ArticleMolecular biology of the cell2025
Microglia express Tie2 in a longitudinal imaging study of acute neural injury in mice.
Article in Molecular biology of the cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
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Who cites it
3 citing papers in PubMed.
- Dysregulated TIE-2 expression is associated with blood-brain barrier leakiness and Alzheimer's disease-related neuropathology.Brain pathology (Zurich, Switzerland) · 2026Article
- Dysregulated TIE-2 expression in Alzheimer's disease: Further considerations on regional specificity and shedding evidence.Brain pathology (Zurich, Switzerland) · 2026Article
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Authors and funding
9 authors.
Funding
Abstract
The Tie2 receptor tyrosine kinase is expressed both in stroke recovery and cancer progression by vascular endothelial and myeloid lineage cells. Tie2 mechanisms have been described in vascular maturation, but the receptor's immune role remains poorly understood. Here, we describe the expression of Tie2 in microglia in response to an acute neural injury, uncovering a potential new role for these cells. Using magnetic resonance imaging (MRI) and the Ts-Biotag multimodal reporter mouse, we noninvasively imaged Tie2 expression dynamics in a longitudinal study of neural injury to identify key timepoints in wound signaling and healing. Using labeled bone marrow chimeras, we further determined that Tie2 is expressed in brain-resident microglia but not invading macrophages. Our results establish the utility of noninvasive molecular imaging for longitudinal studies of neuroimmune function and present a new role for Tie2 as a uniquely expressed marker of microglial function during wound healing.
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