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

Inserm U689, Hôpital Lariboisière, 41, Bd de la Chapelle, 75010 Paris, France.
Arteriosclerosis Thrombosis and Vascular Biology (Impact Factor: 6). 06/2008; 28(8):1429-31. DOI: 10.1161/ATVBAHA.108.169078
Source: PubMed


To study the role of Mer receptor tyrosine kinase (mertk) in atherosclerosis.
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.
Mertk expression by bone marrow-derived cells is required for the disposal of apoptotic cells and controls lesion development and inflammation.

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Available from: Kiyoka Kinugawa
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    • "This counterbalance comes through the alteration or down regulation of ‘don’t eat me’ signals, expressed on viable cells. These include CD300a,68 CD3169 and CD47,45 which all vary in mechanism of function. CD300a is newly identified as an inhibitor of AC engulfment via competitive phospholipid binding on apoptotic cells.99,101 "
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