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Arandarcikaite 2017 Abstract MITOEAGLE Barcelona

From Bioblast

Age-related responses of brain mitochondria to ischemic insult. Arandarcikaite_Presenation

Link: MitoEAGLE

Arandarcikaite O, Balion Z, Veniulyte E, Borutaite V (2017)

Event: MitoEAGLE Barcelona 2017


Stroke is one of most common diseases leading to disability or mortality with limited therapeutic options. The risk for stroke increases with aging. However, molecular mechanisms leading to increased neuronal death in aging brains are not well understood. Most of the research on ischemia-induced cellular perturbations are performed using young adult animals and there are just a few studies on mitochondrial functions and ischemia-induced mitochondrial permeability transition during the lifespan. It is also important to note that brain regions have a different composition of neurons and glial cells, and this may cause different sensitivity to ischemia-induced damages. In this study, we performed a comparative analysis of respiratory functions and calcium retention capacity of mitochondria isolated from cortex and cerebellum of rats (normal and exposed to simulated in vitro ischemia) at various ages: neonatal (7 dyas), young adults (2-3 months), mature adults (7-10 months), and aged (24 months). We found that ischemia caused persistent inhibition of respiration of mitochondria isolated from cortex (characterized as glial-rich region) at all ages of animals. However, calcium retention capacity (a measure of mitochondrial permeability transition) of cortical mitochondria was decreased after ischemia only in young and mature adults and aging rats, whereas neonatal mitochondrial calcium retention capacity was not affected by ischemia. Ischemia induced inhibition of cerebellar mitochondrial respiration at the age of 7 days, 2-3 and 24 months, whereas calcium retention capacity after ischemia decreased only in mitochondria from cerebellum of mature adults and aging rats. These data revealed age-dependent differences in mitochondrial respiratory functions and permeability transition induced by total brain ischaemia in two brain regions – cortex and cerebellum.

β€’ Bioblast editor: Kandolf G β€’ O2k-Network Lab: LT Kaunas Borutaite V

Labels: MiParea: Respiration  Pathology: Aging;senescence  Stress:Ischemia-reperfusion, Permeability transition  Organism: Rat  Tissue;cell: Nervous system  Preparation: Isolated mitochondria 

HRR: Oxygraph-2k  Event: B2 


Lithuanian Univ Health Sc, Neuroscience Inst, Kaunas, Lithuania