Chronic inhibition of endoplasmic reticulum calcium-release channels and calcium-ATPase lengthens the period of hepatic clock gene <it>Per1</it>
<p>Abstract</p> <p>Background</p> <p>The role played by calcium as a regulator of circadian rhythms is not well understood. The effect of the pharmacological inhibition of the ryanodine receptor (RyR), inositol 1,4,5-trisphosphate receptor (IP<sub>3</sub>R),...
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Ubiquity Press
2011-07-01
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Series: | Journal of Circadian Rhythms |
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Online Access: | http://www.jcircadianrhythms.com/content/9/1/6 |
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author | Díaz-Muñoz Mauricio Báez-Ruiz Adrián |
author_facet | Díaz-Muñoz Mauricio Báez-Ruiz Adrián |
author_sort | Díaz-Muñoz Mauricio |
collection | DOAJ |
description | <p>Abstract</p> <p>Background</p> <p>The role played by calcium as a regulator of circadian rhythms is not well understood. The effect of the pharmacological inhibition of the ryanodine receptor (RyR), inositol 1,4,5-trisphosphate receptor (IP<sub>3</sub>R), and endoplasmic-reticulum Ca<sup>2+</sup>-ATPase (SERCA), as well as the intracellular Ca<sup>2+</sup>-chelator BAPTA-AM was explored on the 24-h rhythmicity of the liver-clock protein PER1 in an experimental model of circadian synchronization by light and restricted-feeding schedules.</p> <p>Methods</p> <p>Liver explants from <it>Period1-luciferase </it>(<it>Per1-luc</it>) transgenic rats with either free food access or with a restricted meal schedule were treated for several days with drugs to inhibit the activity of IP<sub>3</sub>Rs (2-APB), RyRs (ryanodine), or SERCA (thapsigargin) as well as to suppress intracellular calcium fluctuations (BAPTA-AM). The period of <it>Per1-luc </it>expression was measured during and after drug administration.</p> <p>Results</p> <p>Liver explants from rats fed ad libitum showed a lengthened period in response to all the drugs tested. The pharmacological treatments of the explants from meal-entrained rats induced the same pattern, with the exception of the ryanodine treatment which, unexpectedly, did not modify the <it>Per1-luc </it>period. All effects associated with drug application were reversed after washout, indicating that none of the pharmacological treatments was toxic to the liver cultures.</p> <p>Conclusions</p> <p>Our data suggest that Ca<sup>2+ </sup>mobilized from internal deposits modulates the molecular circadian clock in the liver of rats entrained by light and by restricted meal access.</p> |
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spelling | doaj.art-933b5c9d62bf4bd99e9c2830f6ef4ac72022-12-22T03:11:00ZengUbiquity PressJournal of Circadian Rhythms1740-33912011-07-0191610.1186/1740-3391-9-6Chronic inhibition of endoplasmic reticulum calcium-release channels and calcium-ATPase lengthens the period of hepatic clock gene <it>Per1</it>Díaz-Muñoz MauricioBáez-Ruiz Adrián<p>Abstract</p> <p>Background</p> <p>The role played by calcium as a regulator of circadian rhythms is not well understood. The effect of the pharmacological inhibition of the ryanodine receptor (RyR), inositol 1,4,5-trisphosphate receptor (IP<sub>3</sub>R), and endoplasmic-reticulum Ca<sup>2+</sup>-ATPase (SERCA), as well as the intracellular Ca<sup>2+</sup>-chelator BAPTA-AM was explored on the 24-h rhythmicity of the liver-clock protein PER1 in an experimental model of circadian synchronization by light and restricted-feeding schedules.</p> <p>Methods</p> <p>Liver explants from <it>Period1-luciferase </it>(<it>Per1-luc</it>) transgenic rats with either free food access or with a restricted meal schedule were treated for several days with drugs to inhibit the activity of IP<sub>3</sub>Rs (2-APB), RyRs (ryanodine), or SERCA (thapsigargin) as well as to suppress intracellular calcium fluctuations (BAPTA-AM). The period of <it>Per1-luc </it>expression was measured during and after drug administration.</p> <p>Results</p> <p>Liver explants from rats fed ad libitum showed a lengthened period in response to all the drugs tested. The pharmacological treatments of the explants from meal-entrained rats induced the same pattern, with the exception of the ryanodine treatment which, unexpectedly, did not modify the <it>Per1-luc </it>period. All effects associated with drug application were reversed after washout, indicating that none of the pharmacological treatments was toxic to the liver cultures.</p> <p>Conclusions</p> <p>Our data suggest that Ca<sup>2+ </sup>mobilized from internal deposits modulates the molecular circadian clock in the liver of rats entrained by light and by restricted meal access.</p>http://www.jcircadianrhythms.com/content/9/1/6Food-entrainable oscillatorliver explantsclock proteinsintracellular calciumSERCAIP<sub>3</sub>RRyR. |
spellingShingle | Díaz-Muñoz Mauricio Báez-Ruiz Adrián Chronic inhibition of endoplasmic reticulum calcium-release channels and calcium-ATPase lengthens the period of hepatic clock gene <it>Per1</it> Journal of Circadian Rhythms Food-entrainable oscillator liver explants clock proteins intracellular calcium SERCA IP<sub>3</sub>R RyR. |
title | Chronic inhibition of endoplasmic reticulum calcium-release channels and calcium-ATPase lengthens the period of hepatic clock gene <it>Per1</it> |
title_full | Chronic inhibition of endoplasmic reticulum calcium-release channels and calcium-ATPase lengthens the period of hepatic clock gene <it>Per1</it> |
title_fullStr | Chronic inhibition of endoplasmic reticulum calcium-release channels and calcium-ATPase lengthens the period of hepatic clock gene <it>Per1</it> |
title_full_unstemmed | Chronic inhibition of endoplasmic reticulum calcium-release channels and calcium-ATPase lengthens the period of hepatic clock gene <it>Per1</it> |
title_short | Chronic inhibition of endoplasmic reticulum calcium-release channels and calcium-ATPase lengthens the period of hepatic clock gene <it>Per1</it> |
title_sort | chronic inhibition of endoplasmic reticulum calcium release channels and calcium atpase lengthens the period of hepatic clock gene it per1 it |
topic | Food-entrainable oscillator liver explants clock proteins intracellular calcium SERCA IP<sub>3</sub>R RyR. |
url | http://www.jcircadianrhythms.com/content/9/1/6 |
work_keys_str_mv | AT diazmunozmauricio chronicinhibitionofendoplasmicreticulumcalciumreleasechannelsandcalciumatpaselengthenstheperiodofhepaticclockgeneitper1it AT baezruizadrian chronicinhibitionofendoplasmicreticulumcalciumreleasechannelsandcalciumatpaselengthenstheperiodofhepaticclockgeneitper1it |