PMID- 30519072
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220330
IS  - 1178-7031 (Print)
IS  - 1178-7031 (Electronic)
IS  - 1178-7031 (Linking)
VI  - 11
DP  - 2018
TI  - The upregulated scavenger receptor CD36 is associated with the progression of 
      nontarget lesions after stent implantation in atherosclerotic rabbits.
PG  - 447-456
LID - 10.2147/JIR.S179814 [doi]
AB  - BACKGROUND: The incidence of recurrent cardiovascular events from the progression 
      of nontarget lesions (NTLs) is high for percutaneous coronary 
      intervention-treated patients. However, the underlying mechanisms have not been 
      thoroughly elucidated. METHODS: In this study, ten atherosclerotic rabbits with 
      multiple plaques in the upper and lower segments of abdominal aorta (group A) 
      were randomly divided into two subgroups: group A1 underwent intravascular 
      ultrasound examination and stent implantation in the lower segments of the 
      abdominal aorta (n=5), whereas group A2 was without stenting (n=5). Group B was a 
      control group without balloon injury. The serum levels of high-sensitivity CRP, 
      interleukin-6 (IL-6), oxidized low-density lipoprotein, and CD36 were assessed 
      via ELISA at five time points between the 10th and 18th weeks. The upper 
      abdominal aorta was examined via the immunohistochemical stain and Western 
      blotting of matrix metallopeptidase 9 (MMP-9), CD36, IL-6, and tumor necrosis 
      factor alpha. RESULTS: As a result, we found that stent implantation aggravated serum 
      levels of CD36, oxidative stress, and inflammatory cytokines. Meanwhile, the 
      upper abdominal arterial plaque burden significantly increased after stenting by 
      intravascular ultrasound. Immunohistochemistry and Western blotting showed that 
      the local NTLs' matrix metallopeptidase 9, CD36, IL-6, and tumor necrosis factor 
      alpha expressions in group A1 were significantly higher than those in groups A2 and B 
      (P<0.05-0.01). More importantly, a strong correlation was identified between CD36 
      expression and NTLs' plaque burden before the rabbits were killed. CONCLUSION: 
      Taken together, stent implantation accelerated inflammation, induced oxidative 
      stress, and increased the NTLs' progression, which were associated with the 
      upregulated CD36 expression.
FAU - Li, Ruijian
AU  - Li R
AD  - Department of Emergency, Qilu Hospital, Shandong University, Jinan, China, 
      liruijian2003@sdu.edu.cn; chen82169307@163.com.
AD  - Key Laboratory of Emergency and Critical Care Medicine of Shandong Province, Qilu 
      Hospital, Shandong University, Jinan, China, liruijian2003@sdu.edu.cn; 
      chen82169307@163.com.
AD  - Key Laboratory of Cardiovascular Remodeling & Function Research, Chinese Ministry 
      of Education & Chinese Ministry of Public Health, Qilu Hospital, Shandong 
      University, Jinan, China, liruijian2003@sdu.edu.cn; chen82169307@163.com.
FAU - Cui, Sumei
AU  - Cui S
AD  - Department of Emergency, Qilu Hospital, Shandong University, Jinan, China, 
      liruijian2003@sdu.edu.cn; chen82169307@163.com.
AD  - Key Laboratory of Emergency and Critical Care Medicine of Shandong Province, Qilu 
      Hospital, Shandong University, Jinan, China, liruijian2003@sdu.edu.cn; 
      chen82169307@163.com.
AD  - Key Laboratory of Cardiovascular Remodeling & Function Research, Chinese Ministry 
      of Education & Chinese Ministry of Public Health, Qilu Hospital, Shandong 
      University, Jinan, China, liruijian2003@sdu.edu.cn; chen82169307@163.com.
FAU - Xu, Youshun
AU  - Xu Y
AD  - Qilu Medical College of Shandong University, Jinan, China.
FAU - Xing, Junhui
AU  - Xing J
AD  - Department of Cardiology, First Affiliated Hospital of Zhengzhou University, 
      Zhengzhou, China.
FAU - Xue, Li
AU  - Xue L
AD  - Department of Emergency, Qilu Hospital, Shandong University, Jinan, China, 
      liruijian2003@sdu.edu.cn; chen82169307@163.com.
AD  - Key Laboratory of Emergency and Critical Care Medicine of Shandong Province, Qilu 
      Hospital, Shandong University, Jinan, China, liruijian2003@sdu.edu.cn; 
      chen82169307@163.com.
AD  - Key Laboratory of Cardiovascular Remodeling & Function Research, Chinese Ministry 
      of Education & Chinese Ministry of Public Health, Qilu Hospital, Shandong 
      University, Jinan, China, liruijian2003@sdu.edu.cn; chen82169307@163.com.
FAU - Chen, Yuguo
AU  - Chen Y
AD  - Department of Emergency, Qilu Hospital, Shandong University, Jinan, China, 
      liruijian2003@sdu.edu.cn; chen82169307@163.com.
AD  - Key Laboratory of Emergency and Critical Care Medicine of Shandong Province, Qilu 
      Hospital, Shandong University, Jinan, China, liruijian2003@sdu.edu.cn; 
      chen82169307@163.com.
AD  - Key Laboratory of Cardiovascular Remodeling & Function Research, Chinese Ministry 
      of Education & Chinese Ministry of Public Health, Qilu Hospital, Shandong 
      University, Jinan, China, liruijian2003@sdu.edu.cn; chen82169307@163.com.
LA  - eng
PT  - Journal Article
DEP - 20181113
PL  - New Zealand
TA  - J Inflamm Res
JT  - Journal of inflammation research
JID - 101512684
PMC - PMC6239100
OTO - NOTNLM
OT  - CD36
OT  - atherosclerosis
OT  - inflammation
OT  - oxidative stress
OT  - stent
COIS- Disclosure The authors report no conflicts of interest in this work.
EDAT- 2018/12/07 06:00
MHDA- 2018/12/07 06:01
PMCR- 2018/11/13
CRDT- 2018/12/07 06:00
PHST- 2018/12/07 06:00 [entrez]
PHST- 2018/12/07 06:00 [pubmed]
PHST- 2018/12/07 06:01 [medline]
PHST- 2018/11/13 00:00 [pmc-release]
AID - jir-11-447 [pii]
AID - 10.2147/JIR.S179814 [doi]
PST - epublish
SO  - J Inflamm Res. 2018 Nov 13;11:447-456. doi: 10.2147/JIR.S179814. eCollection 
      2018.