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Deletion of Ppard in CD11c+ cells attenuates atherosclerosis in ApoE knockout mice

Danyang Tian1,2, Huiling Hong1, Wenbin Shang1

  • 1School of Biomedical Sciences, Institute of Vascular Medicine, the Chinese University of Hong Kong, Shatin, Hong Kong.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|January 11, 2020
PubMed

Insights

Peroxisome proliferator-activated receptor delta (PPARδ) in antigen-presenting cells promotes atherosclerosis by activating myeloid dendritic cells and polarizing T cells. Deleting PPARδ in these cells reduces plaque formation and immune cell infiltration.

Area of Science:

  • Immunology
  • Molecular Biology
  • Cardiovascular Research

Background:

  • Peroxisome proliferator-activated receptor delta (PPARδ) is a nuclear receptor involved in lipid metabolism and other cellular functions.
  • The role of antigen-presenting cells (APCs) in atherosclerosis development is complex and not fully understood.
  • PPARδ's function in APCs, particularly dendritic cells (DCs), during atherosclerosis needs further elucidation.

Purpose of the Study:

  • To investigate the role of PPARδ in CD11c+ cells in the development of atherosclerosis.
  • To determine how PPARδ deletion in APCs affects immune cell activation, differentiation, and migration in the context of atherosclerosis.

Main Methods:

  • Conditional deletion of the Ppard gene in CD11c+ cells using the Cre-loxP system in Apoe-/- mice.
  • Induction of atherosclerosis via a high-cholesterol diet.
  • Analysis of atherosclerotic plaque formation, immune cell infiltration, DC activation, and T cell polarization.
  • Assessment of DC migration to lymph nodes and co-stimulatory molecule/cytokine expression in bone marrow-derived DCs.

Main Results:

  • PPARδ deficiency in CD11c+ cells significantly attenuated atherosclerotic plaque formation.
  • Reduced infiltration of myeloid-derived dendritic cells and T lymphocytes was observed.
  • Dendritic cell activation and T cell differentiation into Th1 cells were decreased.
  • DC migration to lymph nodes was diminished, and palmitic acid-induced pro-inflammatory responses in DCs were reduced.

Conclusions:

  • PPARδ activation by fatty acids promotes myeloid DC activation and subsequent T lymphocyte polarization, contributing to atherosclerosis in Apoe-/- mice.
  • PPARδ plays a regulatory role in antigen presentation, orchestrating immune responses during atherosclerosis.
  • Targeting PPARδ in APCs may offer a therapeutic strategy for atherosclerosis.
Keywords:
PPARdeltaatherosclerosisdendritic cellsinflammation

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