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XXII. BIOCHEMICKÝ ZJAZD - Jesseniova lekárska fakulta

XXII. BIOCHEMICKÝ ZJAZD - Jesseniova lekárska fakulta

XXII. BIOCHEMICKÝ ZJAZD - Jesseniova lekárska fakulta

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Lectures<br />

Apoptosis – DOUBLE EDGED SWORD<br />

Peter Račay 1 , Jozef Hatok 1 , Mária Chomová 1 , Jana Jurečeková 1 , Peter Chudý 2 ,<br />

Juraj Chudej 2 , Andrea Štefániková 1 and Dušan Dobrota 1<br />

1<br />

Department of Medical Biochemistry,<br />

2<br />

Clinic of Haematology and Transfusiology, JLF UK Martin<br />

Apoptosis is an evolutionarily conserved process that is crucial for development and homeostasis<br />

of tissues of multicellular organisms. Its deregulation can elicit inappropriate<br />

cell death associated with different diseases (e. g. neurodegenerative diseases, diabetes,<br />

etc.) or is associated with survival of undifferentiated or transformed cells and can lead<br />

to development of cancer.<br />

Here we present results documenting initiation of apoptosis after global brain ischemia as<br />

well as dysfunction of apoptosis execution associated with acute myeloblastic leukaemia.<br />

We have documented that global brain ischemia induces transcription independent p53-<br />

mediated mitochondrial apoptosis. Execution of apoptosis was associated with genomic<br />

DNA fragmentation and death of pyramidal neurones in CA1 layer of rat hippocampus.<br />

On the other hand, RT-PCR analysis documented significant increase of mRNA level of<br />

apoptotic protein Bax in leukaemic cells in comparison to normal leukocytes, indicating<br />

transcription dependent initiation of p53-mediated apoptosis. Despite apoptosis initiation,<br />

survival of leukaemic cells is probably associated with inhibition of apoptosis execution<br />

mediated by increased transcription of both bcl-X and bcl-2 genes.<br />

Our results showed that detailed study of mechanism of apoptosis might by useful in<br />

search for new effective treatment of diseases associated with either cell death or cell<br />

survival due to deregulation of apoptosis.<br />

Acknowledgement: This work was supported by grant VVCE 0064-07<br />

<strong>XXII</strong>. Biochemistry Congress, Martin<br />

91

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