Evidence map›Paper›PMID 16045736›Full record

ArticleClinical and experimental immunology2005

CXCL12 and CXCR4 expression by human gingival fibroblasts in periodontal disease.

Y Hosokawa, I Hosokawa, K Ozaki, H Nakae, K Murakami, Y Miyake, T Matsuo

Open access · bronzeAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.6field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 69 citations in OpenAlex.

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  8. Role of bone marrow adipocytes in leukemia and chemotherapy challenges.Cellular and molecular life sciences : CMLS · 2019
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  18. The role of osteoimmunology in periodontal disease.BioMed research international · 2013
    Review
  19. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Y HosokawaDepartment of Conservative Dentistry, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, Japan. hosokawa@dent.tokushima-u.ac.jp
I Hosokawa
K Ozaki
H Nakae
K Murakami
Y Miyake
T Matsuo
Tokushima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CXCL12 is a CXC chemokine that is related to lymphocyte infiltration and angiogenesis in inflammatory sites such as arthritis. However, the expression and roles of CXCL12 in periodontal disease are uncertain. The aim of this study was to assess the expression of CXCL12 and its receptor, CXCR4, in periodontal tissue and to investigate the properties of CXCL12 and CXCR4 expression by human gingival fibroblasts (HGF). RT-PCR analysis revealed that CXCL12 and CXCR4 mRNA were expressed in both normal gingival tissues and periodontal diseased tissues. Immunohistochemistry disclosed that CXCL12 was expressed and CXCR4 positive cells were found in both normal and periodontal diseased gingival tissues. Our in vitro experiments elucidated that HGF constitutively produced CXCL12, and the levels were enhanced by stimulation with tumour necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), transforming growth factor-beta (TGF-beta), regulated upon activation normal T cell expressed and secreted (RANTES) and macrophage inflammatory protein 3(alpha) (MIP-3(alpha)). On the other hand, heat killed Porphyromonas gingivalis (P. gingivalis) and P. gingivalis LPS reduced the CXCL12 production by HGF. Flow cytometry analysis clarified that CXCR4 was highly expressed on HGF, and CXCR4 expression was abrogated by TNF-alpha, IFN-gamma and P. gingivalis LPS. Moreover, CXCL12 induced vascular endothelial growth factor (VEGF) production by HGF. Our results demonstrated that CXCL12 might be related to CXCR4+ cells infiltration and angiogenesis both in normal periodontal tissues and periodontal diseased tissue. P. gingivalis, a known periodontal pathogen, inhibits the production of CXCL12 and the expression of CXCR4 by HGF. This fact means that P. gingivalis may inhibit CXCR4+ cells infiltration and neovascularization in periodontal tissue and escape from the immune response.

Indexed as

Cells, CulturedChemokine CCL20Chemokine CCL5Chemokine CXCL12Chemokines, CCChemokines, CXCFibroblastsFlow CytometryGingivaHumansImmunohistochemistryInterferon-gammaLipopolysaccharidesMacrophage Inflammatory ProteinsPeriodontal DiseasesPorphyromonas gingivalisCCL20 protein, humanChemokine CCL20Chemokine CCL5Chemokine CXCL12Chemokines, CCChemokines, CXCCXCL12 protein, humanInterferon-gammaLipopolysaccharidesMacrophage Inflammatory ProteinsReceptors, CXCR4RNA, MessengerTransforming Growth Factor betaTumor Necrosis Factor-alphaVascular Endothelial Growth Factor A

Identifiers

PMID16045736
PMCPMC1809465
OpenAlexW2005793412

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.