AI Article Synopsis
- Intracerebral hemorrhage is a type of stroke with no specific treatment, and certain monocytes (Ly6Chi CCR2+) are linked to acute injury after such events.
- The study investigated whether a different monocyte subset (Ly6Clo CX3CR1+) aids in recovery from this type of hemorrhage, but found no significant differences in outcomes or leukocyte recruitment between different genetic models.
- Ultimately, the research concluded that CX3CR1 signaling in these monocytes does not significantly affect the injury or recovery process, suggesting it may not be a viable target for improving treatment outcomes.
Article Abstract
Intracerebral hemorrhage is a subset of stroke for which there is no specific treatment. The Ly6Chi CCR2+ monocytes have been shown to contribute to acute injury after intracerebral hemorrhage. The other murine monocyte subset expresses CX3CR1 and lower Ly6C levels, and contributes to repair in other disease models. We hypothesized that the Ly6Clo CX3CR1+ monocytes would contribute to recovery after intracerebral hemorrhage. Intracerebral hemorrhage was modeled by blood injection in WT and CX3CR1-null bone marrow chimeras. Neurological outcomes and leukocyte recruitment were quantified at various time points. Functional outcomes were equal at 1, 3, 7, and 14 days after intracerebral hemorrhage in both genotypes. No differences were observed in leukocyte recruitment between genotypes on either 3 or 7 days after intracerebral hemorrhage. A few hundred Ly6Clo monocytes were found in the ipsilateral hemisphere in each genotype and they did not change over time. Peripherally derived CX3CR1+ monocytes were observed in the perihematomal brain 7 and 14 days after intracerebral hemorrhage. Our data suggests CX3CR1 signaling on monocytes does not play an influential role in acute injury or functional recovery after intracerebral hemorrhage and therefore CX3CR1 is not a therapeutic target to improve outcome after intracerebral hemorrhage.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4255025 | PMC |
| http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0114472 | PLOS |
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