ArticleMolecular medicine reports2019
Decreased expression of ubiquilin‑1 following neonatal hypoxia‑ischemic brain injury in mice.
Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 4 citations in OpenAlex.
- Mechanisms of Tertiary Neurodegeneration after Neonatal Hypoxic-Ischemic Brain Damage.Pediatric medicine (Hong Kong, China) · 2022Article
- GABAInternational journal of molecular sciences · 2022Article
- Association of the Protein-Quality-Control Protein Ubiquilin-1 With Alzheimer's Disease BothFrontiers in neuroscience · 2022Article
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12 authors at 5 institutions in 1 country.
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Abstract
Ubiquilin‑1 (Ubqln), a ubiquitin‑like protein, regulates degradation of misfolded proteins and has been reported to have a crucial role in multiple pathologic and physiologic conditions. The current study was undertaken to investigate the expression of Ubqln in the brain of a neonatal hypoxia‑ischemic (HI) brain injury model induced using the Rice method with some modifications. Mouse pups at postnatal day 7 day were used in this study. Pups underwent permanent ligation of the left common carotid artery and a consecutive hypoxic challenge (8% O2 and 92% N2 for 120 min). The expression of Ubqln in the brain of pups following HI was analyzed by immunofluorescence staining and western blot analysis. Immunofluorescence staining demonstrated that Ubqln was extensively distributed in the cerebral cortex and hippocampus, and Ubqln was expressed in neurons, astrocytes and microglia in the brains of the HI brain injury model mice. Western blot analyses revealed decreased expression of Ubqln in the HI penumbra of the mouse model compared with Ubqln in the sham control group. The results of this study revealed that HI alters the expression of Ubqln, thus may provide a novel understanding of role of Ubqln in neonatal hypoxic ischemic encephalopathy.
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