ArticleCell stress & chaperones2019
Lipopolysaccharide induces human olfactory ensheathing glial apoptosis by promoting mitochondrial dysfunction and activating the JNK-Bnip3-Bax pathway.
Article in Cell stress & chaperones, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- Research progress of mitochondrial dysfunction induced pyroptosis in acute lung injury.Respiratory research · 2024Review
- Bnip3 expression is strongly associated with reelin-positive entorhinal cortex layer II neurons.Brain structure & function · 2024Article
- Dexmedetomidine Attenuates LPS-Stimulated Alveolar Type II Cells' Injury through Upregulation of miR-140-3p and Partial Suppression of PD-L1 Involving Inactivating JNK-Bnip3 Pathway.Canadian respiratory journal · 2022Article
- Hydrogen Sulfide Ameliorates Lipopolysaccharide-Induced Memory Impairment in Mice by Reducing Apoptosis, Oxidative, and Inflammatory Effects.Neurotoxicity research · 2021Article
- Retraction Note to: Excessive mitochondrial fragmentation triggered by erlotinib promotes pancreatic cancer PANC‑1 cell apoptosis via activating the mROS‑HtrA2/Omi pathways.Cancer cell international · 2019Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Olfactory ensheathing glia (OEG) play an important role in regulating the regeneration of an injured nervous system. However, chronic inflammation damage reduces the viability of OEG via poorly understood mechanisms. We aimed to investigate the pathological responses of OEG in response to LPS-mediated inflammation stress in vitro. The results indicated that lipopolysaccharide (LPS) treatment significantly reduced the viability of OEG in a dose-dependent fashion. Mechanistically, LPS stimuli induced mitochondrial oxidative damage, mitochondrial fragmentation, mitochondrial metabolism disruption, and mitochondrial apoptosis activation. Furthermore, we verified that LPS modulated mitochondrial apoptosis by promoting Bax upregulation, and this process was regulated by the JNK-Bnip3 pathway. Inhibition of the JNK-Bnip3 pathway prevented LPS-mediated Bax activation, thus attenuating OEG apoptosis. Altogether, our data illustrated that LPS-mediated inflammation injury evoked mitochondrial abnormalities in OEG damage via the JNK-Bnip3-Bax pathway. This finding provides a potential target to protect OEG against chronic inflammation stress.
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