Lack of Toll-like receptor 4 or myeloid differentiation factor 88 reduces atherosclerosis and alters plaque phenotype in mice deficient in apolipoprotein E
Cedars-Sinai Medical Center · University of California, Los Angeles · +1 more institution
Abstract
Toll-like receptors (TLRs) and the downstream adaptor molecule myeloid differentiation factor 88 (MyD88) play an essential role in the innate immune responses. Here, we demonstrate that genetic deficiency of TLR4 or MyD88 is associated with a significant reduction of aortic plaque areas in atherosclerosis-prone apolipoprotein E-deficient mice, despite persistent hypercholesterolemia, implying an important role for the innate immune system in atherogenesis. Apolipoprotein E-deficient mice that also lacked TLR4 or MyD88 demonstrated reduced aortic atherosclerosis that was associated with reductions in circulating levels of proinflammatory cytokines IL-12 or monocyte chemoattractant protein 1, plaque lipid…
Citation impact
- FWCI
- 16.38
- Percentile
- 100%
- References
- 58
Authors
9- KSKathrin S. Michelsen
Cedars-Sinai Medical Center, University of California, Los Angeles, The University of Osaka
- MWMichelle Wong
Cedars-Sinai Medical Center, University of California, Los Angeles, The University of Osaka
- PKPrediman K. Shah
Cedars-Sinai Medical Center, University of California, Los Angeles, The University of Osaka
- WZWenxuan Zhang
Cedars-Sinai Medical Center, University of California, Los Angeles, The University of Osaka
- JYJuliana Yano
Cedars-Sinai Medical Center, University of California, Los Angeles, The University of Osaka
Topics & keywords
- TLR4
- Innate immune system
- Proinflammatory cytokine
- Inflammation
- Apolipoprotein B
- Biology
- Immunology
- LDL receptor
- Good health and well-being