Altered differentiation of mouse epidermal cells treated with retinyl acetate in vitro

Yuspa, Stuart H.; Harris, C.C.

doi:10.1016/0014-4827(74)90653-3

Cited by 391 publications

(119 citation statements)

References 14 publications

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“…16 The epidermis was loosened from the dermis through overnight incubation in 5 mg/ml dispase I (Sigma-Aldrich) at 4°C. Primary keratinocytes were isolated from the epidermis according to the protocol provided by CELLnTEC.…”

Section: Keratinocyte Isolation and Culturementioning

confidence: 99%

17β-Estradiol Inhibits Wound Healing in Male Mice via Estrogen Receptor-α

Gilliver

Emmerson

Campbell

et al. 2010

The American Journal of Pathology

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Although estrogens have long been known to accelerate healing in females, their roles in males remain to be established. To address this, we have investigated the influence of 17␤-estradiol on acute wound repair in castrated male mice. We report that sustained exposure to estrogen markedly delays wound re-epithelialization. Our use of hairless mice revealed this response to be largely independent of hair follicle cycling, whereas other studies demonstrated that estrogen minimally influences wound inflammation in males. Additionally , we report reduced collagen accumulation and increased gelatinase activities in the wounds of estrogen-treated mice. Increased wound matrix metalloproteinase (MMP)-2 activity in these animals may i) contribute to their inability to heal skin wounds optimally and ii) stem , at least in part , from effects on the overall levels and spatial distribution of membrane-type 1-MMP and tissue inhibitor of MMP (TIMP)-3 , which respectively facilitate and prevent MMP-2 activation. Using mice rendered null for either the ␣ or ␤ isoform of the estrogen receptor , we identified estrogen receptor-␣ as the likely effector of estrogen's inhibitory effects on healing.

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Section: Keratinocyte Isolation and Culturementioning

confidence: 99%

17β-Estradiol Inhibits Wound Healing in Male Mice via Estrogen Receptor-α

Gilliver

Emmerson

Campbell

et al. 2010

The American Journal of Pathology

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“…PMKs from newborn WT mice were prepared as described by Yuspa et al (69). Briefly, 1-to 2-day-old newborns were euthanized and washed in 70% ethanol.…”

Section: Cell Culturementioning

confidence: 99%

Multiple Signaling Pathways Are Responsible for Prostaglandin E2–Induced Murine Keratinocyte Proliferation

Ansari

Rundhaug

Fischer

2008

Molecular Cancer Research

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Although prostaglandin E 2 (PGE 2 ) has been shown by pharmacologic and genetic studies to be important in skin cancer, the molecular mechanism(s) by which it contributes to tumor growth is not well understood. In this study, we investigated the mechanisms by which PGE 2 stimulates murine keratinocyte proliferation using in vitro and in vivo models. In primary mouse keratinocyte cultures, PGE 2 activated the epidermal growth factor receptor (EGFR) and its downstream signaling pathways as well as increased cyclic AMP (cAMP) production and activated the cAMP response element binding protein (CREB). EGFR activation was not significantly inhibited by pretreatment with a c-src inhibitor (PP2), nor by a protein kinase A inhibitor (H-89). However, PGE 2 -stimulated extracellularly regulated kinase 1/2 (ERK1/2) activation was completely blocked by EGFR, ERK1/2, and phosphatidylinositol 3-kinase (PI3K) pathway inhibitors. In addition, these inhibitors attenuated the PGE 2 -induced proliferation, nuclear factor-KB, activator protein-1 (AP-1), and CREB binding to the promoter regions of the cyclin D1 and vascular endothelial growth factor (VEGF) genes and expression of cyclin D1 and VEGF in primary mouse keratinocytes. Similarly, in vivo, we found that WT mice treated with PGE 2 and untreated cyclooxygenase-2 -overexpressing transgenic mice had higher levels of cell proliferation and expression of cyclin D1 and VEGF, as well as higher levels of activated EGFR, nuclear factor-KB, AP-1, and CREB, than vehicle-treated WT mice. Our findings provide evidence for a link between cyclooxygenase-2 overexpression and EGFR-, ERK-, PI3K-, cAMP-mediated cell proliferation, and the tumor-promoting activity of PGE 2 in mouse skin.

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“…One of these factors is calcium, which is a necessary prerequisite for a variety of differentiative processes, including stratification, assembly of desmosomes, and activation of epidermal transglutaminase (Rice and Green, 1979;Hennings et al, 1980;Watt et al, 1984;Duden and Franke, 1988). Another important group of regu-lators are retinoids, which diminish features of terminal differentiation in stratified squamous epithelia both in vivo (Fell and Mellanby, 1953) and in vitro (Yuspa and Harris, 1974;Fuchs and Green, 1981). When retinol is removed from serum, cultured epidermal cells display many of the morphological and biochemical characteristics of terminal differentiation (Fuchs and Green, 1981).…”

Section: Reproducing Epidermis In Vitromentioning

confidence: 99%

“…Thus, for example, in organ culture of chick epidermis, vitamin A can induce its transition from a keratinizing to a secretory epithelium (mucous metaplasia) (Fell and Mellanby, 1953). Excess retinoids in mammalian epidermal cultures can suppress differentiative features including K1/KI0 expression (Fuchs and Green, 1981), Kt/KI6 expression (Kopan and Fuchs, 1989), cornified envelope production (Yuspa and Harris, 1974), and filaggrin expression (Fleckman et al, 1985). Many of these effects are at least at the level of mRNA expression (Fuchs and Green, 1981;Kopan et al, 1987;Kopan and Fuchs, 1989), and quite likely at the transcriptional level as well (Agarwal et al, 1990;Blumenberg et al, 1990).…”

Section: Retinoidsmentioning

confidence: 99%

Epidermal differentiation: the bare essentials.

Fuchs

1990

The Journal of Cell Biology

609

481

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N the past ten years, there have been a number of major scientific discoveries in the field of epidermal differentiation. We owe many of these findings to the development of model tissue culture systems, and to technological advances in molecular biology. In this article, I will review some important aspects of the biology of terminal differentiation in vivo and in vitro, and highlight the recent advances in elucidating the molecular mechanism underlying these processes.

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Altered differentiation of mouse epidermal cells treated with retinyl acetate in vitro

Cited by 391 publications

References 14 publications

17β-Estradiol Inhibits Wound Healing in Male Mice via Estrogen Receptor-α

17β-Estradiol Inhibits Wound Healing in Male Mice via Estrogen Receptor-α

Multiple Signaling Pathways Are Responsible for Prostaglandin E2–Induced Murine Keratinocyte Proliferation

Epidermal differentiation: the bare essentials.

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