Effect of heat stress and Hsp90 inhibition on T-type calcium currents and voltage-dependent potassium currents in leydig cells

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...

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Veröffentlicht in:Journal of thermal biology 2019-08, Vol.84, p.1-7
Hauptverfasser: Tenorio, Bruno Mendes, Pereira da Silva, Reginaldo, Tenorio, Fernanda das Chagas Angelo Mendes, Costa Rosales, Roberta Ribeiro, Amaro da Silva Junior, Valdemiro, de Albuquerque Nogueira, Romildo
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container_title Journal of thermal biology
container_volume 84
creator Tenorio, Bruno Mendes
Pereira da Silva, Reginaldo
Tenorio, Fernanda das Chagas Angelo Mendes
Costa Rosales, Roberta Ribeiro
Amaro da Silva Junior, Valdemiro
de Albuquerque Nogueira, Romildo
description 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. [Display omitted] •Effect of heat stress and Hsp90 inhibition on K+ and Ca2+ currents in Leydig cells.•Heat stress reduced voltage-dependent K+ currents.•T-type Ca2+ currents did not change after heat stress.•Hsp90 inhibition did not change the K+ and Ca2+ currents.
doi_str_mv 10.1016/j.jtherbio.2019.05.022
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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. [Display omitted] •Effect of heat stress and Hsp90 inhibition on K+ and Ca2+ currents in Leydig cells.•Heat stress reduced voltage-dependent K+ currents.•T-type Ca2+ currents did not change after heat stress.•Hsp90 inhibition did not change the K+ and Ca2+ currents.</description><identifier>ISSN: 0306-4565</identifier><identifier>EISSN: 1879-0992</identifier><identifier>DOI: 10.1016/j.jtherbio.2019.05.022</identifier><identifier>PMID: 31466741</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Animals ; Benzoquinones - pharmacology ; Calcium channels (T-type) ; Calcium channels (voltage-gated) ; Calcium Channels, T-Type - physiology ; Calcium currents ; Calcium efflux ; Calcium influx ; Conductance ; Fertility ; Heat stress ; Heat-Shock Response - physiology ; High temperature ; Hot Temperature ; Hsp90 ; HSP90 Heat-Shock Proteins - antagonists &amp; inhibitors ; HSP90 Heat-Shock Proteins - physiology ; Hsp90 protein ; Ion channels ; Lactams, Macrocyclic - pharmacology ; Leydig cells ; Leydig Cells - drug effects ; Leydig Cells - physiology ; Luteinizing hormone ; Male ; Menopause ; Mice ; Potassium ; Potassium channels (voltage-gated) ; Potassium Channels, Voltage-Gated - physiology ; Potassium currents ; Testosterone</subject><ispartof>Journal of thermal biology, 2019-08, Vol.84, p.1-7</ispartof><rights>2019 Elsevier Ltd</rights><rights>Copyright © 2019 Elsevier Ltd. 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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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inhibitors</topic><topic>HSP90 Heat-Shock Proteins - physiology</topic><topic>Hsp90 protein</topic><topic>Ion channels</topic><topic>Lactams, Macrocyclic - pharmacology</topic><topic>Leydig cells</topic><topic>Leydig Cells - drug effects</topic><topic>Leydig Cells - physiology</topic><topic>Luteinizing hormone</topic><topic>Male</topic><topic>Menopause</topic><topic>Mice</topic><topic>Potassium</topic><topic>Potassium channels (voltage-gated)</topic><topic>Potassium Channels, Voltage-Gated - physiology</topic><topic>Potassium currents</topic><topic>Testosterone</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tenorio, Bruno Mendes</creatorcontrib><creatorcontrib>Pereira da Silva, Reginaldo</creatorcontrib><creatorcontrib>Tenorio, Fernanda das Chagas Angelo Mendes</creatorcontrib><creatorcontrib>Costa Rosales, Roberta Ribeiro</creatorcontrib><creatorcontrib>Amaro da Silva Junior, Valdemiro</creatorcontrib><creatorcontrib>de Albuquerque Nogueira, Romildo</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Animal Behavior Abstracts</collection><collection>Calcium &amp; 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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. [Display omitted] •Effect of heat stress and Hsp90 inhibition on K+ and Ca2+ currents in Leydig cells.•Heat stress reduced voltage-dependent K+ currents.•T-type Ca2+ currents did not change after heat stress.•Hsp90 inhibition did not change the K+ and Ca2+ currents.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>31466741</pmid><doi>10.1016/j.jtherbio.2019.05.022</doi><tpages>7</tpages></addata></record>
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subjects Animals
Benzoquinones - pharmacology
Calcium channels (T-type)
Calcium channels (voltage-gated)
Calcium Channels, T-Type - physiology
Calcium currents
Calcium efflux
Calcium influx
Conductance
Fertility
Heat stress
Heat-Shock Response - physiology
High temperature
Hot Temperature
Hsp90
HSP90 Heat-Shock Proteins - antagonists & inhibitors
HSP90 Heat-Shock Proteins - physiology
Hsp90 protein
Ion channels
Lactams, Macrocyclic - pharmacology
Leydig cells
Leydig Cells - drug effects
Leydig Cells - physiology
Luteinizing hormone
Male
Menopause
Mice
Potassium
Potassium channels (voltage-gated)
Potassium Channels, Voltage-Gated - physiology
Potassium currents
Testosterone
title Effect of heat stress and Hsp90 inhibition on T-type calcium currents and voltage-dependent potassium currents in leydig cells
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