RESUMO
We investigated the involvement of substance P (SP) and the neurokinin-1 receptor (NK(1)R) in the development of radiation-induced hair loss in mice. A dose of 40 Gy of gamma irradiation induced hair loss from the 10th to at least the 60th day after irradiation. A specific NK(1)R antagonist, CP-99,994, significantly delayed radiation-induced hair loss and reduced its severity. Furthermore, gamma irradiation induced the expression of preprotachykinin-A, a precursor protein of SP, mRNA in irradiated murine skin on the 10th and 30th days after irradiation. These results indicated that gamma irradiation-induced hair loss was mediated by SP via NK(1)R.
Assuntos
Alopecia/metabolismo , Lesões Experimentais por Radiação/metabolismo , Receptores da Neurocinina-1/fisiologia , Substância P/fisiologia , Alopecia/tratamento farmacológico , Animais , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Antagonistas dos Receptores de Neurocinina-1 , Piperidinas/farmacologia , Piperidinas/uso terapêutico , Precursores de Proteínas/biossíntese , Precursores de Proteínas/efeitos da radiação , Lesões Experimentais por Radiação/tratamento farmacológico , Receptores da Neurocinina-1/efeitos da radiação , Substância P/efeitos da radiação , Taquicininas/biossíntese , Taquicininas/efeitos da radiaçãoRESUMO
Atopic dermatitis is a pruritic inflammatory skin disorder, involving immunological and non-immunological factors. Substance P seems to be involved in the pathogenesis of atopic dermatitis. Substance P-containing nerve fibers are increased in the lesional skin of patients with atopic dermatitis and a reduced weal and flare reaction to intradermal injection of substance P has been observed. We investigated the distribution of substance P receptors in the involved skin of patients before and after single or repetitive UVA irradiations. Our results indicate that substance P receptors of the NK-1 subtype are expressed on blood vessels and on epidermal keratinocytes of involved skin of patients with atopic dermatitis. UVA irradiations did not modify the epidermal distribution of substance P receptors but decreased their expression intensity on blood vessels. UVA irradiations seem to decrease skin inflammation through the modulation of NK-1 receptor expression on endothelial cells.