| Literature DB >> 27314518 |
Mária Maslaňáková1, Lucia Balogová1, Pavol Miškovský1,2, Ružena Tkáčová3, Katarína Štroffeková4.
Abstract
Understanding apoptosis regulatory mechanisms in endothelial cells (ECs) has great importance for the development of novel therapy strategies for cancer and cardiovascular pathologies. An oxidative stress with the generation of reactive oxygen species (ROS) is a common mechanism causing ECs' dysfunction and apoptosis. The generation of ROS can be triggered by various stimuli including photodynamic therapy (PDT). In most PDT treatments, photosensitizer (PS) is administered systemically, and thus, possibility of high exposure to PS in the ECs remains high. PS accumulation in ECs may be clinically relevant even without PDT, if PS molecules affect the pro-apoptotic cascade without illumination. In the present work, we focused on Hypericin (Hyp) and HypPDT effects on the cell viability, oxidative stress, and the distribution of Bcl2 family members in human coronary artery endothelial (HCAEC) cells. Our findings show that the presence of Hyp itself has an effect on cell viability, oxidative stress, and the distribution of Bcl2 family members, without affecting the mitochondria function. In contrast, HypPDT resulted in mitochondria dysfunction, further increase of oxidative stress and effect on the distribution of Bcl2 family members, and in primarily necrotic type of death in HCAEC cells.Entities:
Keywords: Apoptosis; Bcl2 family of proteins; Hypericin; Oxidative stress; Photodynamic therapy
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Year: 2016 PMID: 27314518 DOI: 10.1007/s12013-016-0740-y
Source DB: PubMed Journal: Cell Biochem Biophys ISSN: 1085-9195 Impact factor: 2.194