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Arterioscler Thromb Vasc Biol. 2008 Aug;28(8):1429-31. doi: 10.1161/ATVBAHA.108.169078. Epub 2008 May 8.

Defective mer receptor tyrosine kinase signaling in bone marrow cells promotes apoptotic cell accumulation and accelerates atherosclerosis.

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  • 1Inserm U689, Hôpital Lariboisière, 41, Bd de la Chapelle, 75010 Paris, France.

Abstract

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.

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PMID:
18467644
[PubMed - indexed for MEDLINE]
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