Defective Mer Receptor Tyrosine Kinase Signaling in Bone Marrow Cells Promotes Apoptotic Cell Accumulation and Accelerates Atherosclerosis

OBJECTIVE—To study the role of Mer receptor tyrosine kinase (mertk) in atherosclerosis. METHODS AND RESULTS—We irradiated and reconstituted atherosclerosis-susceptible C57Bl/6 low-density lipoprotein receptor–deficient female mice (ldlr) with either a mertk or mertk (tyrosine kinase-defective mertk)...

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Veröffentlicht in:Arteriosclerosis, thrombosis, and vascular biology thrombosis, and vascular biology, 2008-08, Vol.28 (8), p.1429-1431
Hauptverfasser: Ait-Oufella, Hafid, Pouresmail, Vahid, Simon, Tabassome, Blanc-Brude, Olivier, Kinugawa, Kiyoka, Merval, Régine, Offenstadt, Georges, Lesèche, Guy, Cohen, Philip L, Tedgui, Alain, Mallat, Ziad
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Sprache:eng
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Zusammenfassung:OBJECTIVE—To study the role of Mer receptor tyrosine kinase (mertk) in atherosclerosis. METHODS AND RESULTS—We irradiated and reconstituted atherosclerosis-susceptible C57Bl/6 low-density lipoprotein receptor–deficient female mice (ldlr) with either a mertk or mertk (tyrosine kinase-defective mertk) bone marrow. The mice were put on high-fat diet for either 8 or 15 weeks. Mertk deficiency led to increased accumulation of apoptotic cells within the lesions, promoted a proinflammatory immune response, and accelerated lesion development. CONCLUSIONS—Mertk expression by bone marrow–derived cells is required for the disposal of apoptotic cells and controls lesion development and inflammation.
ISSN:1079-5642
1524-4636
DOI:10.1161/ATVBAHA.108.169078