ArticleCNS neuroscience & therapeutics2026
Acetylation-like H2BK109Q attenuates acute brain injury and preserves axon-myelin integrity after intracerebral hemorrhage.
Article in CNS neuroscience & therapeutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
aimsAxon-myelin damage contributes to neurological dysfunction after intracerebral hemorrhage (ICH), but the upstream chromatin regulators remain unclear. We aimed to characterize the H2B acetylation response to ICH, test the functional significance of modeled H2BK109 states, and identify a downstream effector of H2BK109Q-mediated protection.
methodsPan-H2B acetylation was examined in mice with collagenase-induced ICH and in hemoglobin-treated HT22 cells, and the histone acetylome of the mouse brain was profiled. H2BK109Q and H2BK109R were used to model acetylation-mimetic and non-acetylated lysine-like states. Injury outcomes, axon-myelin integrity, molecular profiles, and regional Galc knockdown were assessed.
resultsICH and hemoglobin reduced pan-H2B acetylation, and acetylome profiling indicated reduced H2BK109ac. H2BK109Q-expressing mice showed higher pan-H2B acetylation, smaller hematomas, less edema and apoptosis, improved neurological function, and greater preservation of LFB, MBP, NF200, and axon-myelin ultrastructure. Under matched hemoglobin exposure, H2BK109Q-expressing HT22 cells showed higher BCL2/BAX ratios and lower TUNEL positivity than H2BK109R-expressing cells. In vitro analyses highlighted GALC as a candidate downstream effector of H2BK109Q-associated protection. In H2BK109Q-expressing mice, Galc knockdown reduced LFB- and MBP-positive areas and NF200 signals in the caudate putamen and corpus callosum compared with untreated and siNC controls.
conclusionH2BK109Q attenuates acute ICH injury and preserves axon-myelin integrity, with GALC contributing to these protective effects.
Indexed as
Identifiers
What OpenQuestion holds
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.