Inhibition of eicosanoid formation and lipocortin induction by glucocorticoids in human cell lines and in patients with inflammatory lung disease.

Parente, Luca; Solito, Egle; Giannessi, Pier Giorgio; Paggiari, P.; Sicari, Rosa; Caterina, Raffaele De

doi:10.1016/1043-6618(92)90591-x

Cited by 6 publications

(5 citation statements)

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“…We and previous investigators have reported that in U‐937 cells, endogenous ANXA1 could be upregulated and membrane translocated by dexamethasone after PMA treatment (24 h) ( Solito et al , 1991 ; 1993; 1994; Parente et al , 1992 ; De Caterina et al , 1993 ; Parente & Solito, 1994; Comera & Russo, 1995). Data indicate that there is no significant difference in the cell‐surface expression of ANXA1 in cells treated with PMA or PMA+dex.…”

Section: Discussionmentioning

confidence: 72%

“…Incubation of U‐937 cells with 1 n M PMA for 24 h and with 1 μ M dexamethasone for an additional 16 h was used as a standard procedure to increase ANXA1 expression and externalization on the outer surface of the membrane, as previously reported ( Solito et al , 1991 ; 1993; 1994; 2000; Parente et al , 1992 ; De Caterina et al , 1993 ). Figure 1a showed 50% increase of ANXA1 surface level above untreated control cells after PMA treatment, while dexamethasone alone (16 h incubation) failed to induce the protein.…”

Section: Resultsmentioning

confidence: 99%

“…This immortalized cell line has been used in many studies in which the results are generally reported as being applicable to monocytes or macrophages ( Hass et al , 1989 ). In addition to this, our choice was supported by three other specific reasons: first, U‐937 cell line expresses increased amount of endogenous ANXA1 during cell differentiation by phorbol ester (24 h treatment), and subsequent glucocorticoid treatment for 16 h produced translocation of ANXA1 to the external cell surface and facilitated its release in the medium ( Solito et al , 1991 ; Parente et al , 1992 ; De Caterina et al , 1993 ; Solito et al , 1993 ; 1994); second, we have demonstrated that ANXA1 modulates U‐937 cell adhesive properties by interfering with α 4 β 1 (CD49d/CD29) ( Solito et al , 2000 ) for the same time course of PMA and dexamethasone treatment we used in this present study; and, third, we have recently shown U‐937 cell migration in vivo in SCID mice ( Perretti et al , 2002 ).…”

Section: Introductionmentioning

confidence: 99%

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Dexamethasone enhances interaction of endogenous Annexin 1 with L‐selectin and triggers shedding of L‐selectin in the monocytic cell line U‐937

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Solito²,

Levine

2003

British J Pharmacology

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L‐selectin, constitutively expressed by leukocytes, is involved in the initial binding of leukocytes to activated endothelium. Anti‐inflammatory drugs like glucocorticoids can induce shedding of L‐selectin, but the mechanism is still unknown. Annexin 1, a protein whose synthesis and externalization/secretion are induced during the inflammatory response, has been proposed as a mediator of the anti‐inflammatory actions of glucocorticoids. The monocytic cell line U‐937 strongly expresses Annexin 1 after 24 h of phorbol 12‐myristate 13‐acetate (PMA, 1 nM) treatment and externalizes/releases the protein after additional 16 h of dexamethasone (1 μM) treatment. This study investigated the possible regulation of cell surface L‐selectin shedding by endogenous Annexin 1, and its role in glucocorticoid‐induced L‐selectin shedding in the U‐937 cell line. PMA‐ and dexamethasone treatment‐induced L‐selectin shedding was potentially mediated by Annexin 1, since neutralizing antibodies against Annexin 1 reduced dexamethasone‐ and Annexin 1‐induced shedding. Immunoprecipitation and binding assays provided support for the suggestion that this effect could be mediated by an interaction between externalized Annexin 1 and L‐selectin. Such interaction involved the N‐terminal domain of Annexin 1 and was calcium‐dependent. Confocal microscopy studies demonstrated increased colocalization of Annexin 1 and L‐selectin on the cell surface. Overall, our study provides new insights into the potential role of endogenous ANXA1 as a mediator of dexamethasone‐induced L‐selectin shedding, which may contribute to the anti‐inflammatory activity of glucocorticoids. British Journal of Pharmacology (2003) 140, 133–145. doi:

