Effect of heat stress and Hsp90 inhibition on T-type calcium currents and voltage-dependent potassium currents in leydig cells.
J Therm Biol
; 84: 1-7, 2019 Aug.
Article
em En
| MEDLINE
| ID: mdl-31466741
Heat can trigger testicular damage and impair fertility. Leydig cells produce testosterone in response to stimulation by luteinizing hormone (LH), which induces Ca2+ entry and K+ efflux through ion channels in their plasma membrane. Considering that mechanisms coordinating the Leydig cell responses to hyperthermic stress remain unclear; the present study analyzed the effects of heat stress (HS, 43°C, 15 min) and inhibition of Hsp90 on T-type calcium currents and voltage-dependent potassium currents (VKC) in mice Leydig cells. Results show that HS reduced the VKC steady state currents at +80 mV (45.3%) and maximum conductance (71.5%), as well as increased the activation time constant (31.7%) and the voltage for which half the channels are open (30%). Hsp90 inhibition did not change the VKC currents. T-type calcium currents were not affected by HS or Hsp90 inhibition. In conclusion, HS can slow the activation, reduce the currents and voltage dependence of the VKC, suggesting a possible role of these currents in the response to hyperthermic stress in Leydig cells.
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Base de dados:
MEDLINE
Assunto principal:
Proteínas de Choque Térmico HSP90
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Resposta ao Choque Térmico
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Canais de Cálcio Tipo T
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Canais de Potássio de Abertura Dependente da Tensão da Membrana
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Células Intersticiais do Testículo
Limite:
Animals
Idioma:
En
Ano de publicação:
2019
Tipo de documento:
Article