PMID- 22465343
OWN - NLM
STAT- MEDLINE
DCOM- 20140402
LR  - 20220408
IS  - 1874-1754 (Electronic)
IS  - 0167-5273 (Linking)
VI  - 167
IP  - 3
DP  - 2013 Aug 10
TI  - Isoproterenol induced hypertrophy and associated signaling pathways are modulated 
      by somatostatin in H9c2 cells.
PG  - 1012-22
LID - S0167-5273(12)00282-3 [pii]
LID - 10.1016/j.ijcard.2012.03.077 [doi]
AB  - BACKGROUND: Somatostatin (SST), a growth hormone inhibitory peptide plays key 
      role in regulation of cell proliferation via modulation of mitogen activated 
      protein kinases (MAPKs) and cell survival pathway. In cardiac physiology, 
      beta-Adrenergic receptors (beta-ARs) play crucial role in regulation of downstream 
      signaling pathways in receptor specific manner. The aim of the current study was 
      to delineate the mechanistic insight for the role of SST on beta-AR mediated 
      signaling which promotes hypertrophy and apoptosis in rat fetal cardiomyocytes 
      (H9c2 cells). Accordingly, SST dependent changes in signaling molecules including 
      second messenger cAMP, PKA/CREB as well as MAPKs including ERK and p38 which are 
      key mediators of hypertrophy and apoptosis were analyzed. METHODS AND RESULTS: In 
      the present study, we determined receptor specific effects on intracellular cAMP 
      levels, signaling by western blot analysis and apoptosis by using JC-1 and 
      Hoechst-33258 staining. Here, we present the data which indicates that SST 
      inhibits isoproterenol induced hypertrophy and apoptosis in H9c2 cells. 
      Importantly, SST inhibits beta-ARs agonist induced cAMP activation and SST mediated 
      inhibition of cAMP was enhanced in presence of beta-ARs antagonist. SST enhances 
      beta2AR agonist formoterol mediated effects on PKA, CREB and ERK1/2 phosphorylations 
      whereas it inhibits isoproterenol mediated ERK1/2 and p38 signaling in 
      concentration dependent manner. CONCLUSIONS: Taken together, these results 
      presented here provide a novel insight for the potential role of SST in 
      regulation of beta-AR mediated effects on hypertrophy and modulation of hypertrophy 
      promoting signaling in H9c2 cells.
CI  - Copyright (c) 2012 Elsevier Ireland Ltd. All rights reserved.
FAU - Somvanshi, Rishi K
AU  - Somvanshi RK
AD  - Faculty of Pharmaceutical Sciences, The University of British Columbia, 
      Vancouver, BC, Canada V6T1Z3.
FAU - Qiu, Xiaofan
AU  - Qiu X
FAU - Kumar, Ujendra
AU  - Kumar U
LA  - eng
GR  - MOP 10268/Canadian Institutes of Health Research/Canada
GR  - MOP 74465/Canadian Institutes of Health Research/Canada
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120331
PL  - Netherlands
TA  - Int J Cardiol
JT  - International journal of cardiology
JID - 8200291
RN  - 51110-01-1 (Somatostatin)
RN  - L628TT009W (Isoproterenol)
SB  - IM
MH  - Animals
MH  - Cardiomegaly/blood/chemically induced/pathology
MH  - Cell Line
MH  - Isoproterenol/blood/pharmacology/*toxicity
MH  - Myocytes, Cardiac/*drug effects/*pathology
MH  - Rats
MH  - Signal Transduction/*drug effects/physiology
MH  - Somatostatin/blood/*pharmacology
OTO - NOTNLM
OT  - Adrenergic receptor
OT  - Cardiomyocytes
OT  - Hypertrophy
OT  - MAP kinase
OT  - Somatostatin
EDAT- 2012/04/03 06:00
MHDA- 2014/04/03 06:00
CRDT- 2012/04/03 06:00
PHST- 2011/10/18 00:00 [received]
PHST- 2012/01/06 00:00 [revised]
PHST- 2012/03/03 00:00 [accepted]
PHST- 2012/04/03 06:00 [entrez]
PHST- 2012/04/03 06:00 [pubmed]
PHST- 2014/04/03 06:00 [medline]
AID - S0167-5273(12)00282-3 [pii]
AID - 10.1016/j.ijcard.2012.03.077 [doi]
PST - ppublish
SO  - Int J Cardiol. 2013 Aug 10;167(3):1012-22. doi: 10.1016/j.ijcard.2012.03.077. 
      Epub 2012 Mar 31.