Defective Mer Receptor Tyrosine Kinase Signaling in Bone Marrow Cells Promotes Apoptotic Cell Accumulation and Accelerates Atherosclerosis-Reference-Cited by-同舟云学术

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

Published:2008-08 Issue:8 Volume:28 Page:1429-1431
ISSN:1079-5642
Container-title:Arteriosclerosis, Thrombosis, and Vascular Biology
language:en
Short-container-title:ATVB

Author:

Ait-Oufella Hafid¹,Pouresmail Vahid¹,Simon Tabassome¹,Blanc-Brude Olivier¹,Kinugawa Kiyoka¹,Merval Régine¹,Offenstadt Georges¹,Lesèche Guy¹,Cohen Philip L.¹,Tedgui Alain¹,Mallat Ziad¹

Affiliation:

1. From the Institut National de la Santé et de la Recherche Médicale (Inserm), Unit 689 (H.A.-O., V.P., T.S., O.B.-B., K.K., R.M., A.T., Z.M.), Centre de Recherche Cardiovasculaire Lariboisière, Paris, France; Service de Réanimation Médicale (H.A.-O., G.O.), Hôpital Saint-Antoine, Paris, France; Service de Chirurgie Thoracique et Vasculaire (G.L.), Hôpital Bichat, Paris, France; and Philadelphia VA Medical Center (P.L.C.), University of Pennsylvania, Philadelphia.

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.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine

Link

https://www.ahajournals.org/doi/pdf/10.1161/ATVBAHA.108.169078

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