Vulnerability to glucose deprivation injury correlates with glutathione levels in astrocytes

Papadopoulos, Marios C.; Koumenis, Iphigenia L.; Dugan, Laura L.; Giffard, Rona G.

doi:10.1016/s0006-8993(96)01293-0

Cited by 94 publications

(49 citation statements)

References 33 publications

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“…This increase can be caused by compromised production of NADPH and pyruvate (Spitz et al, 2000), cellular compounds with antioxidant properties, and reduced intracellular glutathione levels (Papadopoulos et al, 1997). In our experiments, overexpression of Hsp75 protected astrocytes against GD-induced ROS accumulation.…”

Section: Discussionsupporting

confidence: 47%

“…Many studies have shown that GD promotes a rapid increase of intracellular ROS (Blackburn et al, 1999;Ouyang et al, 2002;Papadopoulos et al, 1997). This increase can be caused by compromised production of NADPH and pyruvate (Spitz et al, 2000), cellular compounds with antioxidant properties, and reduced intracellular glutathione levels (Papadopoulos et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

“…We previously showed that GD induced increased levels of oxidative stress in primary astrocyte cultures (Ouyang et al, 2006;Papadopoulos et al, 1997). Intracellular ROS levels were evaluated using the ROS-sensitive fluorescent dye HEt (Figure 2).…”

Section: Protection From Glucose Deprivationmentioning

confidence: 99%

See 2 more Smart Citations

Overexpression of Mitochondrial Hsp70/Hsp75 Protects Astrocytes against Ischemic Injury in vitro

Voloboueva

Duan

Ouyang

et al. 2007

J Cereb Blood Flow Metab

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109

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Mitochondrial heat shock protein 70 (mtHsp70/Hsp75/Grp75/mortalin/TRAP-1/PBP74) is an essential mitochondrial chaperone and a member of the heat shock protein 70 (HSP70) family. Although many studies have shown the protective properties of overexpression of the cytosolic inducible member of the HSP70 family, Hsp72, few studies have investigated the protective potential of Hsp75 against ischemic injury. Mitochondria are one of the primary targets of ischemic injury in astrocytes. In this study, we analyzed the effects of Hsp75 overexpression on cellular levels of reactive oxygen species (ROS), mitochondrial membrane potential, ATP levels, and viability during the ischemia-like conditions of oxygen-glucose deprivation (OGD) or glucose deprivation (GD) in primary astrocytic cultures. We show that Hsp75 overexpression decreases ROS production and preserves mitochondrial membrane potential during GD, and preserves ATP levels and cell viability during OGD. These findings indicate that Hsp75 can provide protection against ischemia-like in vitro injury and suggest that it should be further studied as a potential candidate for protection against ischemic injury.

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Section: Discussionsupporting

confidence: 47%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Overexpression of Mitochondrial Hsp70/Hsp75 Protects Astrocytes against Ischemic Injury in vitro

Voloboueva

Duan

Ouyang

et al. 2007

J Cereb Blood Flow Metab

Self Cite

109

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show abstract

“…Hep G2 injury was quantitated by measuring LDH released from lysed cells into the bathing medium, utilizing a commercial available kit (Papadopoulos et al, 1997;Koh and Choi, 1987). LDH release from cells was measured by determining LDH activity in the media and total cells.…”

Section: Assessment Of Cell Injurymentioning

confidence: 99%

Effects of tetrabrominated diphenyl ether and hexabromocyclododecanes in single and complex exposure to hepatoma HepG2 cells

2009

Environmental Toxicology and Pharmacology

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“…However, continued exposure to stressors and a prolonged stress response can have maladaptive consequences (Selye, 1956). Specifically, elevated levels of GCs during chronic stress may lead to an increase in the generation of reactive oxygen species (ROS) that can directly induce mitochondrial dysfunction, disruption of energy pathways (Papadopoulos et al, 1997), damage to neuronal precursors, and impairments in neurogenesis (Kroemer, 1997), thus inducing signaling events that result in apoptotic cell death (Cregan et al, 2002). Previous studies have shown that mitochondria and mitochondria-generated ROS contribute to the apoptotic process, whereby p53-mediated apoptotic signaling still remains an important target Dhar et al, 2006).…”

Section: Chronic Isolation Stress Predisposes Thementioning

confidence: 99%

Molecular mechanisms of regulation of antioxidant enzymes in the brain and liver of acutely and/or chronically stressed rats

