ABSTRACTS – ORAL PRESENTATIONS - AMCA, spol. s r.o.

References
De Ruijter, A.J.M., van Gennip, A.H., Caron, H.N., Kemp, S., and van Kuilenburg,
A.B.: Histone deacetylases (HDACs): characterization of the classical HDAC family. –
Biochemical Journal 370(Pt 3): 737-749, 2003.
Dougherty, T.J., Gomer, C.J., Henderson, B.W., Jori, G., Kessel, D., Korbelik, M., Moan, J.,
and Peng, Q.: Photodynamic therapy – Journal of the National Cancer Institute 90(12):
889-905, 1998.
Glaser, K.B.: HDAC inhibitors: clinical update and mechanism-based potential. –
Biochemical Pharmacology 74(5): 659-671, 2007.
P13. MYELOPEROXIDASE DEFICIENCY ATTENUATES THE CELL DEATH OF NEUTROPHILS
INDUCED BY OXIDATIVE BURST
Silvie Kremserová 1,2 , Karel Souček 1,3 , Anna Klinke 4 , Hana Kolářová 1,3 , Stephan Baldus 4 ,
Jason P. Eiserich 5 , Lukáš Kubala 1,3
1
Institute of Biophysics, Academy of Sciences of the Czech Republic;
kremserova.s@gmail.com
2
Department of Animal Physiology, Faculty of Science, Masaryk University, Czech
Republic;
3
International Clinical Research Center - Center of Biomolecular and Cellular
Engineering, St. Anne‘s University Hospital Brno, Brno, Czech Republic;
4
Department of Internal Medicine, School of Medicine, University of California, Davis, CA;
5
Heart Center, University of Cologne, Cologne, Germany
Neutrophils play a critical role in host defense. On the other hand, neutrophils
accumulated at the site of inflammation contribute to tissue injury associated with acute
and chronic inflammatory disease. Thus, a neutrophil clearance by apoptosis is a key
mechanism for the inflammation resolution. (Klebanoff, 2005, Borregaard and Cowland,
1997).
Myeloperoxidase (MPO) is the most abundant enzyme in granules of neutrophils that
is release upon their activation during degranulation process. Interestingly, in mouse
models of acute and chronic inflammation, MPO deficiency is connected with a more
severe course of the inflammatory process (Tsurubuchi et al., 2001). This can be due to
reduced clearance of MPO-deficient neutrophils from the site of inflammation. Thus, the
involvement of MPO in neutrophil cell death was studied.
Neutrophils isolated from MPO-deficient mice exhibited a significantly lower rate of cell
death compared to neutrophils isolated from wild type mice in response to the stimulation
of oxidative burst by the activators phorbol-12-myristate-13-acetate and ionomycin.
Interestingly, the spontaneous cell death rate was similar for neutrophils isolated from
MPO-deficient and wild type mice. The cell death induced by the employed activators
was connected with a massive increase in the surface expression of phosphatidylserine
detected by Annexin V, which was significantly reduced in neutrophils isolated from
MPO-deficient mice. Interestingly, the activation of caspase 3 was not detected in these
Analytical Cytometry VII 103