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- W2315655597 abstract "VEGFR3-signaling in lymphatic endothelial cells (LEC) is critical in immune surveillance. We investigated the effect of conditional LEC-specific deletion of VEGFR3 in mouse cardiac allografts on graft survival. We constructed C57BL/6J mice in which VEGFR3 was conditionally knocked out in LECs (Vegfr3iΔLEC). This was done by crossing mice expressing a tamoxifen inducible Cre recombinase driven by Prox promoter (Prox1iCreERT2 mice) with mice in which VEGFR3 was flanked by loxP sites (Vegfr3flox/flox mice). We treated Vegfr3iΔLEC mice and Vegfr3flox/flox control mice with i.p. injections of tamoxifen for 3 consecutive days. Ten days after the last injection, we removed the hearts, subjected them to 4-h cold and 1-h warm ischemia, and transplanted them to fully MHC-mismatched BALB/c recipients. We treated the recipients with tacrolimus 1.5 mg/kg/day. The conditional deletion of Vegfr3 by tamoxifen was validated by whole mount stainings of the ear skin, by immunofluorescence of the heart, and by qRT-PCR in intestinal tissue. The use of Vegfr3iΔLEC cardiac allografts significantly prolonged graft survival, when compared with littermate controls. Our results reveal that lymphatic endothelial VEGFR3 in cardiac allografts is required for the development of adaptive immune responses and has important clinical implications in the prevention of allograft rejection." @default.
- W2315655597 created "2016-06-24" @default.
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- W2315655597 date "2015-04-01" @default.
- W2315655597 modified "2023-10-17" @default.
- W2315655597 title "Lymphatic Endothelial Cell VEGFR3 Controls Cardiac Allograft Rejection" @default.
- W2315655597 doi "https://doi.org/10.1016/j.healun.2015.01.248" @default.
- W2315655597 hasPublicationYear "2015" @default.
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