Hyperhomocysteinemia regulated SCF expression in cultured cardiomyocytes via modulation of NF-κB activities.

Hyperhomocysteinemia (HHcy) is an important, independent risk factor for coronary artery disease, especially for the myocardial infarction. Our previous study has shown that myocardial stem cell factor (SCF) mediated cardiac stem cells migration, which was involved in cardiac repair. However, it is not clear regarding the action of HHcy on the expression of SCF in cardiomyocytes. In the present study, cultured neonatal rat cardiomyocytes were treated with 20, 50, or 100 μM homocysteine (Hcy) for 5 h. Results showed an significantly increase of SCF expression with 20-50 μM Hcy incubation, which matched with elevated nuclear factor-kappaB (NF-κB) activities. Treatment with NF-κB inhibitor N-acetylcysteine significantly inhibited the increase of SCF. Nevertheless, 100 μM Hcy markedly decreased the expression of SCF, which was in accordance with the suppression of NF-κB activities. The present study indicated that HHcy regulated the expression of SCF in a concentration-dependent manner via modulation of NF-κB activities. Thus, HHcy may increase the risk for cardiovascular diseases not only by causing endothelial dysfunction but also by directly exerting detrimental effects on cardiomyocytes.