Modulation of semaphorin 3A expression by calcium concentration and histamine in human keratinocytes and fibroblasts

Fukamachi, Shoko; Bito, Toshinori; Shiraishi, Noriko; Miwa, Koichi; Kabashima, Kenji; Nakamura, Motonobu; Tokura, Y.

doi:10.1016/j.jdermsci.2010.11.012

Cited by 27 publications

(22 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…32) Several recent studies showed that Sema3A transcripts were expressed in cultured normal human epidermal keratinocytes. 33,34) Sema3A proteins are mainly distributed in the suprabasal layer of normal human skin, 33) consistent with findings showing that Sema3A is expressed in differentiated keratinocyte cultures. 34) Moreover, epidermal Sema3A levels were lower in patients with atopic dermatitis than in healthy controls, while an increase in epidermal nerve density was found in the skin.…”

Section: Nerve Repulsion Factorssupporting

confidence: 80%

“…33,34) Sema3A proteins are mainly distributed in the suprabasal layer of normal human skin, 33) consistent with findings showing that Sema3A is expressed in differentiated keratinocyte cultures. 34) Moreover, epidermal Sema3A levels were lower in patients with atopic dermatitis than in healthy controls, while an increase in epidermal nerve density was found in the skin. 33) Increased epidermal nerve density in acute dry skin mice was also associated with decreased levels of Sema3A expression, 35,36) suggesting that decreasing the expression of Sema3A accelerates epidermal nerve growth in patients with dry skin condition such as atopic dermatitis and xerosis.…”

Section: Nerve Repulsion Factorssupporting

confidence: 80%

See 1 more Smart Citation

An Update on Peripheral Mechanisms and Treatments of Itch

Tominaga

Takamori

2013

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

Histamine H 1 -receptor blockers are used to treat all types of itch resulting from serious skin diseases such as atopic dermatitis, as well as from renal and liver diseases. However, they often lack efficacy in chronic itch, a profound clinical problem that decreases quality of life. The development of effective treatments requires a full understanding of the fundamental mechanisms of itch. Recent studies have indicated that the pathogenic mechanisms of itch also involve agonists other than histamine, including proteases, neuropeptides, cytokines, and opioids, as well as their cognate receptors. Release of these pruritogenic mediators and modulators into the periphery may directly activate itch-mediating C-fibers via specific receptors on the nerve terminals. Histological observations have shown increased epidermal nerve densities in patients with atopic dermatitis, suggesting that the higher density is at least partly responsible for itch sensitization. This

show abstract

Section: Nerve Repulsion Factorssupporting

confidence: 80%

Section: Nerve Repulsion Factorssupporting

confidence: 80%

An Update on Peripheral Mechanisms and Treatments of Itch

Tominaga

Takamori

2013

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

show abstract

“…Histamine increases and decreases the expression of semaphorin 3A and nerve growth factor, respectively, in cultured keratinocytes, which may result in the suppression of nerve fiber elongation in the epidermis (Fukamachi et al, 2011). In addition, histamine increases the proinflammatory cytokines interleukin-6 and interleukin-8 in HaCaT cells, a human skin keratinocyte cell line (Kohda et al, 2002).…”

Section: Surfactant Itch and Keratinocyte Histaminementioning

confidence: 99%

Topical Surfactant-Induced Pruritus: Involvement of Histamine Released from Epidermal Keratinocytes

Inami

Andoh

Sasaki

et al. 2012

J Pharmacol Exp Ther

View full text Add to dashboard Cite

Surfactants, an important component of cleansers, often cause itch in humans. Topical application of sodium laurate and Nlauroylsarcosine sodium salt to the skin of mice immediately (for 1-1.5 hours) increased scratching, and the former increased scratching again between 2 and 3 hours after application. Thus, we examined the mechanisms of sodium laurate-induced delayed scratching. Sodium laurate (0.1%-10%) increased delayed scratching and skin surface pH in a concentrationdependent manner. N-lauroylsarcosine sodium salt had no effect on these parameters, and sodium hydroxide solution did not increase delayed scratching. Sodium laurate-induced delayed scratching was markedly inhibited by the H 1 histamine receptor antagonist terfenadine, but it was not affected by mast cell deficiency. Sodium laurate application had no effect on the number of total and degranulated mast cells, and did not induce plasma extravasation or the infiltration of inflammatory cells in the skin. Sodium laurate application increased the histamine content of the epidermis, but not that of the dermis, in normal and mast cell-deficient mice. Sodium laurate application increased the ratio of 53-kDa L-histidine decarboxylase (HDC, a key enzyme for histamine production) to 74-kDa HDC in the mouse epidermis and in a human keratinocyte culture. Sodium laurate increased histamine in the human keratinocyte culture, without affecting cell viability. The present results suggest that sodium laurate induced delayed scratching at an alkaline pH through the increased production of histamine in keratinocytes, which may be due to enhanced processing of 74-kDa to 53-kDa HDC.

show abstract

“…NGF is produced not only by epidermal keratinocytes but by mast cells, eosinophils, and fibroblasts in inflamed skin (Ikoma et al, 2006;Leon et al, 1994). Several semaphorins are also produced by fibroblasts and immune cells (Suzuki et al, 2008;Fukamachi et al, 2011). UV radiation has been shown to affect dermal fibroblasts, dermal dendritic cells, endothelial cells, and skin-infiltrating inflammatory cells, such as T lymphocytes and mast cells (Krutmann and Morita, 1999).…”

Section: Uv-based Therapy Of Ad Pruritus Involving Epidermal Hyperinnmentioning

confidence: 99%