Laboratory of Molecular Medical Biochemistry

Head: Paweł DOBRZYŃ

Staff: Anna Ochałek (PhD student), Paulina Stokłosa (PhD student), Tomasz Bednarski (PhD student)

Research profile:

Our research is focused on the cellular and molecular mechanisms of heart dysfunction. The research involves in vivo and in vitro studies of signaling pathways and transcription factors associated with cardiomyocyte apoptosis and pathogenesis of left ventricle hypertrophy. One of the main goals is to investigate the role of SCD1 and SCD4 genes and pro- inflammatory cytokine signaling cascades in hypertrophic cardiomyopathy.

Methods:

• cell culture
• gene expression
• fluorescence microscopy
• echocardiography
• chromatography (TLC, GC, HPLC)
• standard biochemical and immunocytochemical methods

Current research activities:

• functional interactions between SCD activity and devel- opment of myocardial hypertrophy
• role of pro-inflammatory cytokines (TNFα, IL-6, IL-8) in the regulation of cardiac function
• signal transduction and genetic abnormalities in obesity related heart dysfunction

Selected publications:

Dobrzyn P, Pyrkowska A, Jazurek M, Dobrzyn A: Increased availability of endogenous and dietary oleic acid contributes to the upregulation of cardiac fatty acid oxidation. Mitochondrion 2012; 12: 132-137.

Dobrzyn P, Dobrzyn A, Miyazaki M, Ntambi JM: Loss of stearoyl-CoA desaturase 1 rescues cardiac function in obese leptin-deficient mice. J Lipid Res. 2010; 51: 2202-2210.

Dobrzyn P, Pyrkowska A, Jazurek M, Szymanski K, Langfort J, Dobrzyn A: Endurance training-induced accumulation of muscle triglycerides is coupled to upregulation of stearoyl-CoA desaturase 1. J. Appl. Physiol. 2010; 109: 1653-1661

Dobrzyn P, Jazurek M, Dobrzyn A: Stearoyl-CoA desaturase and insulin resistance – What is the molecular switch. Biochim Biophys Acta – Bioenerg. 2010; 1797: 1189-1194.

Dobrzyn P, Sampath H, Dobrzyn A, Miyazaki M, Ntambi JM: Loss of stearoyl-CoA desaturase 1 inhibits fatty acid oxidation and increases glucose utilization in the heart. Am J Physiol Endocrinol Metab. 2008; 294: E357-364.