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| Content Provider | MDPI |
|---|---|
| Author | Baburamani, Ana Hurling, Chloe Stolp, Helen Sobotka, Kristina Gressens, Pierre Hagberg, Henrik Thornton, Claire |
| Abstract | Perturbation of mitochondrial function and subsequent induction of cell death pathways are key hallmarks in neonatal hypoxic-ischemic (HI) injury, both in animal models and in term infants. Mitoprotective therapies therefore offer a new avenue for intervention for the babies who suffer life-long disabilities as a result of birth asphyxia. Here we show that after oxygen-glucose deprivation in primary neurons or in a mouse model of HI, mitochondrial protein homeostasis is altered, manifesting as a change in mitochondrial morphology and functional impairment. Furthermore we find that the mitochondrial fusion and cristae regulatory protein, OPA1, is aberrantly cleaved to shorter forms. OPA1 cleavage is normally regulated by a balanced action of the proteases Yme1L and Oma1. However, in primary neurons or after HI in vivo, protein expression of YmelL is also reduced, whereas no change is observed in Oma1 expression. Our data strongly suggest that alterations in mitochondria-shaping proteins are an early event in the pathogenesis of neonatal HI injury. |
| File Size | 2990080 |
| Ending Page | 22526 |
| Page Count | 18 |
| Starting Page | 22509 |
| File Format | |
| e-ISSN | 14220067 |
| DOI | 10.3390/ijms160922509 |
| Journal | International Journal of Molecular Sciences |
| Issue Number | 9 |
| Volume Number | 16 |
| Language | English |
| Publisher Date | 2015-09-17 |
| Access Restriction | Open |
| Subject Keyword | mitochondria OPA1 Oma1 Yme1L oxygen-glucose deprivation (OGD) hypoxia-ischaemia neonatal brain injury |
| Content Type | Text |
| Resource Type | Article |
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