Antiinflammatory aspects of systemic and topically applied retinoids

Hensby, C.N.; Eustache, Jacques; Shroot, Braham; Bouclier, Martine; Chatelus, A.; Luginbuhl, B.

doi:10.1007/bf01966477

Cited by 17 publications

(6 citation statements)

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“…Not only is activin A production stimulated by these proinflammatory cytokines, but present studies also showed that the GM-CSF-stimulated production of activin A and its constitutive production in monocytes are both suppressed by glucocorticoids and all-trans-retinoic acid, both of which are known to have antiinflammatory activities. 26,27 Although the mechanisms responsible for their anti-inflammatory effects are not completely understood, one of the known mechanisms of action is a direct inhibition of the production of pro-inflammatory cytokines. For example, glucocorticoids were reported to down-regulate the production of monocyte pro-inflammatory mediators, including IL-1, 28 TNFa , 29 prostaglandin E 2 , 27 IL-6, 30 IFN-g, IL-2, 31 G-CSF and GM-CSF.…”

Section: Discussionmentioning

confidence: 99%

“…26,27 Although the mechanisms responsible for their anti-inflammatory effects are not completely understood, one of the known mechanisms of action is a direct inhibition of the production of pro-inflammatory cytokines. For example, glucocorticoids were reported to down-regulate the production of monocyte pro-inflammatory mediators, including IL-1, 28 TNFa , 29 prostaglandin E 2 , 27 IL-6, 30 IFN-g, IL-2, 31 G-CSF and GM-CSF.…”

Section: Discussionmentioning

confidence: 99%

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Induced expression of the new cytokine, activin A, in human monocytes: inhibition by glucocorticoids and retinoic acid

Shao

Frigon

et al. 1996

Immunology

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The capacity of recombinant human granulocyte–macrophage colony‐stimulating factor (GM‐CSF), glucocorticoids or all‐trans‐retinoic acid to modulate production of activin A by human monocytes was studied. It was shown that GM‐CSF stimulated monocytes to accumulate activin A RNA after as few as 4 hr of incubation, reaching a peak of stimulation at approximately 16 hr of incubation. The activin A transcripts accumulated in the monocytes after stimulation with only 5 U/ml of GM‐CSF and reached a maximum plateau level of expression between 25 and 50 U/ml of GM‐CSF. Biologically active activin A molecules were detected in the conditioned media by a bioassay, performed both in the absence and presence of a neutralizing antiserum for activin A. Accumulation of bioactive activin A in conditioned medium of monocyte cultures was detected after 24 hr of incubation with GM‐CSF and high levels of activin A were maintained for 72 hr. The production of the dimeric βAβA in these monocytes was further confirmed by a sandwich enzyme‐linked immunosorbent assay (ELISA) specific for activin A. In contrast to the stimulatory effect of GM‐CSF, hydrocortisone, dexamethasone or all‐trans‐retinoic acid at 1 × 10−7 to 1 × 10−5 m inhibited the constitutive expression of activin A and greatly suppressed the GM‐CSF‐stimulated production. Thus, the expression of activin A is modulated in monocytes by different agents. These observations may imply new roles for activin A at sites of inflammation where monocytes accumulate.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Induced expression of the new cytokine, activin A, in human monocytes: inhibition by glucocorticoids and retinoic acid

Shao

Frigon

et al. 1996

Immunology

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“…Whilst much of their therapeutic activity is derived from their ability to modify cellular differentiation, increasing evidence supports the belief that in addition they may have potent antiinflammatory properties [1]. CD 271 (6(3-(1-adamantyl)-4-methoxyphenyl)2-naphthoic acid) is a new stable substance discovered in the CIRD that shares many of the pharmacological properties of all-trans retinoic acid.…”

Section: Introductionmentioning

confidence: 98%

Thein vivo andin vitro anti-inflammatory activity of CD271: A new retinoid-like modulator of cell differentiation

Hensby¹,

Cavey²,

Bouclier³

et al. 1990

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“…Anti-in¯ammatory eects of retinoids have been shown in dermatological diseases in humans 1Y2 and experimental models of in¯ammation such as adjuvant arthritis 3 and ultraviolet-induced erythema. 4 Some anti-in¯ammatory eects of retinoids on monocyte/ macrophage function have been reported. 5 ±7 We also previously examined the eects of alltrans-retinoic acid (ATRA), retinal and retinol, on the production of tumour necrosis factor-a (TNF-a) and nitric oxide (NO) by LPS-stimulated rat Kuper cells, which are the resident macrophages of the liver.…”

Section: Introductionmentioning

confidence: 99%

Effects of retinoids on the production of tumour necrosis factor-alpha and nitric oxide by lipopolysaccharide-stimulated rat Kupffer cellsin vitro: evidence for participation of retinoid X receptor signalling pathway

Motomura

Sakai

Isobe

et al. 1997

Cell Biochem. Funct.

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Kupffer cells play important roles in the development of liver injury by producing cytokines and free radicals. In consequence inhibition of these inflammatory mediators will be one of the targets for treating liver diseases. Retinoids modulate a wide variety of functions of monocytes/macrophages. Cellular effects of retinoids are mediated by two families of nuclear receptors, retinoic acid receptors (RARs) and retinoid X receptors (RXRs). We examined the effects of several kinds of natural and synthetic retinoids on the production of tumour necrosis factor-alpha (TNF-alpha) and nitric oxide (NO) by LPS-stimulated rat Kupffer cells in vitro. Of the various retinoids tested, 9-cis-retinoic acid (9-cis-RA) and Ro 13-6307 which are agonists of both RARs and RXRs, suppressed the production of TNF-alpha and NO in a concentration-dependent fashion, whereas three types of RAR-selective agonists, Ro 13-7410, Ro 40-6055 and Ro 19-0645 did not show any effect. Furthermore, the RAR alpha antagonist, Ro 41-5253, did not prevent the effects induced by 9-cis-RA. The results suggest that these effects of 9-cis RA and Ro 13-6307 were induced by the RXRs-dependent signalling pathway.

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Antiinflammatory aspects of systemic and topically applied retinoids

Cited by 17 publications

References 0 publications

Induced expression of the new cytokine, activin A, in human monocytes: inhibition by glucocorticoids and retinoic acid

Induced expression of the new cytokine, activin A, in human monocytes: inhibition by glucocorticoids and retinoic acid

Thein vivo andin vitro anti-inflammatory activity of CD271: A new retinoid-like modulator of cell differentiation

Effects of retinoids on the production of tumour necrosis factor-alpha and nitric oxide by lipopolysaccharide-stimulated rat Kupffer cellsin vitro: evidence for participation of retinoid X receptor signalling pathway

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