@misc{,
 copyright={Creative Commons Attribution BY 4.0 license},
 howpublished={online},
 abstract={Exitence of brain areas less sensitive to ischemia (such as CA2-4, DG region of hippocampus) offers hope for development of an ischemia effects treatment based on enhancement of endogenous adaptive response nervous cells. The variety of proteins, including protein kinases C (PKC) translocate to mitochondria following ischemia-reperfusion (I/R), which may lead to cell death or its survival. The aim of the study was to verify PKCbeta engagement in endogenous neuroprotection in CA2-4, DG region of hippocampus after I/R and to discover its mechanisms in mitochondria. Two experimental models were used: an in vivo-5-min. ischemia of gerbil brain and an in w=vitro-exitotoxicity evoked in organotypic hippocampal slice culture. Presented results show that immunoractivity and activity of PKCbeta increased in mitochondria of CA2-4, DG following I/R. A specific, peptide-inhibitor of PKCbetaII decreased postischemic translocation of the kinase to mitochondria and enhanced injury of neurons caused by I/R or excitotoxicityin the experimental models. What is more, PKCbeta II located inmitochondrial matrix after I/R.Due to this fact it was studied that PKCbeta II may interact with mitochondrial proteins (such as ATPase, pyruvate dehydrogenase, glutaminase0. Preliminary metabolomics results suggested changes in energy metabolism, mainly pyruvate alternations in CA2-4, DG region in which PKCbeta II may be engaged. Presented research indicates thatPKCbeta II translocation to mitochondria is an element of endogenous neuroprotection in the region of hippocampus less prone to I/R ( CA2-4, DG). Further development of research regarding neuroprotective mechanism of PKCbetaII can reveal new molecular factors, which may become targets of pharmacological treatment imtendent for patients sufferin from braim ischemia.},
 type={Text},
 URL={http://www.rcin.org.pl/Content/72010/PDF/Praca%20doktorska%20OKRUPSKA.pdf},
 keywords={Protein kinase C, Brain ischemia, mitochondria, Endogenous neuroprotection, Hippocampus},
}