PMID- 20207814
OWN - NLM
STAT- MEDLINE
DCOM- 20100518
LR  - 20200930
IS  - 1522-1539 (Electronic)
IS  - 0363-6135 (Linking)
VI  - 298
IP  - 5
DP  - 2010 May
TI  - The calcineurin-myocyte enhancer factor 2c pathway mediates cardiac hypertrophy 
      induced by endoplasmic reticulum stress in neonatal rat cardiomyocytes.
PG  - H1499-509
LID - 10.1152/ajpheart.00980.2009 [doi]
AB  - Endoplasmic reticulum (ER) stress (ERS) is involved in various cardiovascular 
      diseases. Our previous study verified that ERS took part in the development of 
      cardiac hypertrophy; however, its mechanism is still unclear. This study aimed to 
      investigate the roles of the calcineurin (CaN) signal pathway in hypertrophy 
      induced by the ERS inductor thapsigargin (TG) in neonatal cardiomyocytes from 
      Sprague-Dawley rats. Investigation of ER chaperone expression, ER staining, and 
      calreticulin immunofluorescence were used to detect the ERS response. mRNA 
      expression of atrial natriuretic peptide and brain natriuretic peptide, total 
      protein synthesis rate, and cell surface area were used to evaluate cardiac 
      hypertrophy induced by TG. TG induced a significant ERS response along with 
      hypertrophy in a dose- and time-dependent manner in cardiomyocytes, which was 
      verified by treatment with tunicamycin, another ERS inducer. Furthermore, TG 
      induced a significant elevation of the intracellular Ca(2+) level, CaN 
      activation, and myocyte enhancer factor 2c (MEF2c) expression in a dose- and 
      time-dependent manner in cardiomyocytes. Cyclosporine A, a CaN inhibitor, 
      markedly suppressed MEF2c nuclear translocation and inhibited TG-induced 
      hypertrophy. These results demonstrate that ERS induces cardiac hypertrophy and 
      that the CaN-MEF2c pathway is involved in ERS-induced hypertrophy in 
      cardiomyocytes.
FAU - Zhang, Zhen-Ying
AU  - Zhang ZY
AD  - Department of Pathophysiology, Chinese PLA General Hospital, 28 Fuxing Road, 
      Beijing, China.
FAU - Liu, Xiu-Hua
AU  - Liu XH
FAU - Hu, Wei-Cheng
AU  - Hu WC
FAU - Rong, Fei
AU  - Rong F
FAU - Wu, Xu-Dong
AU  - Wu XD
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20100305
PL  - United States
TA  - Am J Physiol Heart Circ Physiol
JT  - American journal of physiology. Heart and circulatory physiology
JID - 100901228
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (MEF2 Transcription Factors)
RN  - 0 (Myogenic Regulatory Factors)
RN  - 11089-65-9 (Tunicamycin)
RN  - 63231-63-0 (RNA)
RN  - 67526-95-8 (Thapsigargin)
RN  - 83HN0GTJ6D (Cyclosporine)
RN  - EC 1.1.1.27 (L-Lactate Dehydrogenase)
RN  - EC 3.1.3.16 (Calcineurin)
RN  - EC 3.6.3.8 (Sarcoplasmic Reticulum Calcium-Transporting ATPases)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Animals
MH  - Animals, Newborn/*physiology
MH  - Apoptosis/drug effects
MH  - Blotting, Western
MH  - Calcineurin/*physiology
MH  - Calcium/metabolism
MH  - Cardiomegaly/*pathology
MH  - Cell Size/drug effects
MH  - Cells, Cultured
MH  - Cyclosporine/pharmacology
MH  - Dose-Response Relationship, Drug
MH  - Endoplasmic Reticulum/*pathology
MH  - Enzyme Inhibitors/pharmacology
MH  - Fluorescent Antibody Technique
MH  - L-Lactate Dehydrogenase/metabolism
MH  - MEF2 Transcription Factors
MH  - Myocytes, Cardiac/*physiology
MH  - Myogenic Regulatory Factors/antagonists & inhibitors/*physiology
MH  - RNA/biosynthesis/isolation & purification
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Sarcoplasmic Reticulum Calcium-Transporting ATPases/metabolism
MH  - Signal Transduction/drug effects/*physiology
MH  - Thapsigargin/pharmacology
MH  - Tunicamycin/pharmacology
EDAT- 2010/03/09 06:00
MHDA- 2010/05/19 06:00
CRDT- 2010/03/09 06:00
PHST- 2010/03/09 06:00 [entrez]
PHST- 2010/03/09 06:00 [pubmed]
PHST- 2010/05/19 06:00 [medline]
AID - 00980.2009 [pii]
AID - 10.1152/ajpheart.00980.2009 [doi]
PST - ppublish
SO  - Am J Physiol Heart Circ Physiol. 2010 May;298(5):H1499-509. doi: 
      10.1152/ajpheart.00980.2009. Epub 2010 Mar 5.