The effects of a mitochondrial targeted peptide (elamipretide/SS31) on BAX recruitment and activation during apoptosis
| العنوان: | The effects of a mitochondrial targeted peptide (elamipretide/SS31) on BAX recruitment and activation during apoptosis |
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| المؤلفون: | Robert W. Nickells, Martin Redmon, Dennis Keefe, Joshua A. Grosser, Rachel L. Fehrman |
| المصدر: | BMC Research Notes BMC Research Notes, Vol 14, Iss 1, Pp 1-7 (2021) |
| بيانات النشر: | Springer Science and Business Media LLC, 2021. |
| سنة النشر: | 2021 |
| مصطلحات موضوعية: | 0301 basic medicine, Programmed cell death, Science (General), QH301-705.5, Mitochondrial outer membrane permeabilization, Cell, Apoptosis, Mitochondrion, Elamipretide (SS31), General Biochemistry, Genetics and Molecular Biology, Q1-390, 03 medical and health sciences, 0302 clinical medicine, medicine, Staurosporine, Biology (General), bcl-2-Associated X Protein, biology, Chemistry, Cytochrome c, Intrinsic apoptosis, General Medicine, Elamipretide, Mitochondria, Cell biology, Research Note, 030104 developmental biology, medicine.anatomical_structure, BAX, biology.protein, Medicine, Mitochondrial fragmentation, Mitochondrial dysfunction, Oligopeptides, 030217 neurology & neurosurgery, medicine.drug |
| الوصف: | Objective Elamipretide (SS31) is a mitochondria-targeted peptide that has reported functions of stabilizing mitochondrial cristae structure and improving mitochondrial bioenergetics. Several studies have documented cell protective features of this peptide, including impairment of intrinsic apoptosis by inhibiting the recruitment and activation of the pro-apoptotic BAX protein. We used live-cell imaging of ARPE-19 cells expressing fluorescently labeled BAX, cytochrome c, and a mitochondrial marker to investigate the effect of elamipretide on the kinetics of BAX recruitment, mitochondrial outer membrane permeabilization (as a function of cytochrome c release), and mitochondrial fragmentation, respectively. Result In nucleofected and plated ARPE-19 cells, elamipretide accelerated the formation of larger mitochondria. In the presence of the apoptotic stimulator, staurosporine, cells treated with elamipretide exhibited moderately slower rates of BAX recruitment. Peptide treatment, however, did not significantly delay the onset of BAX recruitment or the final total amount of BAX that was recruited. Additionally, elamipretide showed no impairment or delay of cytochrome c release or mitochondrial fragmentation, two events associated with normal BAX activation during cell death. These results indicate that the protective effect of elamipretide is not at the level of BAX activity to induce pro-apoptotic mitochondrial dysfunction after the initiation of staurosporine-induced apoptosis. |
| تدمد: | 1756-0500 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6b4af6c2b33b3bbc0d549b091141f275Test https://doi.org/10.1186/s13104-021-05613-9Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....6b4af6c2b33b3bbc0d549b091141f275 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 17560500 |
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