Zlatković¹

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Najveću zahvalnost dugujem upravo mom mentoru, dr Dragani Filipović, koja me je uvela u metode naučnog rada i tokom godina usmeravala u profesionalnom razvoju. Hvala na prenetom znanju, stručnom vođenju, kao i na svim sugestijama i smernicama koje su me formirale kao istraživača.Veliko hvala za svo utrošeno vreme, savete i konstruktivne kritike koje su dovele do krajnjeg oblikovanja ove teze. Dr Nadeždi Nedeljković se zahvaljujem na ukazanom poverenju i korisnim savetima tokom doktorskih studija.Dr Siniši Đuraševiću se zahvaljujem na savetima i pomoći oko interpretacije pojedinih rezultata. Dr Snežani Pajović veliko hvala na omogućenim uslovima za eksperimentalni rad.Neizmerno hvala porodici i prijateljima, na svemu kroz šta su prošli zajedno sa mnom, na ljubavi i smehu, čineći da sve, pa i ova disertacija, dobije sasvim novu dimenziju. . REZIME Molekularni mehanizmi regulacije antioksidativnih enzima u mozgu i jetri akutno i/ili hronično stresiranih pacovaAktivacija hipolamo-hipofizo-adrenalne (HHA) ose predstavlja jedan od odgovora organizma na izlaganje stresnim uslovima. Dok aktivacija HHA ose uzrokovana kratkotrajnim stresorima ima adaptivni karakter, hroničan stres može dovesti do brojnih patoloških promena među kojima su i poremećaji raspoloženja. Uzrok deregulacije HHA ose u stresnim uslovima još uvek nije u potpunosti utvrđen, a smatra se da može biti povezan sa i pojavom oksidativnog stresa. Stoga je ispitana i okarakterisana aktivnost HHA ose, merenjem koncentracije kortikosterona (CORT) kao markera stresnog odgovora, kao i mehanizmi regulacije antioksidativnih enzima CuZnSOD iMnSOD, kao biomarkera oksidativnog stresa, u uslovima akutnog, hroničnog i kombinovanog stresa u hipokampusu i prečeonoj kori mozga i jetri mužjaka pacova Wistar soja. Cilj ove teze je bio bolje razumevanje biohemijskih i molekularnih mehanizama delovanja antioksidativnih enzima u moždanim strukturama i jetri pacova nakon izlaganja 21-dnevnoj socijalnoj izolaciji, koja predstavlja jedan od životinjskih modela depresije. Akutno izlaganje imobilizaciji ili niskoj temperaturi u trajanju od 2 sata korišćeno je kao pokazatelj "normalnog" odgovora na stres, dok je kombinacija hroničnog i akutnog stresa služila kao potvrda maladaptivnog efekta hroničnog stresa.Rezultati istraživanja su pokazali povećanu koncentraciju CORT-a u serumu životinja izloženih akutnim stresorima, dok su kod životinja izlaganih hroničnoj socijalnoj izolaciji vrednosti ostale nepromenjene. Međutim, značajno niža koncentracija CORT-a između životinja koje su izlagane kombinovanom i odgovarajućem akutnom stresu ukazala je na poremećaj u regulaciji HHA ose koji je izazvana hroničnom socijalnom izolacijom, a što je rezultovalo u neadekvatnm odgovoru na nove stresne situacije.Akutni stres imobilizacije doveo je do povećanja ekspresije MnSOD proteina u mitohondrijama obe moždane strukture, dok je kod životinja akutno izlaganih niskoj temperaturi ili hroničnom stresu izolacije nivo ovog proteina ostao nepromenjen. Međutim, aktivnostiCuZnSOD i MnSOD-a u prečeonoj kori n...

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Vulnerability to glucose deprivation injury correlates with glutathione levels in astrocytes

Cited by 94 publications

References 33 publications

Overexpression of Mitochondrial Hsp70/Hsp75 Protects Astrocytes against Ischemic Injury in vitro

Overexpression of Mitochondrial Hsp70/Hsp75 Protects Astrocytes against Ischemic Injury in vitro

Effects of tetrabrominated diphenyl ether and hexabromocyclododecanes in single and complex exposure to hepatoma HepG2 cells

Molecular mechanisms of regulation of antioxidant enzymes in the brain and liver of acutely and/or chronically stressed rats

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