These findings indicate that blockade of NF-kappaB induces apoptosis and is an important factor in the development of OFT during cardiogenesis. However, it remains unknown which members of the Rel family are relevant in this process.
The signaling pathways that control the life-death switch of a cell are of primary interest in modern biology. In this respect, NF-kappaB has emerged as a decisive transcription factor in the cell's response to apoptotic challenge and its effects on apoptosis have far-reaching consequences for normal development and/or homeostasis in many cells and tissues, including the immune system, hair follicles, and epidermal appendages, liver, nervous system and recently in heart . In this review we analyze the pivotal role of the transcription factor NF-kappaB in the normal functioning of the cardiac cell and its implication in common cardiac pathologies, such as ischemia-reperfusion injury, ischemic precondition, hypertrophy, atherosclerosis and cardiac arrest. While NF-kappaB is usually cytoprotective, it can also be pro-apoptotic depending on the inducing stimulus and the cellular context. Significant progress has been made in elucidating NF-kappaB's mode of action and its interplay with other key factors. These studies identified some anti- and pro-apoptotic NF-kappaB regulated genes that mediate its activity. These important new insights fuel hope that novel approaches will be developed to control the effects of NF-kappaB in cardiac pathologies.
Carbon nanotubes (CNTs) have been a focus of attention due to their possible applications in medicine, by serving as scaffolds for cell growth and proliferation and improving mesenchymal cell transplantation and engraftment. The emphasis on the benefits of CNTs has been offset by the ample debate on the safety of nanotechnologies. In this study, we determine whether functionalized multiwalled CNTs (fMWCNTs) and functionalized oxygen-doped multiwalled CNTs (fCOxs) have toxic effects on rat mesenchymal stem cells (MSCs) in vitro by analyzing morphology and cell proliferation and, using in vivo models, whether they are able to transform MSCs in cancer cells or induce embryotoxicity. Our results demonstrate that there are statistically significant differences in cell proliferation and the cell cycle of MSCs in culture. We identified dramatic changes in cells that were treated with fMWCNTs. Our evaluation of the transformation to cancer cells and cytotoxicity process showed little effect. However, we found a severe embryotoxicity in chicken embryos that were treated with fMWCNTs, while fCOxs seem to exert cardioembryotoxicity and a discrete teratogenicity. Furthermore, it seems that the time of contact plays an important role during cell transformation and embryotoxicity. A single contact with fMWCNTs is not sufficient to transform cells in a short time; an exposure of fMWCNTs for 2 weeks led to cell transformation risk and cardioembryotoxicity effects.
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