Reduced atherosclerosis lesion size, inflammatory response in miR-150 knockout mice via macrophage effects

• DOI: 10.1194/jlr.m082651
• Publication Date: 2018-02-20T22:50:20Z
• Authors: Fu-Han Gong; Wen-Lin Cheng; Haiping Wang; Maomao Gao; Juan-Juan Qin; Yan Zhang; Xia Li; Xueyong Zhu; Hao Xia; Zhi-Gang She
• Keywords: Knockout mouse; Inflammatory response

Atherosclerosis is considered to be a chronic inflammatory disease that can lead severe clinically important cardiovascular events. miR-150 small noncoding RNA significantly enhances responses by upregulating endothelial cell proliferation and migration, as well intravascular environmental homeostasis. However, the exact role of in atherosclerosis remains unknown. Here, we investigated effect deficiency on development. Using double-knockout (miR-150-/- ApoE-/-) mice, measured atherosclerotic lesion size stability. Meanwhile, conducted vivo bone marrow transplantation identify cellular-level components response. Compared with mice deficient only ApoE, had smaller lesions displayed an attenuated Moreover, ablation promoted plaque stabilization via increases smooth muscle collagen content decreased macrophage infiltration lipid accumulation. The vitro experiments indicated response results directly from upregulated expression cytoskeletal protein, PDZ LIM domain 1 (PDLIM1), macrophages. More importantly, decreases phosphorylated p65 cytokine secretion induced were reversed PDLIM1 knockdown. These findings suggest promising target for management atherosclerosis.