Perinatal Hypoxic and Ischemic Damage to the Central Nervous System Causes Changes in the Expression of Connexin 43 and CD38 and ADP-Ribosyl Cyclase Activity in Brain Cells

Салмина, А. Б.; Malinovskaya, N. A.; Окунева, О. С.; Taranushenko, T. E.; Fursov, A. A.; Mikhutkina, S. V.; Моргун, А. В.; Прокопенко, С. В.; Зыкова, Л. Д.

doi:10.1007/s10517-009-0385-6

Cited by 8 publications

(7 citation statements)

References 12 publications

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“…Interestingly, the NAD + glycohydrolase activity appeared to be much higher in nonsynaptic mitochondria compared with mitochondria isolated from synaptosomes (Masmoudi et al, 1988). Insofar as nonsynaptic mitochondria represent mitochondria from both neurons and nonneuronal brain cells (e.g., astrocytes, oligodendroglia and microglia), this finding is in agreement with the report that astrocytes and microglia are the main CD38‐expressing cells in brain (Salmina et al, 2008). Taken together, these data suggest that NAD + depletion can occur more rapidly in astrocytes following ischemic insult, compromising the ability of astrocytes to support neuronal functions.…”

Section: Cd38 Is a Major Nad+ Glycohydrolasesupporting

confidence: 92%

Mitochondrial dysfunction and nicotinamide dinucleotide catabolism as mechanisms of cell death and promising targets for neuroprotection

Kristián

Balan

Schuh

et al. 2011

J of Neuroscience Research

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Both acute and chronic neurodegenerative diseases are frequently associated with mitochondrial dysfunction as an essential component of mechanisms leading to brain damage. Although loss of mitochondrial functions resulting from prolonged activation of the mitochondrial permeability transition (MPT) pore has been shown to play a significant role in perturbation of cellular bioenergetics and in cell death, the detailed mechanisms are still elusive. Enzymatic reactions linked to glycolysis, the tricarboxylic acid cycle, and mitochondrial respiration are dependent on the reduced or oxidized form of nicotinamide dinucleotide [NAD(H)] as a cofactor. Loss of mitochondrial NAD(+) resulting from MPT pore opening, although transient, allows detrimental depletion of mitochondrial and cellular NAD(+) pools by activated NAD(+) glycohydrolases. Poly(ADP-ribose) polymerase (PARP) is considered to be a major NAD(+) degrading enzyme, particularly under conditions of extensive DNA damage. We propose that CD38, a main cellular NAD(+) level regulator, can significantly contribute to NAD(+) catabolism. We discuss NAD(+) catabolic and NAD(+) synthesis pathways and their role in different strategies to prevent cellular NAD(+) degradation in brain, particularly following an ischemic insult. These therapeutic approaches are based on utilizing endogenous intermediates of NAD(+) metabolism that feed into the NAD(+) salvage pathway and also inhibit CD38 activity.

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Section: Cd38 Is a Major Nad+ Glycohydrolasesupporting

confidence: 92%

Mitochondrial dysfunction and nicotinamide dinucleotide catabolism as mechanisms of cell death and promising targets for neuroprotection

Kristián

Balan

Schuh

et al. 2011

J of Neuroscience Research

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“…Известно, что коннексин 43 (Cx43) является белком каналов щелевых контактов, сопряженным с CD38 и играющим роль в нейрон-астроглиальных взаимодействиях (экспрессируется на астроцитах и функционально взаимодействует, согласно литературным данным, в мембранах ряда клеток с CD38, обеспечивая доступность НАД + в качестве субстрата для каталитической реакции CD38) [3,7]. /0%11(( CD38, *.=*1/0%11(( CD38 ( , 0*%0."…”

Section: рис 1 а -коэкспрессия Cd38 и маркеров вида клеток (Nse Thunclassified

Expression of Cd38 and Сх43 in the Midbrain Cells at Experimental Parkinson's Disease

Malinovskaya¹,

Салмина²,

Прокопенко³

et al. 2014

SMR

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ГБОУ ВПО Красноярский государственный медицинский университет имени проф. В. Ф. Войно-Ясенецкого Министерства здравоохранения РФ, ректор-д. м. н., проф. И. П. Артюхов; кафедра биохимии с курсами медицинской, фармацевтической и токсикологической химии, зав.-д. м. н., проф. А. Б. Салмина; НИИ молекулярной медицины и патобиохимии, руководитель-д. м. н.. проф. А. Б. Салмина. v%+< (11+%$."-(?. Выяснить роль потенциальных молекул-маркеров нейрон-астроглиальных взаимодействий (CD38, Cx43, лактат) в патогенезе болезни Паркинсона в эксперименте. l 2%0(+; (,%2.$;. На гомогенатах и срезах среднего мозга крыс с ротеноновой моделью болезни Паркинсона (БП) и в контроле проведена оценка содержания лактата спектрофометрическим методом, иммуногистохимическая оценка экспрессии CD38, коннексина 43 и маркеров вида клеток. p%'3+<2 2;. При болезни Паркинсона выявлено значимое увеличение концентрации лактата, усиление экспрессии CD38 на дофаминергических нейронах, астроцитах и микроглии и его коэкспрессии с Cx43. g *+>7%-(%. Обнаружена важная роль CD38, коннексина 43 и лактата как участников нейрон-астроглиальных взаимодействий при развитии БП.

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“…Астроциты, которые в условиях ишемии экспрессируют больше CD38, напротив, становятся более устойчивыми к действию повреждающих факторов. Эти события способны нарушить метаболическое сопряжение между нейронами и астроцитами за счет изменения интенсивности продукции лактата, регулируемого соотношением цитозольного НАД + и НАДН [20,[61][62][63].…”

Section: Cd38 в регуляции нейрон-астроглиальных взаимодействий при ишunclassified

Nad+-Converting Enzymes in Neuronal and Glial Cells: Cd38 as a Novel Target for Neuroprotection

et al. 2012

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The review contains current data on molecular mechanisms which control NAD+ homeostasis in brain cells. It also deals with the role of NAD+-converting enzymes in regulation of functional activity, viability and intercellular communication of neuronal and glial cells. Special attention is paid to involvement of CD38 into regulation of NAD+ levels in brain cells in normal and pathological conditions.

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Perinatal Hypoxic and Ischemic Damage to the Central Nervous System Causes Changes in the Expression of Connexin 43 and CD38 and ADP-Ribosyl Cyclase Activity in Brain Cells

Cited by 8 publications

References 12 publications

Mitochondrial dysfunction and nicotinamide dinucleotide catabolism as mechanisms of cell death and promising targets for neuroprotection

Mitochondrial dysfunction and nicotinamide dinucleotide catabolism as mechanisms of cell death and promising targets for neuroprotection

Expression of Cd38 and Сх43 in the Midbrain Cells at Experimental Parkinson's Disease

Nad+-Converting Enzymes in Neuronal and Glial Cells: Cd38 as a Novel Target for Neuroprotection

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