ArticleBrain hemorrhages2020
Time-dependent progression of hemorrhagic transformation after transient ischemia and its association with GPR68-dependent protection.
Article in Brain hemorrhages, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- CD8+ regulatory T cells shorten neutrophil lifespan to reduce hemorrhagic transformation after ischemic stroke.The Journal of clinical investigation · 2026Article
- Potentiation of GPR68 alleviates post-ischemia BBB dysfunction and brain edema in mice.Experimental neurology · 2026Article
- A novel transgenic reporter of extracellular acidification in zebrafish elucidates skeletal muscle T-tubule pH regulation.Developmental dynamics : an official publication of the American Association of Anatomists · 2025Article
- Recent advances in acid sensing by G protein coupled receptors.Pflugers Archiv : European journal of physiology · 2024Review
- Redefining the Koizumi model of mouse cerebral ischemia: A comparative longitudinal study of cerebral and retinal ischemia in the Koizumi and Longa middle cerebral artery occlusion models.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022Article
- pH and proton-sensitive receptors in brain ischemia.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022Article
- RNA-Seq analysis of knocking out the neuroprotective proton-sensitive GPR68 on basal and acute ischemia-induced transcriptome changes and signaling in mouse brain.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- GPR68 Contributes to Persistent Acidosis-Induced Activation of AGC Kinases and Tyrosine Phosphorylation in Organotypic Hippocampal Slices.Frontiers in neuroscience · 2021Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Hemorrhagic transformation (HT) following ischemia is one complication which worsens stroke outcome. During and after ischemia-reperfusion, persistent reduction of brain pH occurs. In a recent study, we found that GPR68 functions as a neuronal proton receptor and mediates a protective pathway in brain ischemia. Here, we asked whether GPR68 contributes HT after ischemia. At 24 hr after transient middle cerebral artery occlusion (tMCAO), 58% of the wild-type (WT) mice exhibited some degrees of mild HT. At 72 hr, 95% of the WT showed HT with 42% exhibited large "parenchymal" type hemorrhage. In the GPR68-/- mice, there was a trend of increase in both the incidence and severity of HT at both time points. Mice with severe hemorrhage exhibited significantly larger infarct than those with no to mild hemorrhage. Next, we compared % infarct of GPR68-/- vs WT based on their HT categories. GPR68 deletion increased % infarct when the HT severity is mild. In contrast, for mice exhibiting large area HT, the two genotypes had no difference in % infarct. These data showed that GPR68-dependent signaling leads to protection when HT is mild.
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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.