Production of catecholamines in the human epidermis

Schallreuter, Karin U.; Wood, John M.; Lemke, Regina; LePoole, Caroline; Das, Pranab; Westerhof, W.; Pittelkow, Mark R.; Thody, A. J.

doi:10.1016/0006-291x(92)91527-w

Cited by 114 publications

(91 citation statements)

References 17 publications

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“…In the skin, catecholamines and their regulating enzymes have been detected in nerve fibers (420), keratinocytes (715,718), and melanocytes (714,715,717). Moreover, catecholamines may regulate the activity of certain lymphocytes (natural killer cells) (610) and monocytes (687,946) and induce apoptosis in lymphocytes (166).…”

Section: Catecholaminesmentioning

confidence: 99%

Neuronal Control of Skin Function: The Skin as a Neuroimmunoendocrine Organ

Roosterman¹,

Goerge

Schneider

et al. 2006

Physiological Reviews

552

521

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This review focuses on the role of the peripheral nervous system in cutaneous biology and disease. During the last few years, a modern concept of an interactive network between cutaneous nerves, the neuroendocrine axis, and the immune system has been established. We learned that neurocutaneous interactions influence a variety of physiological and pathophysiological functions, including cell growth, immunity, inflammation, pruritus, and wound healing. This interaction is mediated by primary afferent as well as autonomic nerves, which release neuromediators and activate specific receptors on many target cells in the skin. A dense network of sensory nerves releases neuropeptides, thereby modulating inflammation, cell growth, and the immune responses in the skin. Neurotrophic factors, in addition to regulating nerve growth, participate in many properties of skin function. The skin expresses a variety of neurohormone receptors coupled to heterotrimeric G proteins that are tightly involved in skin homeostasis and inflammation. This neurohormone-receptor interaction is modulated by endopeptidases, which are able to terminate neuropeptide-induced inflammatory or immune responses. Neuronal proteinase-activated receptors or transient receptor potential ion channels are recently described receptors that may have been important in regulating neurogenic inflammation, pain, and pruritus. Together, a close multidirectional interaction between neuromediators, high-affinity receptors, and regulatory proteases is critically involved to maintain tissue integrity and regulate inflammatory responses in the skin. A deeper understanding of cutaneous neuroimmunoendocrinology may help to develop new strategies for the treatment of several skin diseases.

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Section: Catecholaminesmentioning

confidence: 99%

Neuronal Control of Skin Function: The Skin as a Neuroimmunoendocrine Organ

Roosterman¹,

Goerge

Schneider

et al. 2006

Physiological Reviews

552

521

View full text Add to dashboard Cite

show abstract

“…One pathogenic mechanism advanced by the work of Schallreuter and colleagues implicates the beta2AR signaling pathway and catecholamine synthetic network within the epidermis (recently reviewed in [13]). Both keratinocytes and melanocytes express beta2AR [4,10,11,53], both cell types have the enzymatic machinery for catecholamine synthesis [53,54], and indeed, both have been demonstrated to generate norepinephrine (keratinocytes, but not melanocytes can generate epinephrine) [53][54][55]. Stimulation of the beta2AR on melanocytes results in an increase in intracellular levels of cAMP, and subsequently, increased melanogenesis [53].…”

Section: Vitiligo and Beta2armentioning

confidence: 99%

“…Circulating levels of epinephrine are increased posttrauma [101,102] and thus exogenously added beta blockers could be preventing their action on beta2AR in keratinocytes, thereby enhancing migratory speed and wound epithelialization. Alternatively, since keratinocytes have the enzymatic machinery to generate catecholamines [1,28], they can, and do synthesize endogenous epinephrine [28,103], which could be locally secreted into the wound and function in an autocrine manner. In either scenario, the pharmacologic use of beta blockers would result in the observed increase in wound epithelialization.…”

Section: Wound Healingmentioning

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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“…Epinephrine has recently been revealed to be produced by epidermal keratinocytes, and its high affinity receptor, β 2 -adrenergic receptor, is also expressed in epidermal keratinocytes (24). β 2 -Adrenergic receptors are expressed in undifferentiated keratinocytes, but is suppressed in differentiated keratinocytes.…”

Section: Adrenergic and Cholinergic Responsesmentioning

confidence: 99%

Analysis of the Mechanism for the Development of Allergic Skin Inflammation and the Application for Its Treatment: Keratinocytes in Atopic Dermatitis — Their Pathogenic Involvement

Komine

2009

J Pharmacol Sci

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Abstract. Atopic dermatitis frequently accompanies bronchial asthma, allergic rhinitis, and allergic conjunctivitis, the pathogenesis of which has frequently focused on the immunological aspects; however, skin eruption in atopic dermatitis occurs mainly in the epidermis, whose barrier function and cytokine expression have been revealed to be abnormal. In addition, the epidermis contains Langerhans cells, antigen-presenting cells, which could be considered the sentinel of the immune system. Some atopic dermatitis patients have been revealed to have mutations or SNPs (single-nucleotide polymorphisms) in the filaggrin gene, which affect the epidermal barrier function. Proteinases in the epidermis are of importance in maintaining the epidermal barrier, abnormalities of which have been reported in atopic dermatitis. Abnormalities of various cytokines and chemokines produced by keratinocytes have also been reported. Thymic stromal lymphopoietin (TSLP) produced by keratinocytes has recently been a focus in atopic dermatitis. Adrenergic/cholinergic responses in the epidermis could also influence the pathogenesis of atopic dermatitis. Considering epidermal keratinocytes as a trigger of immune abnormalities, not only as a peripheral effector, would be important to further disclose the pathogenesis of this enigmatic disorder.

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Production of catecholamines in the human epidermis

Cited by 114 publications

References 17 publications

Neuronal Control of Skin Function: The Skin as a Neuroimmunoendocrine Organ

Neuronal Control of Skin Function: The Skin as a Neuroimmunoendocrine Organ

Beta Adrenergic Receptors in Keratinocytes

Analysis of the Mechanism for the Development of Allergic Skin Inflammation and the Application for Its Treatment: Keratinocytes in Atopic Dermatitis — Their Pathogenic Involvement

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