PMID- 20375266
OWN - NLM
STAT- MEDLINE
DCOM- 20100615
LR  - 20220318
IS  - 1522-1490 (Electronic)
IS  - 0363-6119 (Linking)
VI  - 298
IP  - 6
DP  - 2010 Jun
TI  - Female sex and estrogen receptor-beta attenuate cardiac remodeling and apoptosis 
      in pressure overload.
PG  - R1597-606
LID - 10.1152/ajpregu.00825.2009 [doi]
AB  - We investigated sex differences and the role of estrogen receptor-beta (ERbeta) 
      on myocardial hypertrophy in a mouse model of pressure overload. We performed 
      transverse aortic constriction (TAC) or sham surgery in male and female wild-type 
      (WT) and ERbeta knockout (ERbeta(-/-)) mice. All mice were characterized by 
      echocardiography and hemodynamic measurements and were killed 9 wk after surgery. 
      Left ventricular (LV) samples were analyzed by microarray profiling, real-time 
      RT-PCR, and histology. After 9 wk, WT males showed more hypertrophy and heart 
      failure signs than WT females. Notably, WT females developed a concentric form of 
      hypertrophy, while males developed eccentric hypertrophy. ERbeta deletion 
      augmented the TAC-induced increase in cardiomyocyte diameter in both sexes. Gene 
      expression profiling revealed that WT male hearts had a stronger induction of 
      matrix-related genes and a stronger repression of mitochondrial genes than WT 
      female hearts. ERbeta(-/-) mice exhibited a different transcriptional response. 
      ERbeta(-/-)/TAC mice of both sexes exhibited induction of proapoptotic genes with 
      a stronger expression in ERbeta(-/-) males. Cardiac fibrosis was more pronounced 
      in male WT/TAC than in female mice. This difference was abolished in ERbeta(-/-) 
      mice. The number of apoptotic nuclei was increased in both sexes of 
      ERbeta(-/-)/TAC mice, most prominent in males. Female sex offers protection 
      against ventricular chamber dilation in the TAC model. Both female sex and ERbeta 
      attenuate the development of fibrosis and apoptosis, thus slowing the progression 
      to heart failure.
FAU - Fliegner, Daniela
AU  - Fliegner D
AD  - Institute of Gender in Medicine, Charite-Medical University Berlin, Germany. 
      daniela.fliegner@charite.de
FAU - Schubert, Carola
AU  - Schubert C
FAU - Penkalla, Adam
AU  - Penkalla A
FAU - Witt, Henning
AU  - Witt H
FAU - Kararigas, Georgios
AU  - Kararigas G
FAU - Dworatzek, Elke
AU  - Dworatzek E
FAU - Staub, Eike
AU  - Staub E
FAU - Martus, Peter
AU  - Martus P
FAU - Ruiz Noppinger, Patricia
AU  - Ruiz Noppinger P
FAU - Kintscher, Ulrich
AU  - Kintscher U
FAU - Gustafsson, Jan-Ake
AU  - Gustafsson JA
FAU - Regitz-Zagrosek, Vera
AU  - Regitz-Zagrosek V
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20100407
PL  - United States
TA  - Am J Physiol Regul Integr Comp Physiol
JT  - American journal of physiology. Regulatory, integrative and comparative 
      physiology
JID - 100901230
RN  - 0 (Estrogen Receptor beta)
SB  - IM
EIN - Am J Physiol Regul Integr Comp Physiol. 2010 Sep;299(3):R981. Kararigas, George 
      [corrected to Kararigas, Georgios]
MH  - Animals
MH  - Aorta/pathology
MH  - Apoptosis
MH  - Constriction, Pathologic/pathology
MH  - Echocardiography
MH  - Estrogen Receptor beta/*genetics/*metabolism
MH  - Female
MH  - Gene Expression Profiling
MH  - Heart/*physiopathology
MH  - Heart Failure/pathology
MH  - Heart Ventricles/pathology
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Myocardium/metabolism/pathology
MH  - Myocytes, Cardiac/metabolism/pathology
MH  - Pressure
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - *Sex Characteristics
EDAT- 2010/04/09 06:00
MHDA- 2010/06/16 06:00
CRDT- 2010/04/09 06:00
PHST- 2010/04/09 06:00 [entrez]
PHST- 2010/04/09 06:00 [pubmed]
PHST- 2010/06/16 06:00 [medline]
AID - ajpregu.00825.2009 [pii]
AID - 10.1152/ajpregu.00825.2009 [doi]
PST - ppublish
SO  - Am J Physiol Regul Integr Comp Physiol. 2010 Jun;298(6):R1597-606. doi: 
      10.1152/ajpregu.00825.2009. Epub 2010 Apr 7.