2008
DOI: 10.1134/s1990519x08030139
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The effect of oxidized glutathione and its pharmacological analogue glutoxim on intracellular Ca2+ concentration in macrophages Ca2+

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Cited by 17 publications
(12 citation statements)
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“…The results about suppression by compound CK0944666 of Ca 2+ entry induced by glutoxim and molixan in mac rophages agree with our data about participation of elements of cytoskeleton in regulation of Ca 2+ entry evoked by glutoxim or molixan [8] and also purinergic agonists ATP and UTP and inhibitors of endoplasmic Ca 2+ ATPases thapsigargin and cyclopiazonic acid in rat peritoneal macrophages [20]. The glutoxim or molixan evoked Ca 2+ entry into cell occurs by a store dependent mechanism [3]. Earlier [20] in the experi ments with the use of ATP, UTP, thapsigargin and cyclopiazonic acid we have shown that store depen dent Ca 2+ entry in rat peritoneal macrophages occurs according to a store dependent Ca 2+ entry model named "secretion like coupling," implying reversible translocation of the Ca 2+ store to the plasmalemma, including active participation of actin filaments [21].…”
Section: Resultssupporting
confidence: 87%
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“…The results about suppression by compound CK0944666 of Ca 2+ entry induced by glutoxim and molixan in mac rophages agree with our data about participation of elements of cytoskeleton in regulation of Ca 2+ entry evoked by glutoxim or molixan [8] and also purinergic agonists ATP and UTP and inhibitors of endoplasmic Ca 2+ ATPases thapsigargin and cyclopiazonic acid in rat peritoneal macrophages [20]. The glutoxim or molixan evoked Ca 2+ entry into cell occurs by a store dependent mechanism [3]. Earlier [20] in the experi ments with the use of ATP, UTP, thapsigargin and cyclopiazonic acid we have shown that store depen dent Ca 2+ entry in rat peritoneal macrophages occurs according to a store dependent Ca 2+ entry model named "secretion like coupling," implying reversible translocation of the Ca 2+ store to the plasmalemma, including active participation of actin filaments [21].…”
Section: Resultssupporting
confidence: 87%
“…Earlier we have shown for the first time that glu toxim and molixan increase the intracellular concen tration of Ca 2+ ([Ca 2+ ] i ), causing mobilization of Ca 2+ from thapsigargin sensitive Ca 2+ stores and subse quent Ca 2+ entry into rat peritoneal macrophages [2][3][4]. Using a wide range of agents affecting components of intracellular signaling systems in cells, we have shown for the first time that key players in a signal cas cade triggered by GSSG and glutoxim and leading to [Ca 2+ ] i increase in macrophages are tyrosine kinases and tyrosine phosphatases [3,5], phosphatidylinositol kinases [6], key enzymes of the phosphoinositide sig nal pathway -phospholipase C and protein kinase C [7].…”
Section: Introductionmentioning
confidence: 99%
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“…Earlier we found that GSSG and glutoxim increase intracellular Ca 2+ concentration, [Ca 2+ ] i , inducing Ca 2+ mobilization from thapsigargin sensitive Ca 2+ stores and subsequent Ca 2+ entry into the rat perito neal macrophages (Kruretskaya et al, 2007a;Kurilova et al, 2008). Later we demonstrated that the same effect on [Ca 2+ ] i is observed in macrophages treated with molixan (Krutetskaya et al, 2010).…”
mentioning
confidence: 58%
“…Так, установлено, что GSSG (фармакологический аналог -глутамил-цистеинил-глицин) в концентрациях, близких или превышающих те, что определяются вне клеток, про-демонстрировал способность оказывать рецептор-опосре-дованное Са 2+ -зависимое влияние на клеточные процессы при ряде заболеваний [17]. Обнаружено модулирующее влияние окисленного глутатиона на регуляцию функций цитокинов и воспалительные процессы [18].…”
Section: результаты и обсуждениеunclassified