Overexpression of Cellular Retinoic Acid-Binding Protein Type II (CRABP-II) and Down-Regulation of CRABP-I in Psoriatic Skin

Siegenthaler, Georges; Tomatis, Isabelle; Didierjean, Liliane; Jaconi, Stefano; Saurat, Jean‐Hilaire

doi:10.1159/000247462

Cited by 24 publications

(19 citation statements)

References 11 publications

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“…Third, squamous cell carcinomas frequently display reduced RARγ expression [21,22], and the RAR and RXR levels are progressively suppressed during malignant transformation of human epidermis [10]. Fourth, studies of psoriatic epidermis, characterized by abnormal differentiation and hyperproliferation, have disclosed reduced mRNA expression of RARα and RXRα [23] and increased expression of CRABPII [24,25] that fails to respond to RA treatment [25]. Nonetheless, RArelated drugs (i.e.…”

Section: Introductionmentioning

confidence: 99%

Keratinocyte differentiation induced by calcium, phorbol ester or interferon-γ elicits distinct changes in the retinoid signalling pathways

Karlsson¹,

Vahlquist²,

Törmä³

2010

Journal of Dermatological Science

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This is an author produced version of a paper published in Journal ofDermatological Science. This paper has been peer-reviewed but does not include the final publisher proof-corrections or journal pagination. Access to the published version may require subscription. Published with permission from: ElsevierThe final publication is available at www.elsevier.com Conclusions:Retinoid signalling is profoundly altered upon differentiation of keratinocytes and the effects depend on how cellular differentiation is initiated.

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Section: Introductionmentioning

confidence: 99%

Keratinocyte differentiation induced by calcium, phorbol ester or interferon-γ elicits distinct changes in the retinoid signalling pathways

Karlsson¹,

Vahlquist²,

Törmä³

2010

Journal of Dermatological Science

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“…A number of gene products have been described whose expression is altered in psoriasis. Among these are the low molecular weight proteins cellular retinoic acid-binding protein type II (CRABP II) and psoriasin [1][2][3]. CRABP II is an intracellular protein which binds retinoic acid and may serve to regulate cellular retinoic acid concentrations and thus the effects of retinoic acid on differentiation.…”

Section: Introductionmentioning

confidence: 99%

Differential expression of CRABP II, psoriasin and cytokeratin 1 mRNA in human skin diseases

et al. 1996

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In order to confirm and further explore the significance of the overexpression of the CRABP II (cellular retinoic acid binding protein type II) and psoriasin genes in psoriatic versus normal skin, we examined the mRNA expression levels of these two genes by in situ hybridization in skin samples from psoriatic plaques and in one case from the border between a psoriatic plaque and uninvolved skin. Both genes were markedly upregulated in lesional skin, with a shift from low to high expression in the transitional zone of the plaque. Expression of the cytokeratin 1 (K1) gene was, in contrast, high in normal skin and decreased in the transition from uninvolved skin to psoriatic plaque, Examination of mRNA levels of CRABP II and psoriasin in other hyperproliferative and inflammatory skin diseases showed high expression of psoriasin, and in some cases also of CRABP II, in atopic dermatitis, mycosis fungoides, Darier's disease and inflammatory lichen sclerosus et atrophicus. In atrophic lesions of lichen sclerosus et atrophicus that lacked an inflammatory infiltrate, these changes were only weakly expressed. These findings demonstrate that altered epidermal gene expression of K1, psoriasin and CRABP II is not disease-specific and may reflect instead an altered state of epidermal differentiation and/or may be linked to the inflammation and cellular infiltration common to all the conditions studied.

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“…We showed that CRABP-I and -II arc expressed in normal skin to approximately the same extent. However, in abnormal skin differentiation, the level of CRABP-II strongly increases while that of CRABP-I decreases below the threshold of detection [ 19], In submerged keratinoevte cultures, where cells stratify and differentiate without reaching terminal differentia tion states such as skin, CRABP-II levels were increased only in differentiating cells, whereas CRABP-II was unde tectable in nondifferentiated cells (basal layer) [20]. CRABP-I was never detected in the various in vitro sys tems analyzed [21].…”

Section: Intracellular Transport: Cytosolic Retinoid-binding Proteinsmentioning

confidence: 94%

Extra- and Intracellular Transport of Retinoids: A Reappraisal

Siegenthaler¹

1996

Horm Res

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Retinoids are a family of compounds including retinol (ROL; vitamin A) and ROL derivatives that exert a powerful control over cell differentiation. Retinol-binding protein (RBP) is the specific blood carrier transporting ROL, the precursor of the retinoic acid (RA) hormone, to target tissues. Recently, it was reported that, in addition to the native RBP, two truncated forms of RBP, RBP₁ and RBP₂, are also present in normal serum. RBP₂, the form which has lost the two N-terminal Leu is dramatically increased in serum of patients with chronic renal failure (CRF) whereas this form is very low in normal serum. There is strong evidence that RBP₂ is formed in vitamin A target tissues, and that after its release into blood circulation, it is cleared by the kidney in healthy people but accumulates in the serum of CRF patients. It appears that RBP₂ may play an important physiological role in ROL transport and recycling. Within the cell, two cellular retinoic acid-binding proteins (CRABP-I and -II) and a ROL-binding protein (CRBP-I) regulate the levels of free RA and ROL. The expression of these retinoid-binding proteins in a given tissue may reflect the extent of retinoid metabolism. The most intense traffic of retinoids was found in differentiating keratinocytes, whereas nondifferentiated keratinocytes showed very low activities, suggesting that retinoids control cell differentiation in keratinocytes committed to differentiate. Moreover, these data indicate that normal function of epidermis requires precise amounts of CRABP-I and -II and that a dysregulation of these carriers can alter keratinocyte differentiation by inducing inadequate intracellular levels of RA.

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Overexpression of Cellular Retinoic Acid-Binding Protein Type II (CRABP-II) and Down-Regulation of CRABP-I in Psoriatic Skin

Cited by 24 publications

References 11 publications

Keratinocyte differentiation induced by calcium, phorbol ester or interferon-γ elicits distinct changes in the retinoid signalling pathways

Keratinocyte differentiation induced by calcium, phorbol ester or interferon-γ elicits distinct changes in the retinoid signalling pathways

Differential expression of CRABP II, psoriasin and cytokeratin 1 mRNA in human skin diseases

Extra- and Intracellular Transport of Retinoids: A Reappraisal

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