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

In English

Författare

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

Summary, in English

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.

Publiceringsår

2014

Språk

Engelska

Publikation/Tidskrift/Serie

Cardiovascular Diabetology

Volym

13

Dokumenttyp

Artikel i tidskrift

Förlag

BioMed Central (BMC)

Ämne

  • Cardiac and Cardiovascular Systems

Nyckelord

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

Status

Published

Forskningsgrupp

  • Cardiovascular Research - Immunity and Atherosclerosis

ISBN/ISSN/Övrigt

  • ISSN: 1475-2840