PMID- 25703422
OWN - NLM
STAT- MEDLINE
DCOM- 20160212
LR  - 20201231
IS  - 1874-1754 (Electronic)
IS  - 0167-5273 (Linking)
VI  - 184
DP  - 2015 Apr 1
TI  - Transient carotid ischemia as a remote conditioning stimulus for myocardial 
      protection in anesthetized rabbits: Insights into intracellular signaling.
PG  - 140-151
LID - S0167-5273(15)00106-0 [pii]
LID - 10.1016/j.ijcard.2015.01.079 [doi]
AB  - BACKGROUND: We investigated the effectiveness of perconditioning (Perc) applied 
      at different time points along with the role of RISK, SAFE, STAT5 and eNOS 
      pathways. METHODS AND RESULTS: Anesthetized rabbits were subjected to 30-min 
      ischemia/3-hour reperfusion. Perc, consisted of 4 cycles of 1-min 
      ischemia/reperfusion, was applied in the carotid artery at different time points. 
      Perc was started and ended during ischemia, started during ischemia and ended at 
      the beginning of reperfusion, started at the end of ischemia and ended at 
      reperfusion and started and ended during reperfusion. The PI3K inhibitor 
      wortmannin, or the JAK-2 inhibitor AG490, was also applied and the infarct size 
      was assessed. In another series assigned to the previous groups, the 
      phosphorylation of Akt, PI3K, ERKs1/2, GSK3beta, STAT3, and STAT5 was evaluated. All 
      Perc groups had smaller infarction compared to those without Perc, independently 
      of PI3K or JAK-2 inhibition. STAT5 was the only molecule that was phosphorylated 
      in parallel with cardioprotection. Since Src and angiotensin II mediate the STAT5 
      pathway, we administered the Scr inhibitor PP1 and the angiotensin II receptor 
      antagonist valsartan. PP1 and valsartan prevented STAT5 phosphorylation, but did 
      not abrogate the effect of Perc. Furthermore, the NOS inhibitor L-NAME was 
      administered and abrogated the infarct size limiting effect of Perc. In parallel, 
      the expression of cleaved caspase-3 was elevated only in the control and 
      Perc-A-L-NAME groups. CONCLUSION: Perc reduces infarction independently of RISK, 
      SAFE and STAT5 pathways. Src kinase and angiotensin II play a predominant role in 
      STAT5 activation. eNOS may protect the myocardium through inhibition of 
      apoptosis.
CI  - Copyright (c) 2015 Elsevier Ireland Ltd. All rights reserved.
FAU - Andreadou, Ioanna
AU  - Andreadou I
AD  - Department of Pharmaceutical Chemistry, University of Athens School of Pharmacy, 
      Athens, Greece. Electronic address: jandread@pharm.uoa.gr.
FAU - Bibli, Sofia-Iris
AU  - Bibli SI
AD  - Department of Pharmaceutical Chemistry, University of Athens School of Pharmacy, 
      Athens, Greece.
FAU - Mastromanolis, Emmanuel
AU  - Mastromanolis E
AD  - Second Department of Cardiology, University of Athens Medical School, Attikon 
      University Hospital, Athens, Greece.
FAU - Zoga, Anastasia
AU  - Zoga A
AD  - Second Department of Cardiology, University of Athens Medical School, Attikon 
      University Hospital, Athens, Greece.
FAU - Efentakis, Panagiotis
AU  - Efentakis P
AD  - Department of Pharmaceutical Chemistry, University of Athens School of Pharmacy, 
      Athens, Greece.
FAU - Papaioannou, Nikolaos
AU  - Papaioannou N
AD  - Department of Pathology, School of Health Sciences, Faculty of Veterinary 
      Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece.
FAU - Farmakis, Dimitrios
AU  - Farmakis D
AD  - Second Department of Cardiology, University of Athens Medical School, Attikon 
      University Hospital, Athens, Greece.
FAU - Kremastinos, Dimitrios Th
AU  - Kremastinos DT
AD  - Second Department of Cardiology, University of Athens Medical School, Attikon 
      University Hospital, Athens, Greece.
FAU - Iliodromitis, Efstathios K
AU  - Iliodromitis EK
AD  - Second Department of Cardiology, University of Athens Medical School, Attikon 
      University Hospital, Athens, Greece.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150207
PL  - Netherlands
TA  - Int J Cardiol
JT  - International journal of cardiology
JID - 8200291
SB  - IM
CIN - Int J Cardiol. 2015 May 6;187:443-4. PMID: 25841145
MH  - Animals
MH  - Carotid Arteries/*metabolism/pathology
MH  - Intracellular Fluid/*metabolism
MH  - Ischemic Preconditioning, Myocardial/*methods
MH  - Male
MH  - Myocardial Infarction/*metabolism/pathology/prevention & control
MH  - Myocardial Ischemia/metabolism/pathology/prevention & control
MH  - Rabbits
MH  - Signal Transduction/*physiology
OTO - NOTNLM
OT  - Cardioprotection
OT  - Perconditioning
OT  - RISK
OT  - SAFE
OT  - STAT5
OT  - eNOS
EDAT- 2015/02/24 06:00
MHDA- 2016/02/13 06:00
CRDT- 2015/02/24 06:00
PHST- 2014/09/30 00:00 [received]
PHST- 2014/12/09 00:00 [revised]
PHST- 2015/01/25 00:00 [accepted]
PHST- 2015/02/24 06:00 [entrez]
PHST- 2015/02/24 06:00 [pubmed]
PHST- 2016/02/13 06:00 [medline]
AID - S0167-5273(15)00106-0 [pii]
AID - 10.1016/j.ijcard.2015.01.079 [doi]
PST - ppublish
SO  - Int J Cardiol. 2015 Apr 1;184:140-151. doi: 10.1016/j.ijcard.2015.01.079. Epub 
      2015 Feb 7.