Mu-Opiate Receptor and Beta-Endorphin Expression in Nerve Endings and Keratinocytes in Human Skin

Bigliardi-Qi, Mei; Sumanovski, Lazar T.; Büchner, S.; Rufli, T; Bigliardi, Paul L.

doi:10.1159/000079887

Cited by 99 publications

(80 citation statements)

References 10 publications

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“…Recent findings point to an involvement of ␤-endorphin in the pathophysiology of acne (972) and atopic dermatitis (65,67), although direct evidence is still lacking. Animal studies, however, indicate that ␤-endorphin also has a role in cutaneous inflammatory processes.…”

Section: ␤-Endorphinmentioning

confidence: 99%

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

Roosterman¹,

Goerge

Schneider

et al. 2006

Physiological Reviews

536

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: ␤-Endorphinmentioning

confidence: 99%

“…Bigliardi et al (67) investigated the role of ␤-endorphin in the pathophysiology of atopic dermatitis. They found immunoreactivity for ␤-endorphin in keratinocytes and unmyelinated sensory nerve fibers by immunofluorescence.…”

Section: Atopic Dermatitismentioning

confidence: 99%

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

Roosterman¹,

Goerge

Schneider

et al. 2006

Physiological Reviews

536

521

View full text Add to dashboard Cite

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“…Remarkably, keratinocytes also have the ability express opioid receptors and release opioids [172,173,182]. A recent study by Moffett et al (2012) used pulsed radio frequency energy to increase precursor mRNA for enkaphalin and dynorphin in both human dermal fibroblasts and keratinocytes, suggesting that both non-neural cell types have the ability to create and release opioids [183].…”

Section: The Role Of the Endocannabinoid System In Dry Needling-mediamentioning

confidence: 99%

Peripheral and Spinal Mechanisms of Pain and Dry Needling Mediated Analgesia: A Clinical Resource Guide for Health Care Professionals

Butts¹,

Dunning²

2016

Int J Phys Med Rehabil

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There are a number of biochemical, biomechanical, endocrinological and neurovascular mechanisms underpinning the anti-nociceptive and anti-inflammatory effects of dry needling (DN). While myofascial trigger points likely play a role in peripheral pain, a diagnostic tool for localizing them has not been validated, and DN studies that have targeted trigger points to elicit localized twitch responses have reported mixed results. Therefore, the mechanism responsible for DN-mediated analgesia may be more complicated. DN activates opioid-based pain reduction, mediated by endogenous cannabinoids and the sympathetic nervous system, and non-opioid pain relief via serotonin and norepinephrine from the brain stem. DN also triggers the hypothalamic-pituitary-adrenal axis centrally and the corticotropin releasing hormone-proopiomelanocortin-corticosteroid axis locally to inhibit cox-2, reducing inflammatory cytokines. Recent studies demonstrate that DN combined with mechanical and/or electrical stimulation may reverse PKC-mediated peripheral hyperalgesic priming by normalizing nociceptive channels, to include TRPV, ASIC, TTX and P2X/Y. Electrical DN (EDN) stimulates immune cells, fibroblasts and keratinocytes to release CGRP and substance-P, altering the stimulation of TTX receptors to reverse hyperalgesia. It also encourages the supraoptic nucleus to release oxytocin to quiet ASIC receptors peripherally and stimulate opioid interneurons spinally. Moreover, EDN inhibits ERK1/2 kinase pathways of inflammation in the spinal cord and stimulates Aδ fibers and N/OFQ to reverse C-fiber mediated central changes. Mechanotransduction of fibroblasts and peripheral nerves via TRPV1 and P2X/Y-mediated intracellular Ca 2+ wave propagation and subsequent activation of the nucleus accumbens inhibits spinal pain transmission via glycinergic and opioidergic interneurons. The increased ATP is metabolized to adenosine, which activates P1 purinergic receptors, events considered key to DN analgesia and rho kinase-based tissue remodeling. Mechanotransduction-mediated release of histamine further explains analgesia secondary to needling points distal to pain. DN-mediated analgesia is dependent on a number of synergistic physiologic events involving biochemical and mechanical processes in neural, connective and muscle tissue.

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“…Recently, β-endorphin (β-END) has been detected not just in the central nervous system (CNS), where it has various functions (30), but also in the periphery regulating processes such as cell differentiation, cell communication, and modulation of inflammation (4). β-END binding sites have been detected in rat chondrocytes (6), and β-END has been found in articular chondrocytes, synovial membrane, and fibrous joint capsule of dogs (16), suggesting the possible existence of an opiate modulation of articular cartilage.…”

Section: Introductionmentioning

confidence: 99%

β-Endorphin Regulation of MAPKs in Cultured Human Articular Chondrocytes: MAPK Inhibitors Prevent the Increase of IL-1β Protein Levels During β-Endorphin Stimulation

Andjelkov¹,

Elvenes²,

Knutsen³

et al. 2007

Cell Communication & Adhesion

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We investigated the effect of β-endorphin on the activities of mitogen-activated protein kinases in cultured human articular chondrocytes in order to elucidate its effect on cartilage. Monolayer cultures of chondrocytes obtained from patients undergoing total knee arthroplasty were treated with 60, 600, or 6000 ng/ml β-endorphin, or 100 ng/ml naltrexone combined with 600 ng/ml β-endorphin. The regulation of three major mitogen-activated protein kinases phosphorylation, ERKp44/p42, p38, and JNK, was determined by Western blotting. We also examined the influence of specific mitogen-activated protein kinase inhibitors on IL-1β protein levels during β-endorphin stimulation. The results demonstrate that β-endorphin, dependent on concentration and duration of stimulation, significantly affected the activation of the three mitogen-activated protein kinases in cultured human articular chondrocytes. Naltrexone in some cases significantly regulated the mitogen-activated protein kinases in different ways when added to β-endorphin 600 ng/ml. Furthermore, specific mitogen-activated protein kinase inhibitors hindered the increase of IL-1β during β-endorphin incubation. The effect of β-endorphin seen in this study is considered critical for the production of several mediators of cartilage damage in an arthritic joint.

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Mu-Opiate Receptor and Beta-Endorphin Expression in Nerve Endings and Keratinocytes in Human Skin

Cited by 99 publications

References 10 publications

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

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

Peripheral and Spinal Mechanisms of Pain and Dry Needling Mediated Analgesia: A Clinical Resource Guide for Health Care Professionals

β-Endorphin Regulation of MAPKs in Cultured Human Articular Chondrocytes: MAPK Inhibitors Prevent the Increase of IL-1β Protein Levels During β-Endorphin Stimulation

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