ArticleJournal of molecular histology2015
Phosphorylation of p38 MAPK mediates aquaporin 9 expression in rat brains during permanent focal cerebral ischaemia.
Article in Journal of molecular histology, 2015. 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, 16 citations in OpenAlex.
- Aquaporins in Acute Brain Injury: Insights from Clinical and Experimental Studies.Biomedicines · 2025Review
- Aquaporins in Nervous System.Advances in experimental medicine and biology · 2023Article
- G-CSF upregulates the expression of aquaporin-9 through CEBPB to enhance the cytotoxic activity of arsenic trioxide to acute myeloid leukemia cells.Cancer cell international · 2022Article
- Metformin inhibits MAPK signaling and rescues pancreatic aquaporin 7 expression to induce insulin secretion in type 2 diabetes mellitus.The Journal of biological chemistry · 2021Article
- Investigate of AQP gene expression in the liver of mice after ischemia-reperfusion.Molecular biology reports · 2018Article
- Lack of Aquaporin 9 Reduces Brain Angiogenesis and Exaggerates Neuronal Loss in the Hippocampus Following Intracranial Hemorrhage in Mice.Journal of molecular neuroscience : MN · 2017Article
- Tozasertib attenuates neuronal apoptosis via DLK/JIP3/MA2K7/JNK pathway in early brain injury after SAH in rats.Neuropharmacology · 2016Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aquaporin 9 (AQP9), an aquaglyceroporin, is an important aquaporin in the brain. This study examined the expression patterns of AQP9 and p38 mitogen-activated protein kinases (MAPK) in ischaemic brains from rats with permanent middle cerebral artery occlusion (pMCAO) to elucidate the function and regulation of AQP9 after ischaemia. AQP9 was co-localised with glial fibrillary acidic protein-positive astrocytes and neuronal nuclei-positive neurons in rat brains. Expression of AQP9 increased continuously until 24 h after pMCAO in the ischaemic core region and the border region. Importantly, this increase in expression of AQP9 correlated with brain oedema. AQP9 expression was predominant in astrocytes within 3 h after pMCAO and then in neurons 6 h after pMCAO. Phosphorylated p38 MAPK was also induced in the ischaemic core region and the border region at different time points after pMCAO. Interestingly, intracerebroventricular injection of the p38 MAPK inhibitor SB203580 attenuated AQP9 expression after pMCAO. Taken together, these results indicate that dynamic changes in AQP9 expression, mediated in part via the p38 MAPK signal transduction pathway, may contribute to the development of cerebral oedema after brain ischaemia.
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