ArticleHistochemistry and cell biology2003
Immunohistochemical localization of macrophage migration inhibitory factor (MIF) in human gingival tissue and its pathophysiological functions.
Article in Histochemistry and cell biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 18 citations in OpenAlex.
- Clinically Healthy Human Gingival Tissues Show Significant Inter-individual Variability in GCF Chemokine Expression and Subgingival Plaque Microbial Composition.Frontiers in oral health · 2021Article
- Macrophage migration inhibitory factor promotes cyst growth in polycystic kidney disease.The Journal of clinical investigation · 2015Article
- Expression of macrophage migration inhibitory factor in the mouse neocortex and posterior piriform cortices during postnatal development.Cellular and molecular neurobiology · 2014Article
- News and views in Histochemistry and Cell Biology.Histochemistry and cell biology · 2004Review
- Innovative techniques and applications in histochemistry and cell biology.Histochemistry and cell biology · 2003Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent reports have indicated that macrophage migration inhibitory factor (MIF) plays a key role in systemic as well as local inflammatory and immune responses. In this study, the presence and localization of MIF in human gingival tissue were examined. The expression of MIF was confirmed by western blot analysis, which demonstrated the same band at 12.5 kDa in different gingival tissues. Immunohistochemical studies showed that MIF protein existed in the cytoplasm of keratinocytes, especially in free gingival epithelium and junctional epithelium. It was also found in basal cells, fibroblasts, and various cells. These cells were considered to be stimulated mechanically at all times. To determine the effect of mechanical stimuli, Gin-1 cells were cyclically stretched for a short time by using a Flexercell Strain Unit. RT-PCR analysis demonstrated upregulation of MIF mRNA in these Gin-1 cells. In this study, MIF existed not only in inflammatory parts but also in those areas with high cell proliferative activity subjected to external stimulus. Moreover, the finding that MIF protein levels of the control determined by immunohistochemical detection were quite similar to those for grown and stretched Gin-1 cells suggested that MIF protein was stored in the cytoplasm for some time and that MIF is an important autocrine mediator of homeostatic-dependent signaling events. These results suggest that MIF plays an important role in the homeostatic process of periodontal inflammation.
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Registered trials
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