioning

confidence: 99%

“…Firstly, we had observed that MIF expression correlates with the expression of galectin-3 in relation to recurrences in human cholesteatomas (34). Secondly, recent studies suggest that MIF, first identified nearly 40 years ago as a potent proinflammatory cytokine, may also contribute to the multiple aspects of tumor progression and neoplasia including impairment of p53 activity (35)(36)(37).…”

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confidence: 96%

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Prognostic Values of Galectin-3 and the Macrophage Migration Inhibitory Factor (MIF) in Human Colorectal Cancers

et al. 2003

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Detection of Macrophage Migration Inhibitory Factor (MIF) in Human Cholesteatomas and Functional Implications of Correlations to Recurrence Status and to Expression of Matrix Metalloproteinases‐3/9, Retinoic Acid Receptor‐β, and Anti‐apoptotic Galectin‐3

Cited by 26 publications

References 39 publications

Regulation of p53 by macrophage migration inhibitory factor in inflammatory arthritis

Regulation of p53 by macrophage migration inhibitory factor in inflammatory arthritis

REVIEW ARTICLE: Governing the Invasive Trophoblast: Current Aspects on Intra‐ and Extracellular Regulation

Prognostic Values of Galectin-3 and the Macrophage Migration Inhibitory Factor (MIF) in Human Colorectal Cancers

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