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IMPACT OF CLONAL HAEMATOPOIESIS ON THE INFLAMMATORY RESPONSE TO ISCHEMIC STROKE
Polina Bugaevaand 14 co-authors
Charité Universitätsmedizin Berlin
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS04-08PM-091
Presentation
Date TBA
Board: PS04-08PM-091
Event Information
Poster Board
PS04-08PM-091
Poster
View posterAbstract
Clonal haematopoiesis refers to the clonal expansion of haematopoietic stem cells triggered by mutations in genes regulating epigenetic modifications and DNA repair. Specifically, TET2 mutations were associated with systemic inflammation and elevated risk of recurrent cardiovascular events (recurrency, myocardial infarction, or death) after stroke. This preclinical study aims to investigate the impact of TET2-mediated clonal haematopoiesis on the local and systemic responses to ischaemic stroke.
One-leg irradiated mice engrafted with either WT or TET2-knockout bone marrow underwent 30-minute middle cerebral artery occlusion or sham surgery at the age of 7 months. We assessed stroke lesion size on day 1 and post-stroke atrophy on day 26 using T2-MRI. Blood samples were analysed by means of spectral flow cytometry at baseline, on day 7, and on day 28 after stroke, and cytokine profiles were determined using the Olink proximity extension assay. Brain and heart tissues underwent full spectral flow cytometry-based immunophenotyping on day 28 after stroke.
We detected no difference in stroke lesion size or post-stroke atrophy between the TET2-KO and WT groups. Cytometric analysis identified the expansion of Tet2 KO leukocytes, in particular myeloid cells, in peripheral blood of TET2 KO mice after stroke compared to WT animals.
We observed evidence of systemic inflammation in TET2 KO animals that correlates with clinical findings. However, deeper molecular phenotyping of the brain tissue is required to characterise the local response to ischemic stroke.
One-leg irradiated mice engrafted with either WT or TET2-knockout bone marrow underwent 30-minute middle cerebral artery occlusion or sham surgery at the age of 7 months. We assessed stroke lesion size on day 1 and post-stroke atrophy on day 26 using T2-MRI. Blood samples were analysed by means of spectral flow cytometry at baseline, on day 7, and on day 28 after stroke, and cytokine profiles were determined using the Olink proximity extension assay. Brain and heart tissues underwent full spectral flow cytometry-based immunophenotyping on day 28 after stroke.
We detected no difference in stroke lesion size or post-stroke atrophy between the TET2-KO and WT groups. Cytometric analysis identified the expansion of Tet2 KO leukocytes, in particular myeloid cells, in peripheral blood of TET2 KO mice after stroke compared to WT animals.
We observed evidence of systemic inflammation in TET2 KO animals that correlates with clinical findings. However, deeper molecular phenotyping of the brain tissue is required to characterise the local response to ischemic stroke.
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