Expression of genes coding for proangiogenic factors and their receptors in human placenta complicated by preeclampsia and intrauterine growth restriction.

The aim of the study was to investigate the expression of genes coding for vascular endothelial growth factor (VEGF) and placenta growth factor (PlGF) as well as their receptors, fms-like tyrosine kinase receptor 1 (VEGFR-1/Flt-1) and VEGF receptor 2 (VEGFR-2/KDR) in the placentae of patients with pregnancies complicated by preeclampsia (PE) and intrauterine growth restriction (IUGR). Tissue samples were collected from placentae of women with PE (n=31) and IUGR syndrome (n=25) as well as of healthy control women (n=31). Total RNA was extracted and purified, mRNA reversely transcribed, and amplified using real-time PCR. Expression of the examined genes was normalized to ß-actin. Higher levels of PlGF (p<0.001) and Flt-1 (p<0.05) transcription were found in PE placentae compared to normal ones. A positive correlation between PlGF and Flt-1 expression was revealed in the PE patients. In conclusion, the presented data indicate the upregulation of both PlGF and Flt-1 in placentae of women with PE, which could be induced by a pathological process possibly due to endothelial dysfunction.

Cell-based therapy for heart failure: skeletal myoblasts.

Satellite cells are committed precursor cells residing in the skeletal muscle. These cells provide an almost unlimited regeneration potential to the muscle, contrary to the heart, which, although proved to contain cardiac stem cells, possesses a very limited ability for self-renewal. The idea that myoblasts (satellite cell progenies) may repopulate postinfarction scar occurred around the mid-1990s. Encouraging results of preclinical studies triggered extensive research, which led to the onset of clinical trials. These trials have shown that autologous skeletal myoblast transplantation to cure heart failure is feasible and relatively safe (observed incidences of arrhythmia). Because most of the initial studies on myoblast application into postischemic heart have been carried out as an adjunct to routine surgical procedures, the true clinical outcome of such therapy in regard to cell implantation is blurred and requires to be elucidated. The mechanism by which implantation of skeletal myoblast may improve heart function is not clear, especially in the light of inability of these cells to couple electromechanically with a host myocardium. Successful myoblast therapy depends on a number of factors, including: delivery to the target tissue, long-term survival, efficacious engraftment, differentiation into cardiomyocytes, and integration into the new, unique microenvironment. All these steps constitute a potential goal for cell manipulation aiming to improve the overall outcome of such therapy. Precise understanding of the mechanism by which cells improve cardiac function is essential in giving the sensible direction of further research.