ArticleNeurochemical research2010
Translocation of the serine protease Omi/HtrA2 from mitochondria into the cytosol upon seizure-induced hippocampal injury in the neonatal rat brain.
Article in Neurochemical research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 19 citations in OpenAlex.
- Role of high-temperature requirement serine protease A 2 in rheumatoid inflammation.Arthritis research & therapy · 2023Article
- Serine protease HtrA2/Omi regulates adaptive mitochondrial reprogramming in the brain cortex after ischemia/reperfusion injury via UCP2-SIRT3-PGC1 axis.Human cell · 2022Article
- Omi inhibition ameliorates neuron apoptosis and neurological deficit after subarachnoid hemorrhage in rats.Genes & genomics · 2021Article
- Increased Active OMI/HTRA2 Serine Protease Displays a Positive Correlation with Cholinergic Alterations in the Alzheimer's Disease Brain.Molecular neurobiology · 2019Article
- Mitochondria mediates caspase-dependent and independent retinal cell death in Staphylococcus aureus endophthalmitis.Cell death discovery · 2016Article
- Specific alterations of the HtrA2/HAX-1 ratio in the penumbra upon focal cerebral ischemia in mice.Neurochemical research · 2012Article
- Alterations in the expression of the anti-apoptotic factor HAX-1 upon seizures-induced hippocampal injury in the neonatal rat brain.Neurochemical research · 2012Article
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Omi/HtrA2 is a pro-apoptotic mitochondrial serine protease involved in caspase-dependent as well as caspase-independent cell death upon various brain injuries. However, the role of Omi/HtrA2 in neuronal death induced by status epilepticus (SE) in the immature brain has not been reported. In this study, we analyzed the contribution of serine protease Omi/HtrA2, its substrate X-linked inhibitor of apoptosis protein (XIAP) and the caspase-3 activation to damage of hippocamplal CA1 cells following lithium-pilocarpine SE in P14 rat pups. Status epilepticus in the immature brain significantly induced translocation of Omi/HtrA2 from mitochondria into the cytosol, increased cytosolic accumulation of Omi/HtrA2, induced appearance of XIAP-breakdown products and enhanced caspase-3 activity in the selectively vulnerable hippocampal CA1-subfield. Taken together, these results demonstrate for the first time that SE in the immature brain results in Omi/HtrA2 accumulation in the cytosol, where it probably promotes neuronal death by neutralizing and cleaving XIAP, one of the most potent endogenous inhibitors of apoptosis.
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