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

H Ait-Oufella, V Pouresmail, T Simon… - … , and vascular biology, 2008 - Am Heart Assoc
H Ait-Oufella, V Pouresmail, T Simon, O Blanc-Brude, K Kinugawa, R Merval, G Offenstadt…
Arteriosclerosis, thrombosis, and vascular biology, 2008Am Heart Assoc
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 …
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.
Am Heart Assoc