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Section: Discussionmentioning

confidence: 72%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Dexamethasone enhances interaction of endogenous Annexin 1 with L‐selectin and triggers shedding of L‐selectin in the monocytic cell line U‐937

Coupade

Solito²,

Levine

2003

British J Pharmacology

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“…Different groups of investigators have shown that glucocorticoids induce the synthesis of annexin I (31)(32)(33)(34)(35). Thus we tested the following hypothesis: whether glucocorticoids can further increase the expression or alter the distribution of annexin I.…”

Section: Modulation Of the Expression And Cellular Distribution Of Anmentioning

confidence: 97%

Annexin I modulates cell functions by controlling intracellular calcium release

et al. 1999

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Annexin I is an intracellular protein in search of a function. Ex vivo it has calcium- and phospholipid-binding properties. To evaluate its role in vivo, MCF-7 cells were stably transfected with annexin I in sense or antisense orientations. In cells overexpressing annexin I, calcium release was abrogated on stimulation of purinergic or bradykinin receptors, whereas non-transfected cells or cells with down-regulated annexin I released calcium within seconds. Basal calcium and calcium stores were not affected. The impaired calcium release was paralleled by a down-regulation of the activities of phospholipase C, group II phospholipase A2, and E-cadherin with altered adhesion and enhanced tumor growth on soft agar. Significantly smaller tumors, with the histologically most differentiated cells, were observed in nude mice inoculated with cells transfected with the antisense rather than with the sense plasmid. These observations indicate that annexin I modulates cell functions by controlling intracellular calcium release. Frey, B. M., Reber, B. F. X., Vishwanath, B. S., Escher, G., Frey, F. J. Annexin I modulates cell functions by controlling intracellular calcium release.

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“…Early hypotheses as to the mechanism of corticosteroid actions concentrated on their ability to increase the production of the protein lipocortin-1, an endogenous inhibitor of phospholipase A 2 (PLA 2 ), the family of enzymes responsible for the first step in the production of both eicosanoids and platelet-activating factor. Lipocortin-1 has been shown to be increased in bronchial epithelial cells in response to corticosteroids [3]. However, similar reports using other cell types showed decreased eicosanoid production, but failed to demonstrate changes in lipocortin-1 in response to corticosteroid treatment [4].…”

Section: Why Topical Corticosteroids Are Not Enoughmentioning

confidence: 99%

Novel immunomodulators for topical skin disease therapy

Travers

2000

Expert Opinion on Investigational Drugs

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The use of topical corticosteroids has revolutionised the treatment of inflammatory skin diseases. However, problems including pharmacological resistance, as well as the side effect profile of potent topical corticosteroids, has prompted studies to investigate into other topical non-corticosteroidal agents in inflammatory skin diseases. This review outlines the major types of inflammatory skin diseases and discusses emerging therapies based on topical immunosuppressive macrolide antibiotics. In particular, tacrolimus and ascomycin derivatives have been shown to be effective for treating atopic dermatitis with a surprising lack of side effects. It is expected that these agents will play an important role in future dermatological therapy. Accumulating evidence suggests the importance of lipid-derived mediators of inflammation (eicosanoids and platelet-activating factor) in cutaneous inflammatory diseases. The role of these mediators in skin inflammation is also addressed in this review. Though there appears to be a large amount of redundancy in the activities of these lipid mediators, this family of agents could potentially serve as targets for anti-inflammatory therapy. Inasmuch as the phospholipase A(2) family of enzymes serve to synthesise both eicosanoids and platelet-activating factor, inhibition at this step could have important therapeutic benefits in designing therapy for inflammatory skin diseases.

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Inhibition of eicosanoid formation and lipocortin induction by glucocorticoids in human cell lines and in patients with inflammatory lung disease.

Cited by 6 publications

References 4 publications

Dexamethasone enhances interaction of endogenous Annexin 1 with L‐selectin and triggers shedding of L‐selectin in the monocytic cell line U‐937

Dexamethasone enhances interaction of endogenous Annexin 1 with L‐selectin and triggers shedding of L‐selectin in the monocytic cell line U‐937

Annexin I modulates cell functions by controlling intracellular calcium release

Novel immunomodulators for topical skin disease therapy

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