PMID- 30936987
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200930
IS  - 1792-0981 (Print)
IS  - 1792-1015 (Electronic)
IS  - 1792-0981 (Linking)
VI  - 17
IP  - 4
DP  - 2019 Apr
TI  - PDCD4 expression in coronary atherosclerosis rat models and its mechanism.
PG  - 3150-3154
LID - 10.3892/etm.2019.7296 [doi]
AB  - This study investigated the expression of programmed cell death protein 4 (PDCD4) 
      in rat models of coronary atherosclerosis (AS) and analyzed its role and 
      mechanism. A total of 80 Wistar rats were selected and divided into the control 
      group (n=40) and research group (n=40) according to the principle of similar body 
      weight, of which coronary AS models were established in rats in the research 
      group. PDCD4 expression in coronary artery tissues was detected using western 
      blotting, and the expression of interleukin-6 (IL-6) and IL-8 in the coronary 
      artery tissues were measured by means of reverse transcription-polymerase chain 
      reaction (RT-PCR). The apoptotic rate of coronary artery smooth muscle cells was 
      determined via terminal deoxynucleotidyl transferase-mediated dUTP nick end 
      labeling (TUNEL). The relative expression of PDCD4 in coronary artery tissues in 
      the research group was obviously higher than that in the control group, and the 
      difference was statistically significant (t=6.121, P<0.01). In terms of the 
      relative expression of messenger ribonucleic acid (mRNA) of IL-6 in the coronary 
      artery tissues, the research group had a remarkably higher level than the control 
      group, with a statistically significant difference (t=21.03, P<0.01). The 
      difference in the relative expression of IL-8 mRNA between the research group and 
      the control group was statistically significant, of which a much higher level was 
      detected in the research group (t=19.96, P<0.01). The apoptotic rate of smooth 
      muscle cells in the research group was increased notably compared with that in 
      the control group, and the difference was statistically significant (t=5.985, 
      P<0.01). PDCD4 may participate in the formation of coronary AS plaque, and its 
      possible function in the process is to inhibit the proliferation of vascular 
      smooth muscle cells and promote the upregulation of IL-6 and IL-8.
FAU - Gao, Yuhong
AU  - Gao Y
AD  - Department of Cardiology, Yidu Central Hospital of Weifang, Weifang, Shandong 
      262500, P.R. China.
FAU - Li, Hongmei
AU  - Li H
AD  - Department of Cardiology, Yidu Central Hospital of Weifang, Weifang, Shandong 
      262500, P.R. China.
FAU - Zhou, Yanchun
AU  - Zhou Y
AD  - Department of Psychology, Yidu Central Hospital of Weifang, Weifang, Shandong 
      262500, P.R. China.
FAU - Lv, Hongmei
AU  - Lv H
AD  - Department of Cardiovascular Medicine, Yidu Central Hospital of Weifang, Weifang, 
      Shandong 262500, P.R. China.
FAU - Chen, Yanping
AU  - Chen Y
AD  - Department of Cardiovascular Medicine, Weifang People's Hospital, Weifang, 
      Shandong 261041, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20190222
PL  - Greece
TA  - Exp Ther Med
JT  - Experimental and therapeutic medicine
JID - 101531947
PMC - PMC6434255
OTO - NOTNLM
OT  - IL-6
OT  - IL-8
OT  - PDCD4
OT  - coronary atherosclerosis
OT  - rat models
EDAT- 2019/04/03 06:00
MHDA- 2019/04/03 06:01
PMCR- 2019/02/22
CRDT- 2019/04/03 06:00
PHST- 2018/03/30 00:00 [received]
PHST- 2019/02/06 00:00 [accepted]
PHST- 2019/04/03 06:00 [entrez]
PHST- 2019/04/03 06:00 [pubmed]
PHST- 2019/04/03 06:01 [medline]
PHST- 2019/02/22 00:00 [pmc-release]
AID - ETM-0-0-7296 [pii]
AID - 10.3892/etm.2019.7296 [doi]
PST - ppublish
SO  - Exp Ther Med. 2019 Apr;17(4):3150-3154. doi: 10.3892/etm.2019.7296. Epub 2019 Feb 
      22.