All-Trans-Retinoic Acid Induces Interleukin-8 via the Nuclear Factor-κB and p38 Mitogen-Activated Protein Kinase Pathways in Normal Human Keratinocytes

Dai, Xiuju; Yamasaki, Kenshi; Shirakata, Yuji; Sayama, Koji; Hashimoto, Koji

doi:10.1111/j.0022-202x.2004.23503.x

Cited by 48 publications

(45 citation statements)

References 56 publications

(61 reference statements)

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“…Activation of the p38 pathway by ATRA is consistent with other reports in different cell types (27,29,35,36). It has also been reported that the effects of ATRA in different models might be mediated by increased TGF-␤1 levels.…”

Section: Discussionsupporting

confidence: 92%

All-trans-retinoic Acid Promotes Trafficking of Human Concentrative Nucleoside Transporter-3 (hCNT3) to the Plasma Membrane by a TGF-β1-mediated Mechanism

Fernández-Calotti

Pastor‐Anglada

2010

Journal of Biological Chemistry

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Human concentrative nucleoside transporter-3 (hCNT3) is a sodium-coupled nucleoside transporter that exhibits high affinity and broad substrate selectivity, making it the most suitable candidate for mediating the uptake and cytotoxic action of most nucleoside-derived drugs. The drug of this class most commonly used in the treatment of chronic lymphocytic leukemia (CLL) is the pro-apoptotic nucleoside analog fludarabine (Flu), which enters CLL cells primarily through human equilibrative nucleoside transporters (hENTs). Although CLL cells lack hCNT3 activity, they do express this transporter protein, which is located mostly in the cytosol. The aim of our study was to identify agents and mechanisms capable of promoting hCNT3 trafficking to the plasma membrane. Here, we report that all-transretinoic acid (ATRA), currently used in the treatment of acute promyelocytic leukemia (APL), increases hCNT3-related activity through a mechanism that involves trafficking of pre-existing hCNT3 proteins to the plasma membrane. This effect is mediated by the autocrine action of transforming growth factor (TGF)-␤1, which is transcriptionally activated by ATRA in a p38-dependent manner. TGF-␤1 acts through activation of ERK1/2 and the small GTPase RhoA to promote plasma membrane trafficking of the hCNT3 protein.

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Section: Discussionsupporting

confidence: 92%

All-trans-retinoic Acid Promotes Trafficking of Human Concentrative Nucleoside Transporter-3 (hCNT3) to the Plasma Membrane by a TGF-β1-mediated Mechanism

Fernández-Calotti

Pastor‐Anglada

2010

Journal of Biological Chemistry

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“…Rapid activation of p38MAPK by RA has previously been reported in keratinocytes, but in these cells RA alone was able to activate the kinase. 58 In our experiments, RA enhanced the phosphorylation of p38MAPK only in combination with CpG. This indicates that RA has a more costimulatory role in B cells.…”

Section: Org Fromsupporting

confidence: 56%

Vitamin A potentiates CpG-mediated memory B-cell proliferation and differentiation: involvement of early activation of p38MAPK

