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Arteriosclerosis, Thrombosis, and Vascular Biology 2008-Aug

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

Samo registrirani uporabniki lahko prevajajo članke
Prijava / prijava
Povezava se shrani v odložišče
Hafid Ait-Oufella
Vahid Pouresmail
Tabassome Simon
Olivier Blanc-Brude
Kiyoka Kinugawa
Régine Merval
Georges Offenstadt
Guy Lesèche
Philip L Cohen
Alain Tedgui

Ključne besede

Povzetek

OBJECTIVE

To study the role of Mer receptor tyrosine kinase (mertk) in atherosclerosis.

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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