Sodium butyrate selectively antagonizes the inhibitory effect of retinoids on cornified envelope formation in cultured human keratinocytes

Schmidt, Rainer; Cathelineau, C.; Cavey, Marie T.; Dionisius, Veronique.; Michel, Serge; Shroot, Braham; Reichert, Uwe

doi:10.1002/jcp.1041400213

Cited by 34 publications

(29 citation statements)

References 45 publications

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“…Mansbridge & Hanawalt (1988) reported that the synthesis of keratins 6 and 16, which are usually associated with hyperproliferation of keratinocytes, was increased after treatment with TGF-1, while synthesis of keratin 1, associated with keratinocyte differentiation, was inhibited. In other studies, sodium butyrate enhanced cornified envelope formation in cultured human keratinocytes (Schmidt et al 1989). Neutralising antibodies to TGF-1 effectively reduced this effect (Wang et al 1992) while additional TGF-1 significantly enhanced the effect of sodium butyrate on keratinocyte differentiation.…”

Section: Discussionmentioning

confidence: 73%

Modulation of skin cell functions by transforming growth factor-beta1 and ACTH after ultraviolet irradiation

Dissanayake

Mason²

1998

Journal of Endocrinology

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The adaptive responses in skin to ultraviolet (UV) radiation include increased cornification of keratinocytes and increased synthesis and distribution of melanin by melanocytes.The possible involvement of paracrine factors in the generation of these responses was studied in a novel twostage culture model. Human melanocytes or keratinocytes were first irradiated or sham-irradiated and then the conditioned media collected from these cells after 24 h were used to treat unirradiated skin cells.Immunofluorescent staining for transforming growth factor (TGF)-1 was increased in UV-irradiated keratinocytes compared with sham-irradiated cells. Increased TGF-1 was also detected in the culture media of irradiated keratinocytes. Treatment of unirradiated keratinocytes with conditioned media collected from UVirradiated keratinocytes resulted in increased absolute numbers and percentages of cornified envelopes per well compared with treatment with conditioned media from sham-irradiated keratinocytes. The magnitude of this effect increased with increased dose of initial irradiation. The effects of conditioned media from UVR-treated cells were mimicked by authentic TGF-1. Treatment of conditioned media from irradiated cells with an antibody shown to neutralise the effects of TGF-1 but not with a non-immune antibody of similar isotype, abolished this bioactivity of the conditioned media from UV-irradiated cells. Immunofluorescent staining for ACTH was also increased in UV-irradiated keratinocytes. Conditioned media from UV-irradiated keratinocytes increased tyrosinase activity of unirradiated melanocytes, an effect which was mimicked by authentic ACTH. This bioactivity of conditioned media from irradiated keratinocytes was abolished in the presence of an antibody which neutralised the activity of ACTH but not MSH. These results provide evidence to support the involvement of TGF-1 and ACTH in the cornification and pigmentary responses respectively of skin cells after UV exposure.

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Section: Discussionmentioning

confidence: 73%

Modulation of skin cell functions by transforming growth factor-beta1 and ACTH after ultraviolet irradiation

Dissanayake

Mason²

1998

Journal of Endocrinology

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“…Transcriptional regulation in eukaryotic cells is heavily dependent upon histone acetylation and methylation (reviewed in reference 24). Keratinocyte differentiation and growth arrest can be induced by inhibitors of histone deacetylase, such as sodium butyrate (72,82) and tricostatin A (71). The KSHV Rta promoter can also be induced by these histone deacetylase inhibitors (52,89), and Rta itself is involved in the recruitment of cellular factors (32,35) that influence chromatin remodeling and access to cellular transcription factors (52).…”

Section: Discussionmentioning

confidence: 99%

Activation of Kaposi's Sarcoma-Associated Herpesvirus Lytic Gene Expression during Epithelial Differentiation

Johnson¹,

Maronian

Vieira³

2005

J Virol

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The oral cavity has been identified as the major site for the shedding of infectious Kaposi's sarcomaassociated herpesvirus (KSHV). While KSHV DNA is frequently detected in the saliva of KSHV seropositive persons, it does not appear to replicate in salivary glands. Some viruses employ the process of epithelial differentiation for productive viral replication. To test if KSHV utilizes the differentiation of oral epithelium as a mechanism for the activation of lytic replication and virus production, we developed an organotypic raft culture model of epithelium using keratinocytes from human tonsils. This system produced a nonkeratinized stratified squamous oral epithelium in vitro, as demonstrated by the presence of nucleated cells at the apical surface; the expression of involucrin and keratins 6, 13, 14, and 19; and the absence of keratin 1. The activation of KSHV lytic-gene expression was examined in this system using rKSHV.219, a recombinant virus that expresses the green fluorescent protein during latency from the cellular EF-1␣ promoter and the red fluorescent protein (RFP) during lytic replication from the viral early PAN promoter. Infection of keratinocytes with rKSHV.219 resulted in latent infection; however, when these keratinocytes differentiated into a multilayered epithelium, lytic cycle activation of rKSHV.219 occurred, as evidenced by RFP expression, the expression of the late virion protein open reading frame K8.1, and the production of infectious rKSHV.219 at the epithelial surface. These findings demonstrate that KSHV lytic activation occurs as keratinocytes differentiate into a mature epithelium, and it may be responsible for the presence of infectious KSHV in saliva.

