ArticleNeurochemical research2017
Suppression of Inner Mitochondrial Membrane Peptidase 2-Like (IMMP2L) Gene Exacerbates Hypoxia-Induced Neural Death Under High Glucose Condition.
Article in Neurochemical research, 2017. 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, 10 citations in OpenAlex.
- Inner Mitochondrial Membrane Peptidase 2-Like Deletion Aggravates Mitochondrial Apoptosis and Inhibits Autophagy After Hyperglycemia Stroke.Molecular neurobiology · 2025Article
- Genome-wide association research on the reproductive traits of Qianhua Mutton Merino sheep.Animal bioscience · 2024Article
- Immp2l Enhances the Structure and Function of Mitochondrial Gpd2 Dehydrogenase.International journal of molecular sciences · 2024Article
- Antioxidant Behavioural Phenotype in theGenes · 2023Article
- Immp2l Mutation Induces Mitochondrial Membrane Depolarization and Complex III Activity Suppression after Middle Cerebral Artery Occlusion in Mice.Current medical science · 2023Article
- PRG5 Knockout Precipitates Late-Onset Hypersusceptibility to Pilocarpine-Induced Juvenile Seizures by Exacerbating Hippocampal Zinc Signaling-Mediated Mitochondrial Damage.Frontiers in neuroscience · 2021Article
- Substrain- and sex-dependent differences in stroke vulnerability in C57BL/6 mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is known that diabetes hyperglycemia enhances cerebral ischemia and reperfusion induced damage. We have previously shown that mutation of inner mitochondrial membrane peptidase 2-like (IMMP2L) increases brain damage caused by transient cerebral ischemia. In this study, we attempt to examine the impact of IMMP2L deficiency on an in vitro model that mimics the diabetic hypoxic conditions. Normal IMMP2L wild type and IMMP2L gene deleted HT22 cells were cultured. Hypoxia was induced under high glucose and acidic conditions with 4 h of oxygen deprivation. Cell viability was assessed by CCK-8 assay and cell death was determined using Annexin V/7-AAD assay. Superoxide production was measured using dihydroethidium staining and mitochondrial membrane potential was detected using JC-1 probe. Suppression of IMMP2L reduced the cell viability, increased the ROS production and decreased the mitochondrial membrane potential. In conclusion, our study demonstrated that deficiency of IMMP2L in cells, cultured under hypoxia, high glucose and acidic conditions, exacerbated neuronal death under a condition that mimics in vivo cerebral ischemia in diabetic condition.
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