Constitutive production of angiotensin converting enzyme from rheumatoid nodule cells under serum free conditions.

Goto, Makoto; Sasano, Minoru; Fuzisawa, M; Okabe, Tetsuro; Nishizawa, Kaho

doi:10.1136/ard.51.6.741

Cited by 21 publications

(13 citation statements)

References 12 publications

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“…Angiotensin converting enzyme is expressed in the synovial membranes from patients with the adult form of rheumatoid arthritis (RA), and a role for this enzyme in the pathophysiology has been suggested [27][28][29]. However, a recent study did not Wnd a signiWcant diVerence between the prevalence of ACE gene polymorphism in adults with rheumatoid arthritis (RA) and controls, and between severe and non-severe RA [30].…”

Section: Discussionmentioning

confidence: 99%

Angiotensin-converting enzyme gene polymorphism in patients with psoriatic arthritis

et al. 2007

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To investigate the frequency of angiotensinconverting enzyme (ACE) gene insertion/deletion (I/D) polymorphism genotypes in adults with psoriatic arthritis (PsA), a heterogeneous chronic disease with autoimmune pathology. ACE gene I/D polymorphism inXuences the plasma and tissue levels of ACE and has an involvement in inXammatory mechanism. The frequency of ACE gene I/D polymorphism genotypes was determined in 51 adults with PsA from Kuwait, and compared to that in 100 ethnically matched healthy controls using polymerase chain reaction. The distribution of ACE I/D polymorphism and allele frequencies in PsA patients were not signiWcantly diVerent from controls (P > 0.05). Further analyses of PsA patients showed that ACE I/D gene polymorphism was not associated with family history, clinical manifestations, and disease severity. However, the frequency of II genotype was signiWcantly higher in patients with late disease onset than in those with early onset (25 vs. 3%; P = 0.04). No diVerence was found between the distribution of the ACE genotype in PsA patients and the general population in Kuwait.However, the presence of II genotype may confer susceptibility to the development of late onset PsA.

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Section: Discussionmentioning

confidence: 99%

Angiotensin-converting enzyme gene polymorphism in patients with psoriatic arthritis

et al. 2007

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“…Macrophages, for example, express AT 1 receptors and produce angiotensin II by ACE. 62,63 Furthermore, elevated ACE activity is found in nodules 64 and synovium 65 in patients with rheumatoid arthritis, and AT 1 receptors have appeared in human synovium. 66 Evidence also suggests that angiotensin II regulates immune responses by using a calcineurin-dependent pathway through AT 1 receptors, indicating a direct effect on T cells.…”

Section: Rheumatoid Arthritismentioning

confidence: 99%

Protective Effects of Angiotensin II Interruption: Evidence for Antiinflammatory Actions

Dagenais

Jamali

2005

Pharmacotherapy

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Angiotensin II, the major effector molecule produced from the renin-angiotensin-aldosterone axis, is a vasoconstrictor contributing to hypertension. Evidence indicates, however, that angiotensin II also is a potent proinflammatory mediator with growth and remodeling effects. In vitro and in vivo studies have shown that angiotensin II blockade significantly reduces concentrations of proinflammatory mediators and oxidative stress products in numerous inflammatory models. Interruption of angiotensin II activity with angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers has been beneficial for patients with inflammatory diseases. Much of this benefit occurs independent of the antihypertensive effect of angiotensin II interruption, suggesting a distinctive protective mechanism. Angiotensin II receptor blockers may represent a novel class of antiinflammatory drugs with indications far beyond cardiovascular diseases.

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“…In rheumatoid nodules macrophages migrate towards a central necrotic focus [1]. Altered expression of macrophage surface molecules [1,2] and production of angiotensin converting enzyme (ACE) [3] and IL-l^S [4] provide evidence of macrophage activation. The earliest foci of necrosis occur within small collections of macrophages characterized by sustained expression of the p8,14 molecule [5], a calcium binding dimer of unknown function [6].…”

Section: Introductionmentioning

confidence: 99%

Changes in the phenotype of monocytes/macrophages and expression of cytokine mRNA in peripheral blood and synovial fluid of patients with rheumatoid arthritis

Highton

Carlisle

Palmer

1995

Clinical and Experimental Immunology

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SUMMARY Data from a previous study suggested that peripheral blood monocytes in patients with rheumatoid arthritis (RA) may be activated. Therefore, in this study we sought further evidence of ‘presynovial’ activation of monocytes. Our results show that phenotypic changes are demonstrable in peripheral blood monocytes in patients with RA, including increased expression of CR3 (CDllb/CD18) and FcRI (CD64). However, changes are most extensive in synovial monocytes/macrophages and especially for HLA‐DR and intercellular adhesion molecule‐1 (ICAM‐1) (CD54). We conclude that monocyte/macrophage activation is most evident within the joint, and that ‘presynovial’ changes occur but are of limited extent.

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Constitutive production of angiotensin converting enzyme from rheumatoid nodule cells under serum free conditions.

Cited by 21 publications

References 12 publications

Angiotensin-converting enzyme gene polymorphism in patients with psoriatic arthritis

Angiotensin-converting enzyme gene polymorphism in patients with psoriatic arthritis

Protective Effects of Angiotensin II Interruption: Evidence for Antiinflammatory Actions

Changes in the phenotype of monocytes/macrophages and expression of cytokine mRNA in peripheral blood and synovial fluid of patients with rheumatoid arthritis

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