TRPV1 antagonist can suppress the atopic dermatitis-like symptoms by accelerating skin barrier recovery

Yun, Jun Won; Seo, Jung A.; Jeong, Yeon Su; Bae, Il-Hong; Jang, Won Hee; Lee, Jihae; Kim, Sun Young; Shin, Song Seok; Woo, Byoung Young; Lee, Ki Wha; Lim, Kyung Min; Park, Young Ho

doi:10.1016/j.jdermsci.2010.10.014

Cited by 55 publications

(68 citation statements)

References 49 publications

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“…In contrast to other TRP channels discussed here, activation of TRPV1 in keratinocytes appears to suppress cell growth and induce apoptosis and, hence, to have a negative role in epidermal barrier formation and recovery (Denda et al, 2007;Tóth et al, 2011;Yun et al, 2011). Nonetheless, TRPV1-mediated Ca 2+ influx might still be necessary for keratinocyte polarity and migration (Graham et al, 2013).…”

Section: Trpv Channelsmentioning

confidence: 86%

Defective channels lead to an impaired skin barrier

Blaydon¹,

Kelsell²

2014

Journal of Cell Science

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Channels are integral membrane proteins that form a pore, allowing the passive movement of ions or molecules across a membrane (along a gradient), either between compartments within a cell, between intracellular and extracellular environments or between adjacent cells. The ability of cells to communicate with one another and with their environment is a crucial part of the normal physiology of a tissue that allows it to carry out its function. Cell communication is particularly important during keratinocyte differentiation and formation of the skin barrier. Keratinocytes in the skin epidermis undergo a programme of apoptosis-driven terminal differentiation, whereby proliferating keratinocytes in the basal (deepest) layer of the epidermis stop proliferating, exit the basal layer and move up through the spinous and granular layers of the epidermis to form the stratum corneum, the external barrier. Genes encoding different families of channel proteins have been found to harbour mutations linked to a variety of rare inherited monogenic skin diseases. In this Commentary, we discuss how human genetic findings in aquaporin (AQP) and transient receptor potential (TRP) channels reveal different mechanisms by which these channel proteins function to ensure the proper formation and maintenance of the skin barrier.

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Section: Trpv Channelsmentioning

confidence: 86%

Defective channels lead to an impaired skin barrier

Blaydon¹,

Kelsell²

2014

Journal of Cell Science

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“…Character of lesion scoring was adapted from previous studies (Hampton et al, 2012; Liu et al, 2013; Yun et al, 2011). …”

Section: Methodsmentioning

confidence: 99%

HTR7 Mediates Serotonergic Acute and Chronic Itch

Morita

McClain

Batia

et al. 2015

Neuron

161

172

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SUMMARY Chronic itch is a prevalent and debilitating condition for which few effective therapies are available. We harnessed the natural variation across genetically distinct mouse strains to identify transcripts co-regulated with itch behavior. This survey led to the discovery of the serotonin receptor, HTR7, as a key mediator of serotonergic itch. Activation of HTR7 promoted opening of the ion channel TRPA1, which in turn triggered itch behaviors. In addition, acute itch triggered by serotonin or a selective serotonin reuptake inhibitor required both HTR7 and TRPA1. Aberrant serotonin signaling has long been linked to a variety of human chronic itch conditions, including atopic dermatitis. In a mouse model of atopic dermatitis, mice lacking HTR7 or TRPA1 displayed reduced scratching and skin lesion severity. These data highlight a role for HTR7 in acute and chronic itch, and suggest that HTR7 antagonists may be useful for treating a variety of pathological itch conditions.

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“…107,114 PAC-14028 antagonist of TRPV1, tested in atopic animals, was able to suppress the symptoms of AD resulting from stimulation of these receptors. 115-117 Antagonists of these channels can also suppress the symptoms of AD by accelerating the recovery of the skin barrier. 115 …”

Section: Introductionmentioning

confidence: 99%

“…115-117 Antagonists of these channels can also suppress the symptoms of AD by accelerating the recovery of the skin barrier. 115 …”

Section: Introductionmentioning

confidence: 99%

Atopic dermatitis: allergic dermatitis or neuroimmune dermatitis?

Gaspar

Aidé²

2016

An. Bras. Dermatol.

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Advances in knowledge of neurocellulars relations have provided new directions in the understanding and treatment of numerous conditions, including atopic dermatitis. It is known that emotional, physical, chemical or biological stimuli can generate more accentuated responses in atopic patients than in non-atopic individuals; however, the complex network of control covered by these influences, especially by neuropeptides and neurotrophins, and their genetic relations, still keep secrets to be revealed. Itching and airway hyperresponsiveness, the main aspects of atopy, are associated with disruption of the neurosensory network activity. Increased epidermal innervation and production of neurotrophins, neuropeptides, cytokines and proteases, in addition to their relations with the sensory receptors in an epidermis with poor lipid mantle, are the aspects currently covered for understanding atopic dermatitis.

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TRPV1 antagonist can suppress the atopic dermatitis-like symptoms by accelerating skin barrier recovery

Cited by 55 publications

References 49 publications

Defective channels lead to an impaired skin barrier

Defective channels lead to an impaired skin barrier

HTR7 Mediates Serotonergic Acute and Chronic Itch

Atopic dermatitis: allergic dermatitis or neuroimmune dermatitis?

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