ArticleNeuroprotection (Chichester, England)2026
Mesenchymal stem cells as cellular factories for targeted P2X7 blockade after traumatic brain injury.
Article in Neuroprotection (Chichester, England), 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
Background: Traumatic brain injury (TBI) causes long-term disability, with inflammation contributing to both primary and secondary brain damage. Extracellular adenosine triphosphate (ATP) and its receptor purinergic receptor X7 (P2X7) drive neuroinflammation and represent promising therapeutic targets. Therefore, we developed a strategy to mitigate acute post-TBI inflammation using mesenchymal stem cells (MSCs) engineered to deliver a P2X7-blocking nanobody (P2X7nb). Methods: Primary MSCs were transfected in vitro with bicistronic messenger RNA (mRNA) encoding P2X7nb and a haloalkane dehalogenase Tag reporter, with nanobody secretion confirmed by enzyme-linked immunosorbent assay (ELISA). In vivo, TBI was induced in mice using the closed-head injury model. Twenty-4 hours post-TBI, MSCs labeled with iron oxide nanoparticles were administered via intra-arterial injection into the internal carotid artery. Dynamic 9.4 T magnetic resonance imaging (MRI) using susceptibility-weighted imaging (SWI) allowed real-time monitoring of cellular accumulation. Behavioral performance was assessed using the beam walk test, while mice were euthanized on Day 4 post-TBI for immunofluorescence analysis of cell localization. Data were analyzed using either an unpaired Results: Transfection (38.9% efficiency) and release of P2X7nb were confirmed, with a peak secretion of 17.29 ± 1.84 ng/mL. SWI MRI revealed accumulation of labeled MSCs in the brain post-injection, with a persistent hypointense signal ranging from 2.45% ± 2.93% to 0.77% ± 0.88% of cell area (% of right hemisphere) over 3 days. Behavioral assessment using the beam walk test revealed no cell transplantation-related motor impairment, while histology confirmed the presence of transfected MSCs in injured brain tissue. Conclusion: MSCs expressing a P2X7nb are detectable in the injured brain following intra-arterial delivery for at least 3 days, without producing adverse effects. These findings provide insights into cell-based immunomodulatory therapies targeting neuroinflammation in TBI and highlight the utility of noninvasive MRI to monitor therapeutic cell biodistribution and persistence.
Indexed as
Identifiers
What Socratic 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 Socratic graph.