Catecholamines in Human Keratinocyte Differentiation

Schallreuter, Karin U.; Lemke, K Regina; Pittelkow, Mark R.; Wood, John M.; Körner, Christa; Malik, Ruth

doi:10.1111/1523-1747.ep12606218

Cited by 121 publications

(104 citation statements)

References 25 publications

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“…The skin also expresses epidermal equivalents of another bioamine-based system, the catecholaminergic systems ( 29,30 ). This also includes a 6-tetrahydrobiopterin (6BH 4 ) generating system ( 30,31 ), which acts as a co-factor for phenylalanine, tyrosine, and tryptophan hydroxylases.…”

Section: Cutaneous Pathway For Melatonin Synthesismentioning

confidence: 99%

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On the Role of Melatonin in Skin Physiology and Pathology

Słomiński

Fischer

Żmijewski

et al. 2005

ENDO

230

281

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Melatonin has been experimentally implicated in skin functions such as hair growth cycling, fur pigmentation, and melanoma control, and melatonin receptors are expressed in several skin cells including normal and malignant keratinocytes, melanocytes, and fibroblasts. Melatonin is also able to suppress ultraviolet (UV)-induced damage to skin cells and shows strong antioxidant activity in UV exposed cells. Moreover, we recently uncovered expression in the skin of the biochemical machinery involved in the sequential transformation of L-tryptophan to serotonin and melatonin. Existence of the biosynthetic pathway was confirmed by detection of the corresponding genes and proteins with actual demonstration of enzymatic activities for tryptophan hydroxylase, serotonin Nacetyl-transferase, and hydroxyindole-O-methyltransferase in extracts from skin and skin cells. Initial evidence for in vivo synthesis of melatonin and its metabolism was obtained in hamster skin organ culture and in one melanoma line. Therefore, we propose that melatonin (synthesized locally or delivered topically) could counteract or buffer external (environmental) or internal stresses to preserve the biological integrity of the organ and to maintain its homeostasis. Furthermore, melatonin could have a role in protection against solar radiation or even in the management of skin diseases.

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Section: Cutaneous Pathway For Melatonin Synthesismentioning

confidence: 99%

“…This also includes a 6-tetrahydrobiopterin (6BH 4 ) generating system ( 30,31 ), which acts as a co-factor for phenylalanine, tyrosine, and tryptophan hydroxylases. Expression and activity of aromatic amino acid decarboxylase (AAD) has also been demonstrated in human skin cells ( 29 ).…”

Section: Cutaneous Pathway For Melatonin Synthesismentioning

confidence: 99%

On the Role of Melatonin in Skin Physiology and Pathology

Słomiński

Fischer

Żmijewski

et al. 2005

ENDO

230

281

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“…Physiologically, however, EPI and NE could be derived from other sources. Epidermal keratinocytes and melanocytes are capable of producing catecholamines (51) and EPI of adrenomedullary origin may reach skin cells as a hormone. Thus, the true physiological roles of ARs on LC and their function in states of sympathetic arousal remain to be elucidated.…”

Section: Figure 5 Intradermal Injection Of Epi Inhibits Chs Inductionmentioning

confidence: 99%

Catecholamines Inhibit the Antigen-Presenting Capability of Epidermal Langerhans Cells

Seiffert¹,

Hosoi²,

Torii³

et al. 2002

The Journal of Immunology

120

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The sympathetic nervous system modulates immune function at a number of levels. Within the epidermis, APCs (Langerhans cells (LC)) are frequently anatomically associated with peripheral nerves. Furthermore, some neuropeptides have been shown to regulate LC Ag-presenting function. We explored the expression of adrenergic receptors (AR) in murine LC and assessed their functional role on Ag presentation and modulation of cutaneous immune responses. Both purified LC and the LC-like cell lines XS52-4D and XS106 expressed mRNA for the ARs α1A and β2. XS106 cells and purified LC also expressed β1-AR mRNA. Treatment of murine epidermal cell preparations with epinephrine (EPI) or norepinephrine inhibited Ag presentation in vitro. Furthermore, pretreatment of epidermal cells with EPI or norepinephrine in vitro suppressed the ability of these cells to present Ag for elicitation of delayed-type hypersensitivity in previously immunized mice. This effect was blocked by use of the β2-adrenergic antagonist ICI 118,551 but not by the α-antagonist phentolamine. Local intradermal injection of EPI inhibited the induction of contact hypersensitivity to epicutaneously administered haptens. Surprisingly, injection of EPI at a distant site also suppressed induction of contact hypersensitivity. Thus, catecholamines may have both local and systemic effects. We conclude that specific ARs are expressed on LC and that signaling through these receptors can decrease epidermal immune reactions.

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“…Interestingly, it has been shown that keratinocytes are capable of producing epinephrine [28,29], an endogenous adrenergic agonist with selectivity for the beta2AR, and basal layer keratinocytes produce higher levels of epinephrine than suprabasal keratinocytes [29]. Thus, it has been proposed that epinephrine activates keratinocyte beta2AR to modulate calcium influx and begin the differentiation cascade crucial to the native architecture of the epidermis [29]. The beta2AR desensitizes upon repeated activation through several mechanisms, including downregulation of the number of beta2AR receptors (reviewed in [30,31]).…”

mentioning

confidence: 99%

Beta Adrenergic Receptors in Keratinocytes

Sivamani

Lam

Isseroff

2007

Dermatologic Clinics

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SynopsisBeta2 adrenergic receptors were identified in keratinocytes more than 30 years ago, but their function in the epidermis continues to be elucidated. Abnormalities in their expression, signaling pathway, or in the generation of endogenous catecholamine agonists by keratinocytes have been implicated in the pathogenesis of cutaneous diseases such as atopic dermatitis, vitiligo and psoriasis. New studies also indicate that the beta2AR also modulates keratinocyte migration, and thus can function to regulate wound re-epithelialization. This review focuses on the function of these receptors in keratinocytes and their contribution to cutaneous physiology and disease.Keywords beta-adrenergic; keratinocyte; atopic dermatitis; psoriasis; vitiligo; wound Physiology of the beta2 adrenergic receptor in keratinocytesOf the several identified classes of adrenergic receptors (alpha and beta, and their subtypes), it is of particular interest to note that human keratinocytes, the cells the make up the majority of the epidermis, express only beta2 adrenergic receptors (beta2AR) [1][2][3][4]. The beta adrenergic receptor is a classic seven transmembrane G protein coupled receptor. These receptors serve as the endogenous receptor to the catecholamine hormones norepinephrine and epinephrine, and can be further subdivided into beta1, beta2, and beta3 subtypes, based on their differential pharmacological response to catecholamines and specific antagonists, as well as differences in their protein sequences [5][6][7].The first studies to suggest the presence of betaAR in the epidermis were functional ones that demonstrated an increase in levels of cAMP in keratinocytes after stimulation with non-specific betaAR agonists [8,9]. Subsequently, work using agonists and antagonists with specificity for the different adrenergic receptor subtypes demonstrated that the increase in keratinocyte

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Catecholamines in Human Keratinocyte Differentiation

Cited by 121 publications

References 25 publications

On the Role of Melatonin in Skin Physiology and Pathology

On the Role of Melatonin in Skin Physiology and Pathology

Catecholamines Inhibit the Antigen-Presenting Capability of Epidermal Langerhans Cells

Beta Adrenergic Receptors in Keratinocytes

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