Ertesvag

Aasheim

Naderi

et al. 2007

Blood

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Foreign CpG-DNA from viruses and bacteria can activate memory B cells through binding to toll-like receptor 9, and this pathway has been hypothesized to be involved in the continuous activation of memory B cells ensuring life-long humoral immunity. In this study, we demonstrate that retinoic acid (RA) is a potent coactivator of this pathway in human B cells. RA enhanced the CpG-mediated proliferation of CD27 ؉ memory B cells, and the proliferative response was accompanied by increased immunoglobulin (Ig) secretion indicative of plasma-cell formation. The RA-induced proliferation was preceded by enhanced expression of cyclin D3, and both the expression of cyclin D3 and the induced Ig secretion were found to be dependent on IL-10. Of importance, RA increased the CpG-induced phosphorylation of ERK1/2, p38MAPK, and IB as early as 30 minutes after stimulation. By using specific inhibitors, all the RA-mediated events, including proliferation, cyclin D3 expression, IL-10 se- IntroductionVitamin A is important for an optimal functioning of the immune system, but the mechanisms involved are not fully understood. A part of the increased resistance to infection has been attributed to improved epithelial integrity, but a direct effect on cells of the immune system is also established. [1][2][3] We and others have shown that all-trans retinoic acid has a stimulatory role in T lymphocytes. [4][5][6][7][8][9][10][11] However, there has been some controversy regarding the importance of vitamin A for B-cell activity. Some reports document that retinoids are required for B-cell activity 12 and have the potential to enhance differentiation and antibody responses of B cells, [13][14][15][16] and that B-cell responses are impaired in vitamin A-deficient rats. 17 We have previously shown that RA inhibits the proliferation of human and murine B-cell precursors 18 as well as peripheral-blood B cells stimulated via B-cell receptor (BcR). 19 We also demonstrated that the inhibition of B-cell proliferation was accompanied by inhibition of the cell-cycle machinery driving the cells from G 1 to S phase. 20 In the primary immune response, naive B cells proliferate and differentiate into plasma cells that secrete antibodies mainly of the immunoglobulin-M (IgM) class. During this process, somatic hypermutation and isotype switching take place, producing highaffinity antibodies of the IgG class. 21 Some B cells embark on a different program to become long-lived memory B cells, which are characterized by lower threshold for activation and differentiation. 22 In the past 2 decades, it has become clear that B cells can be activated by DNA from bacteria and viruses. 23 The discrimination between human and bacterial/viral DNA is based on the fact that CpG dinucleotides are underrepresented and generally methylated in vertebrate DNA, while they are present at expected frequency and are unmethylated in bacteria and viruses. 23,24 Unmethylated CpG DNA is recognized by toll-like receptor 9 (TLR9), which is primarily expressed in memory B cells and plas...

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“…in ICD models in previous in vivo and in vitro studies, although most of the studies were performed in the early induction stage of irritant dermatitis. TNF-α and IL-8 were also reported to be up-regulated in retinoid dermatitis [18][19][20] .…”

Section: Discussionmentioning

confidence: 97%

Epidermal Hyperplasia and Elevated HB-EGF are More Prominent in Retinoid Dermatitis Compared with Irritant Contact Dermatitis Induced by Benzalkonium Chloride

et al. 2010

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Background: 'Retinoid dermatitis' is a retinoid-induced irritant contact dermatitis (ICD). The mechanism of retinoid dermatitis may be different from that of other ICDs. However, it remains uncertain how topical retinoid induce ICD. Objective: We compared several aspects of contact dermatitis induced by topical retinol and benzalkonium chloride (BKC) on hairless mice skin. Methods: 2% retinol or 2.5% BKC was applied to hairless mice and transepidermal water loss (TEWL), ear thickness, histologic and immunohistochemical findings were compared. We also compared mRNA expression of inflammatory cytokines, epidermal differential markers, cyclooxygenases (COXs) and heparin binding epidermal growth factor like growth factor (HB-EGF). Results: Topical application of 2% retinol and 2.5% BKC increased TEWL and ear thickness in similar intensity. Epidermal hyperplasia was more prominent in retinol treated skin. Proliferating cell nuclear antigen, involucrin and loricrin expression were higher in retinol-treated skin than in BKC-treated skin. Filaggrin, however, was more expressed in BKC-treated skin. The mRNA expression of IL-8, TNF-α, COX-2, involucrin, loricrin and filaggrin were increased in both retinol-and BKC-treated skin in similar intensity. HB-EGF was more significantly increased in retinol-treated skin. Conclusion: Elevated HB-EGF and epidermal hyperplasia are more prominent features of retinoid dermatitis than in BKC-induced ICD. (Ann Dermatol 22(3) 290∼299,

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All-Trans-Retinoic Acid Induces Interleukin-8 via the Nuclear Factor-κB and p38 Mitogen-Activated Protein Kinase Pathways in Normal Human Keratinocytes

Cited by 48 publications

References 56 publications

All-trans-retinoic Acid Promotes Trafficking of Human Concentrative Nucleoside Transporter-3 (hCNT3) to the Plasma Membrane by a TGF-β1-mediated Mechanism

All-trans-retinoic Acid Promotes Trafficking of Human Concentrative Nucleoside Transporter-3 (hCNT3) to the Plasma Membrane by a TGF-β1-mediated Mechanism

Vitamin A potentiates CpG-mediated memory B-cell proliferation and differentiation: involvement of early activation of p38MAPK

Epidermal Hyperplasia and Elevated HB-EGF are More Prominent in Retinoid Dermatitis Compared with Irritant Contact Dermatitis Induced by Benzalkonium Chloride

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