PMID- 30018722
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201001
IS  - 1943-8141 (Print)
IS  - 1943-8141 (Electronic)
IS  - 1943-8141 (Linking)
VI  - 10
IP  - 6
DP  - 2018
TI  - Apolipoprotein B-100 peptide 210 antibody inhibits atherosclerosis by regulation 
      of macrophages that phagocytize oxidized lipid.
PG  - 1817-1828
AB  - Immunization with peptides derived from apolipoprotein B-100 (ApoB-100) has been 
      shown to ameliorate atherosclerosis in apolipoprotein E knockout (ApoE(-/-)) 
      mice. However, the exact mechanism underlying the therapeutic effects remains 
      elusive. To shed light on this mechanism, we immunized ApoE(-/-) mice that were 
      fed a Western diet with either malondialdehyde-modified ApoB-100 peptide 210 
      (P210) emulsified in Freund's adjuvant or anti-malondialdehyde-modified P210 
      antibody (P210-Ab). Mice immunized with Freund's adjuvant or bovine serum albumin 
      served as controls. Macrophages were incubated in vitro with oxidized low-density 
      lipoprotein (ox-LDL) or ox-LDL plus P210-Ab. Our results show that P210-Ab 
      promoted cholesterol efflux, inhibited lipid accumulation in vitro, and reduced 
      plasma levels of high-sensitivity C-reactive protein (hsCRP), monocyte 
      chemoattractant protein-1 (MCP-1), tumor necrosis factor-alpha (TNF-alpha), and 
      interleukin-6 (IL-6). Furthermore, dramatically increased the expression of Fc 
      receptors (FcR) on peripheral blood mononuclear macrophages, suggesting that the 
      mechanism of phagocytosis of ox-LDL by mononuclear macrophages may rely more on 
      FcR than the cluster of differentiation 36 (CD36) scavenger receptor with 
      P210-Ab. Both in vitro and in vivo, P210-Ab triggered the promoter of ATP-binding 
      cassette transporter A1 (ABCA1) to increase peroxisome proliferator-activated 
      receptor alpha (alpha) activity and inhibit the nuclear factor 
      kappa-light-chain-enhancer of activated B cells (NF-kappaB) pathway. In addition, 
      P210-Ab significantly attenuated macrophage infiltration and markedly improved 
      the stability of atheromatous plaque. In conclusion, the anti-atherosclerotic 
      effect of P210-Ab is related to its preferential inhibition of inflammation and 
      reversion of cholesterol transportation by altering the pathway by which 
      macrophages phagocytize ox-LDL.
FAU - Zeng, Zhuanglin
AU  - Zeng Z
AD  - Laboratory of Cardiovascular Immunology, Key Laboratory of Molecular Targeted 
      Therapies of The Ministry of Education, Institute of Cardiology, Union Hospital, 
      Tongji Medical College of Huazhong University of Science and Technology Wuhan 
      430022, Hubei, China.
FAU - Cao, Bingxin
AU  - Cao B
AD  - Laboratory of Cardiovascular Immunology, Key Laboratory of Molecular Targeted 
      Therapies of The Ministry of Education, Institute of Cardiology, Union Hospital, 
      Tongji Medical College of Huazhong University of Science and Technology Wuhan 
      430022, Hubei, China.
FAU - Guo, Xiaopeng
AU  - Guo X
AD  - Department of Interventional Radiology, Union Hospital, Tongji Medical College of 
      Huazhong University of Science and Technology Wuhan 430022, Hubei, China.
FAU - Li, Weijuan
AU  - Li W
AD  - Laboratory of Cardiovascular Immunology, Key Laboratory of Molecular Targeted 
      Therapies of The Ministry of Education, Institute of Cardiology, Union Hospital, 
      Tongji Medical College of Huazhong University of Science and Technology Wuhan 
      430022, Hubei, China.
FAU - Li, Songhai
AU  - Li S
AD  - Laboratory of Cardiovascular Immunology, Key Laboratory of Molecular Targeted 
      Therapies of The Ministry of Education, Institute of Cardiology, Union Hospital, 
      Tongji Medical College of Huazhong University of Science and Technology Wuhan 
      430022, Hubei, China.
FAU - Chen, Juan
AU  - Chen J
AD  - Laboratory of Cardiovascular Immunology, Key Laboratory of Molecular Targeted 
      Therapies of The Ministry of Education, Institute of Cardiology, Union Hospital, 
      Tongji Medical College of Huazhong University of Science and Technology Wuhan 
      430022, Hubei, China.
FAU - Zhou, Wenping
AU  - Zhou W
AD  - Laboratory of Cardiovascular Immunology, Key Laboratory of Molecular Targeted 
      Therapies of The Ministry of Education, Institute of Cardiology, Union Hospital, 
      Tongji Medical College of Huazhong University of Science and Technology Wuhan 
      430022, Hubei, China.
FAU - Zheng, Chuansheng
AU  - Zheng C
AD  - Department of Interventional Radiology, Union Hospital, Tongji Medical College of 
      Huazhong University of Science and Technology Wuhan 430022, Hubei, China.
FAU - Wei, Yumiao
AU  - Wei Y
AD  - Laboratory of Cardiovascular Immunology, Key Laboratory of Molecular Targeted 
      Therapies of The Ministry of Education, Institute of Cardiology, Union Hospital, 
      Tongji Medical College of Huazhong University of Science and Technology Wuhan 
      430022, Hubei, China.
LA  - eng
PT  - Journal Article
DEP - 20180615
PL  - United States
TA  - Am J Transl Res
JT  - American journal of translational research
JID - 101493030
PMC - PMC6038070
OTO - NOTNLM
OT  - P210
OT  - atherosclerosis
OT  - cholesterol efflux
OT  - inflammation
OT  - macrophages
COIS- None.
EDAT- 2018/07/19 06:00
MHDA- 2018/07/19 06:01
PMCR- 2018/06/15
CRDT- 2018/07/19 06:00
PHST- 2018/01/25 00:00 [received]
PHST- 2018/05/14 00:00 [accepted]
PHST- 2018/07/19 06:00 [entrez]
PHST- 2018/07/19 06:00 [pubmed]
PHST- 2018/07/19 06:01 [medline]
PHST- 2018/06/15 00:00 [pmc-release]
PST - epublish
SO  - Am J Transl Res. 2018 Jun 15;10(6):1817-1828. eCollection 2018.