PMID- 27487299
OWN - NLM
STAT- MEDLINE
DCOM- 20170509
LR  - 20220318
IS  - 1423-0135 (Electronic)
IS  - 1018-1172 (Linking)
VI  - 53
IP  - 1-2
DP  - 2016
TI  - C-Reactive Protein and Inflammatory Cytokines during Percutaneous Coronary 
      Intervention.
PG  - 39-48
AB  - BACKGROUND: C-reactive protein (CRP) is significantly associated with 
      cardiovascular diseases; however, whether CRP plays a causal role in coronary 
      artery disease has yet to be determined. In addition, the relationship between 
      CRP, atherosclerosis, and inflammation remains controversial. METHODS AND 
      RESULTS: Serum interleukin (IL)-6, IL-1beta, and CRP levels were determined in 160 
      patients at time points around percutaneous coronary intervention (PCI) with 
      drug-eluting stent implantation. The levels were found to be at peak at 24 h 
      post-PCI and gradually declined to the level before PCI at day 30 post-PCI. These 
      inflammation markers around PCI have no statistical difference in the different 
      postdilation pressures (</=14, 14-18, and >/=18 atm) and stent number (1 and >/=2 
      stents) groups. Treatment of cultured human vascular smooth muscle cells (VSMCs) 
      with a combination of IL-6 and IL-1beta at concentrations associated with PCI did 
      not result in any significant change in the CRP mRNA levels. The IL-6-augmented 
      CRP expression in human internal mammary arteries (IMAs) stretched with a 
      mechanical strength of 3 g was blocked by the nuclear factor-kappaB (NF-kappaB) peptide 
      inhibitor SN50 and not by the inactive SN50 analog SN50M. IL-6 treatment 
      increased NF-kappaB activity in human IMAs stretched with 3 g, and this effect was 
      further blocked by stretch-activated channel (SAC) inhibitors (streptomycin or 
      GdCl3) and SN50. CONCLUSIONS: The current study provides evidence that increased 
      serum IL-6, IL-1beta, and CRP levels around PCI are not different between different 
      postdilation pressure and stent number groups. The combination of IL-6 and IL-1beta 
      at concentrations associated with PCI cannot induce CRP expression in human 
      VSMCs, but they can augment mechanical strain-induced CRP synthesis via the 
      SAC-NF-kappaB pathway in human IMAs.
CI  - (c) 2016 S. Karger AG, Basel.
FAU - Wu, Mingxin
AU  - Wu M
AD  - Division of Cardiology, Xiangtan Central Hospital, Xiangtan, PR China.
FAU - Gu, Xinyuan
AU  - Gu X
FAU - Li, Xiujuan
AU  - Li X
FAU - Li, Yanhui
AU  - Li Y
FAU - Zhou, Huaineng
AU  - Zhou H
FAU - Lu, Guihua
AU  - Lu G
FAU - Wu, ZhongKai
AU  - Wu Z
FAU - Huang, He
AU  - Huang H
FAU - Tang, Lilong
AU  - Tang L
FAU - Zeng, Jianping
AU  - Zeng J
LA  - eng
PT  - Journal Article
DEP - 20160804
PL  - Switzerland
TA  - J Vasc Res
JT  - Journal of vascular research
JID - 9206092
RN  - 0 (IL1B protein, human)
RN  - 0 (IL6 protein, human)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Interleukin-1beta)
RN  - 0 (Interleukin-6)
RN  - 0 (Ion Channels)
RN  - 0 (NF-kappa B)
RN  - 9007-41-4 (C-Reactive Protein)
SB  - IM
MH  - Aged
MH  - Angioplasty, Balloon, Coronary/instrumentation
MH  - C-Reactive Protein/genetics/*metabolism
MH  - Cells, Cultured
MH  - Coronary Artery Disease/blood/diagnostic imaging/genetics/*therapy
MH  - Drug-Eluting Stents
MH  - Female
MH  - Gene Expression Regulation
MH  - Humans
MH  - Inflammation Mediators/*blood
MH  - Interleukin-1beta/*blood
MH  - Interleukin-6/*blood
MH  - Ion Channel Gating
MH  - Ion Channels/metabolism
MH  - Male
MH  - Mammary Arteries/metabolism
MH  - Mechanotransduction, Cellular
MH  - Middle Aged
MH  - Muscle, Smooth, Vascular/metabolism
MH  - Myocytes, Smooth Muscle/metabolism
MH  - NF-kappa B/metabolism
MH  - Pressure
MH  - Stress, Mechanical
MH  - Time Factors
EDAT- 2016/10/19 06:00
MHDA- 2017/05/10 06:00
CRDT- 2016/08/04 06:00
PHST- 2015/12/16 00:00 [received]
PHST- 2016/06/10 00:00 [accepted]
PHST- 2016/10/19 06:00 [pubmed]
PHST- 2017/05/10 06:00 [medline]
PHST- 2016/08/04 06:00 [entrez]
AID - 000447558 [pii]
AID - 10.1159/000447558 [doi]
PST - ppublish
SO  - J Vasc Res. 2016;53(1-2):39-48. doi: 10.1159/000447558. Epub 2016 Aug 4.