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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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Posters<br />

49.<br />

DIMETHYL-OXALYLGYCINE MODULATES GENE EXPRESION AND PROTEIN<br />

LEVELS OF THE SODIUM CALCIUM EXCHANGER IN HEK 293 CELL LINE<br />

Cagala M. 1 , Lencesova L. 1,2 , Hudecova S. 1 , Csaderova L. 2 , Sirova M. 1 ,<br />

Cholujova D. 3 , Kopacek J. 4 , Pastorekova S. 2,4 and Krizanova O. 1,3<br />

1<br />

IMPG, Center of Excellence for Cardiovascular Research, SAS, Vlarska 5,<br />

833 34 Bratislava, Slovak Republic 2 MMC, SAS, Vlarska 3-7, 831 01 Bratislava,<br />

Slovak Republic 3 IEO, SAS, Vlarska 7, 833 91, Bratislava, Slovak Republic 4 IV,<br />

Center of Excellence for Cardiovascular Research, SAS, Dubravska cesta 9,<br />

845 05 Bratislava, Slovak Republic<br />

Up to now a little is known about the effect of hypoxia on the NCX1 expression and<br />

function. Therefore we studied, how dimethyl-oxalylglycine (DMOG), an activator and<br />

stabilizator of the HIF-1α could affect expression of the NCX1 in HEK 293 cell line. We also<br />

tried to determine, whether this activation can result in the development of apoptosis in<br />

HEK 293 cells. We have found that DMOG treatment for 3 hours significantly increased<br />

gene expression and also protein levels of the NCX1. This increase was accompanied<br />

with the decrease in intracellular pH. Wash-out of DMOG did not result in decrease of<br />

NCX1 mRNA and protein to original, control levels, although pH returned to control<br />

values. In the promoter region of the NCX1 we did not find consensus sequence for<br />

HRE, but we have found consensus NF-kB sequence in this region of the NCX1. Using<br />

luciferase reporter assay we observed increase in NCX1 promoter activity after DMOG<br />

treatment, which suggests that NF-kB is involved in DMOG induced upregulation of<br />

the NCX1. Moreover, we also showed that this upregulation might be involved, at least<br />

partially, in the induction of the process of apoptosis. Nevertheless, further experiments<br />

are needed to clarify this issue.<br />

Ackowledgement: This work was supported by grants APVV 51-0397-07, VEGA 2/0082/10<br />

and TRANSMED.<br />

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

169

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