Immunization with advanced glycation end products modified low density lipoprotein inhibits atherosclerosis progression in diabetic apoE and LDLR null mice

Lin Zhu, Zhiqing He, Feng Wu, Ru Ding, Qixia Jiang, Jiayou Zhang, Min Fan, Xing Wang, Eva Bengtsson, Jan Nilsson, Chun Liang, Zonggui Wu

Research output: Contribution to journalArticlepeer-review

13 Citations (SciVal)
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Abstract

Background: Diabetes accelerates atherosclerosis through undefined molecular mechanisms. Hyperglycemia induces formation of advanced glycation end product (AGE)-modified low-density lipoprotein (LDL). Anti-AGE-LDL autoantibodies favor atherosclerosis (AS) progression in humans, while anti oxidized LDL immunization inhibits AS in hypercholesterolemic, non-diabetic mice. We here investigated if AGE-LDL immunization protects against AS in diabetic mice. Methods: After diabetes induction with streptozotocin and high fat diet, both low density lipoprotein receptor (LDLR)(-/-) and apoE female mice were randomized to: AGE-LDL immunization with aluminum hydroxide (Alum) adjuvant; Alum alone; or PBS. Results: AGE-LDL immunization: significantly reduced AS; induced specific plasma IgM and IgG antibodies; upregulated splenic Th2, Treg and IL-10 levels, without altering Th1 or Th17 cells; and increased serum high density lipoprotein(HDL) while numerically lowering HbA1c levels. Conclusions: Subcutaneous immunization with AGE-LDL significantly inhibits atherosclerosis progression in hyperlipidemic diabetic mice possibly through activation of specific humoral and cell mediated immune responses and metabolic control improvement.
Original languageEnglish
Article number151
JournalCardiovascular Diabetology
Volume13
DOIs
Publication statusPublished - 2014

Subject classification (UKÄ)

  • Cardiac and Cardiovascular Systems

Keywords

  • Immunization
  • Advanced glycation end products
  • Low density lipoprotein
  • Atherosclerosis
  • Diabetes

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