Immunization with advanced glycation end products modified low density lipoprotein inhibits atherosclerosis progression in diabetic apoE and LDLR null mice
Zhu, Lin ; He, Zhiqing ; Wu, Feng ; Ding, Ru ; Jiang, Qixia ; Zhang, Jiayou ; Fan, Min ; Wang, Xing ; Bengtsson, Eva LU
and Nilsson, Jan
LU
, et al.
(2014)
In Cardiovascular Diabetology
13.
- 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... (More)
- 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. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/4965656
- author
- Zhu, Lin
; He, Zhiqing
; Wu, Feng
; Ding, Ru
; Jiang, Qixia
; Zhang, Jiayou
; Fan, Min
; Wang, Xing
; Bengtsson, Eva
LU
and Nilsson, Jan
LU
, et al. (More)
- Zhu, Lin
; He, Zhiqing
; Wu, Feng
; Ding, Ru
; Jiang, Qixia
; Zhang, Jiayou
; Fan, Min
; Wang, Xing
; Bengtsson, Eva
LU
; Nilsson, Jan
LU
; Liang, Chun
and Wu, Zonggui
(Less)
- organization
- publishing date
- 2014
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Immunization, Advanced glycation end products, Low density lipoprotein, Atherosclerosis, Diabetes
- in
- Cardiovascular Diabetology
- volume
- 13
- article number
- 151
- publisher
- BioMed Central (BMC)
- external identifiers
-
- wos:000346064300001
- scopus:84920847396
- pmid:25391642
- ISSN
- 1475-2840
- DOI
- 10.1186/s12933-014-0151-6
- language
- English
- LU publication?
- yes
- id
- 819656da-1cd1-4040-85ff-153ac8433a4f (old id 4965656)
- date added to LUP
- 2016-04-01 13:07:17
- date last changed
- 2022-03-29 05:39:46
@article{819656da-1cd1-4040-85ff-153ac8433a4f,
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.}},
author = {{Zhu, Lin and He, Zhiqing and Wu, Feng and Ding, Ru and Jiang, Qixia and Zhang, Jiayou and Fan, Min and Wang, Xing and Bengtsson, Eva and Nilsson, Jan and Liang, Chun and Wu, Zonggui}},
issn = {{1475-2840}},
keywords = {{Immunization; Advanced glycation end products; Low density lipoprotein; Atherosclerosis; Diabetes}},
language = {{eng}},
publisher = {{BioMed Central (BMC)}},
series = {{Cardiovascular Diabetology}},
title = {{Immunization with advanced glycation end products modified low density lipoprotein inhibits atherosclerosis progression in diabetic apoE and LDLR null mice}},
url = {{https://lup.lub.lu.se/search/files/3170218/7695372}},
doi = {{10.1186/s12933-014-0151-6}},
volume = {{13}},
year = {{2014}},
}