CEACAM2 negatively regulates hemi (ITAM-bearing) GPVI and CLEC-2 pathways and thrombus growth in vitro and in vivo
Key result
Ceacam2(-/-)-deficient mice exhibited enhanced platelet aggregation, increased adhesion, hyperresponsive granule release, and formed larger, more stable thrombi compared with wild-type controls.
Population
Ceacam2(-/-)-deficient mice (Cc2(-/-)) and wild-type controls
Comparison
Genetic deletion of CEACAM2 (Ceacam2(-/-)) vs Wild-type controls
Design
Preclinical
Authors
Discussion
Loading...
Member takes
Implication
CEACAM2 may represent a novel antithrombotic target; animal data leave open human applicability and require validation.
Structured PICO
P
Population
Ceacam2(-/-)-deficient mice (Cc2(-/-)) and wild-type controls
E
Exposure
Genetic deletion of CEACAM2 (Ceacam2(-/-))
C
Comparator
Wild-type controls
O
Outcome
Platelet aggregation, adhesion, granule release, and in vivo thrombus formationsurrogate
CEACAM2 is a novel platelet immunoreceptor that negatively regulates platelet GPVI-collagen interactions and CLEC-2 pathways, limiting thrombus growth.
Cite This Study
Alshahrani et al. (2014) studied this question. Ceacam2(-/-)-deficiency vs. Wild-type controls was evaluated on Platelet aggregation, adhesion, granule release, and thrombus size/stability. Ceacam2(-/-)-deficient mice exhibited enhanced platelet aggregation, increased adhesion, hyperresponsive granule release, and formed larger, more stable thrombi compared with wild-type controls.