ArticleJournal of neurochemistry2010
p90 activation contributes to cerebral ischemic damage via phosphorylation of Na+/H+ exchanger isoform 1.
Article in Journal of neurochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Method parameters' impact on mortality and variability in mouse stroke experiments: a meta-analysis.Scientific reports · 2016Pooled it
- A dangerous liaison: Spreading depolarization and tissue acidification in cerebral ischemia.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2025Review
- RSK1 and RSK2 as therapeutic targets: an up-to-date snapshot of emerging data.Expert opinion on therapeutic targets · 2024Review
- Acidosis in arterial blood gas testing is associated with clinical outcomes after endovascular thrombectomy.Frontiers in neurology · 2022Article
- Role of GPR39 in Neurovascular Homeostasis and Disease.International journal of molecular sciences · 2021Review
- Tissue Acidosis Associated with Ischemic Stroke to Guide Neuroprotective Drug Delivery.Biology · 2020Review
- Pharmacological inhibition of the MEK5/ERK5 and PI3K/Akt signaling pathways synergistically reduces viability in triple-negative breast cancer.Journal of cellular biochemistry · 2020Article
- The Zinc Sensing Receptor, ZnR/GPR39, in Health and Disease.International journal of molecular sciences · 2018Review
- Functional kinomics establishes a critical node of volume-sensitive cation-ClScientific reports · 2016Article
- Review
- Glioma-mediated microglial activation promotes glioma proliferation and migration: roles of Na+/H+ exchanger isoform 1.Carcinogenesis · 2016Article
- Bacterial Expression, Purification and In Vitro Phosphorylation of Full-Length Ribosomal S6 Kinase 2 (RSK2).PloS one · 2016Article
- RhoA Kinase (Rock) and p90 Ribosomal S6 Kinase (p90Rsk) phosphorylation of the sodium hydrogen exchanger (NHE1) is required for lysophosphatidic acid-induced transport, cytoskeletal organization and migration.Cellular signalling · 2015Article
- Proton-sensitive cation channels and ion exchangers in ischemic brain injury: new therapeutic targets for stroke?Progress in neurobiology · 2014Review
- TIPE2, a novel regulator of immunity, protects against experimental stroke.The Journal of biological chemistry · 2012Article
- Role of sodium/hydrogen exchanger isoform 1 in microglial activation and proinflammatory responses in ischemic brains.Journal of neurochemistry · 2011Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Excessive activation of Na+/H+ exchanger isoform 1 (NHE-1) plays a role in cerebral ischemic injury. The current study investigated whether NHE-1 protein in ischemic brains is regulated by extracellular signal-regulated kinase (ERK)/90-kDa ribosomal S6 kinase (p90(RSK)) signaling pathways. A transient focal ischemia in mice was induced by a 60-min-occlusion of the middle cerebral artery followed by reperfusion for 3, 10, or 60 min (Rp). Expression of phosphorylated ERK 1/2 was significantly elevated in the ipsilateral hemispheres at 3-10 min Rp and reduced by 60 min Rp. An increase in phosphorylation of p90(RSK), a known NHE-1 kinase, was also detected at 3-10 min Rp, which was accompanied with a transient elevation of NHE-1 phosphorylation (p-NHE-1). Stimulation of p90(RSK) in ischemic neurons was downstream of ERK activation because inhibition of MEK1 (MAP kinase/ERK kinase) with its inhibitor U0126 blocked phosphorylation of p90(RSK). Moreover, direct inhibition of p90(RSK) by its selective inhibitor fluoromethyl ketone not only reduced p-NHE-1 expression but also ischemic infarct volume. Taken together, our study revealed that reperfusion triggers a transient stimulation of the ERK/p90(RSK) pathway. p90(RSK) activation contributes to cerebral ischemic damage in part via activation of NHE-1 protein.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.