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“…Moreover, inhibition of DNA methylation and histone deacetylation has been shown to promote keratinocyte differentiation (Rosl et al, 1988;Schmidt et al, 1989;Staiano-Coico et al, 1989), and an inverse correlation between DNA methylation and the expression of differentiating genes has been demonstrated in human keratinocytes (Engelkamp et al, 1993;Elder and Zhao, 2002). It has also been suggested that inhibition of differentiation by AEA occurs through changes in chromatin methylation patterns (Paradisi et al, 2008;Pasquariello et al, 2009), and that AEA induces DNA methylation of keratinocyte-differentiating genes by increasing DNA methyltransferase (DNMT) activity via a CB 1-dependent involvement of p38 and p42/p44 MAPK (Paradisi et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Epigenetic control of skin differentiation genes by phytocannabinoids

Pucci

Rapino

Francesco

et al. 2013

British J Pharmacology

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BACKGROUND AND PURPOSEEndocannabinoid signalling has been shown to have a role in the control of epidermal physiology, whereby anandamide is able to regulate the expression of skin differentiation genes through DNA methylation. Here, we investigated the possible epigenetic regulation of these genes by several phytocannabinoids, plant-derived cannabinoids that have the potential to be novel therapeutics for various human diseases. EXPERIMENTAL APPROACHThe effects of cannabidiol, cannabigerol and cannabidivarin on the expression of skin differentiation genes keratins 1 and 10, involucrin and transglutaminase 5, as well as on DNA methylation of keratin 10 gene, were investigated in human keratinocytes (HaCaT cells). The effects of these phytocannabinoids on global DNA methylation and the activity and expression of four major DNA methyltransferases (DNMT1, 3a, 3b and 3L) were also examined. KEY RESULTSCannabidiol and cannabigerol significantly reduced the expression of all the genes tested in differentiated HaCaT cells, by increasing DNA methylation of keratin 10 gene, but cannabidivarin was ineffective. Remarkably, cannabidiol reduced keratin 10 mRNA through a type-1 cannabinoid (CB1) receptor-dependent mechanism, whereas cannabigerol did not affect either CB1 or CB2 receptors of HaCaT cells. In addition, cannabidiol, but not cannabigerol, increased global DNA methylation levels by selectively enhancing DNMT1 expression, without affecting DNMT 3a, 3b or 3L. CONCLUSIONS AND IMPLICATIONSThese findings show that the phytocannabinoids cannabidiol and cannabigerol are transcriptional repressors that can control cell proliferation and differentiation. This indicates that they (especially cannabidiol) have the potential to be lead compounds for the development of novel therapeutics for skin diseases. AbbreviationsAEA, anandamide; 2-AG, 2-arachidonoylglycerol; CB1, cannabinoid receptor type I; CB2, cannabinoid receptor type II; CBD, cannabidiol; CBDV, cannabidivarin; CBG, cannabigerol; CPZ, capsazepine; DAGL, diacylglycerol lipase; DNMT, DNA methyltransferase; eCBs, endocannabinoids; ECS, endocannabinoid system; FAAH, fatty acid amide hydrolase; K1, keratin 1; K10, keratin 10; NAPE-PLD, N-acyl-phosphatidylethanolamines-specific phospholipase D; NHEK, normal human epidermal keratinocytes; MAGL, monoacylglycerol lipase; SR141716, N-piperidino-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-3-pyrazole carboxamide; SR144528, N-[(1)-endo-1,3,3-trimethy-1-bicyclo [2.2.1]-heptan-2-yl]5-(4-chloro-3-methyl-phenyl)-1-(4-methyl-benzyl)-pyrazole-3-carboxamide; TGase 5, transglutaminase 5; THC, Δ 9-tetrahydrocannbinol; TPA, 12-O-tetradecanoylphorbol 13-acetate; TRPV1, transient receptor potential vanilloid 1 IntroductionEndocannabinoids (eCBs) are lipid mediators derived from membrane precursors and are involved in multiple regulatory functions, both in health and disease (Di Marzo and Petrosino, 2007). The two most important eCBs are N-arachidonylethanolamine ('anandamide', AEA) and 2-arachidonoylglycerol (2-AG) that elicit their a...

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Sodium butyrate selectively antagonizes the inhibitory effect of retinoids on cornified envelope formation in cultured human keratinocytes

Cited by 34 publications

References 45 publications

Modulation of skin cell functions by transforming growth factor-beta1 and ACTH after ultraviolet irradiation

Modulation of skin cell functions by transforming growth factor-beta1 and ACTH after ultraviolet irradiation

Activation of Kaposi's Sarcoma-Associated Herpesvirus Lytic Gene Expression during Epithelial Differentiation

Epigenetic control of skin differentiation genes by phytocannabinoids

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