Literature DB >> 7944616

Altered Ca2+ signalling in human neutrophils from inflammatory sites.

E V Davies1, B D Williams, R J Whiston, A M Cooper, A K Campbell, M B Hallett.   

Abstract

OBJECTIVES: To determine whether the intracellular store release of Ca2+ in neutrophils from patients with rheumatoid arthritis, other joint disease and active leg ulceration was different from normal neutrophils.
METHODS: The release into the cytosol of Ca2+ from stores within individual neutrophils was determined using ratiometric imaging of fura2. The size of the elevated Ca2+ 'cloud' and its concentration were quantified in neutrophils from the circulation of patients with rheumatoid arthritis, other joint diseases, and leg ulcers and from the joints of those with joint disease.
RESULTS: In neutrophils isolated from both the synovial fluid of patients with rheumatoid arthritis and other joint conditions, and also arising from leg ulcers, the amount of the cell cytosol occupied by elevated Ca2+ was significantly increased compared with neutrophils from healthy subjects; for neutrophils from rheumatoid, non-rheumatoid joints and leg ulcers p values were 0.0006, < 0.0001, 0.016 respectively (Student's t test). There was also a significant increase in Ca2+ release from circulating neutrophils from patients with rheumatoid arthritis (p = 0.09), but not in circulating neutrophils from patients with leg ulcers or non-rheumatoid joint conditions.
CONCLUSIONS: It is proposed that the increased release of free Ca2+ into the cytosol of neutrophil at inflammatory sites results in increased oxidase activation.

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Year:  1994        PMID: 7944616      PMCID: PMC1005368          DOI: 10.1136/ard.53.7.446

Source DB:  PubMed          Journal:  Ann Rheum Dis        ISSN: 0003-4967            Impact factor:   19.103


  12 in total

1.  Dissociation of store release from transmembrane influx of calcium in human neutrophils.

Authors:  E V Davies; A K Campbell; M B Hallett
Journal:  FEBS Lett       Date:  1992-11-23       Impact factor: 4.124

2.  Calcium signaling capacity of the CD11b/CD18 integrin on human neutrophils.

Authors:  J Ng-Sikorski; R Andersson; M Patarroyo; T Andersson
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3.  White cell accumulation in dependent legs of patients with venous hypertension: a possible mechanism for trophic changes in the skin.

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4.  Ca2+ oscillations in neutrophils triggered by immune complexes result from Ca2+ influx.

Authors:  E V Davies; A K Campbell; M B Hallett
Journal:  Immunology       Date:  1994-05       Impact factor: 7.397

Review 5.  Is intracellular Ca2+ the trigger for oxygen radical production by polymorphonuclear leucocytes?

Authors:  M B Hallett; A K Campbell
Journal:  Cell Calcium       Date:  1984-02       Impact factor: 6.817

6.  The use of fura-2 to determine the relationship between cytoplasmic free Ca2+ and oxidase activation in rat neutrophils.

Authors:  F A Al-Mohanna; M B Hallett
Journal:  Cell Calcium       Date:  1988-02       Impact factor: 6.817

7.  Activation of neutrophils by soluble and insoluble immunoglobulin aggregates from synovial fluid of patients with rheumatoid arthritis.

Authors:  J J Robinson; F Watson; M Phelan; R C Bucknall; S W Edwards
Journal:  Ann Rheum Dis       Date:  1993-05       Impact factor: 19.103

8.  Synchronous free Ca2+ changes in individual neutrophils stimulated by leukotriene B4.

Authors:  E V Davies; A K Campbell; M B Hallett
Journal:  FEBS Lett       Date:  1991-10-07       Impact factor: 4.124

9.  Single cell imaging reveals abnormal intracellular calcium signals within rheumatoid synovial neutrophils.

Authors:  E V Davies; A K Campbell; B D Williams; M B Hallett
Journal:  Br J Rheumatol       Date:  1991-12

10.  Modulation of cytosolic-free calcium transients by changes in intracellular calcium-buffering capacity: correlation with exocytosis and O2-production in human neutrophils.

Authors:  P D Lew; C B Wollheim; F A Waldvogel; T Pozzan
Journal:  J Cell Biol       Date:  1984-10       Impact factor: 10.539

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2.  Signalling through neutrophil Fc gamma RIII, Fc gamma RII, and CD59 is not impaired in active rheumatoid arthritis.

Authors:  J Jones; I Laffafian; T Lawson; B D Williams; B P Morgan
Journal:  Ann Rheum Dis       Date:  1996-05       Impact factor: 19.103

3.  Inhibition of antithrombin by hyaluronic acid may be involved in the pathogenesis of rheumatoid arthritis.

Authors:  Xiaotian Chang; Ryo Yamada; Kazuhiko Yamamoto
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  3 in total

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