scholarly journals Role of 17[beta]‐estradiol and estrogen receptor [beta] in the genomic response to hypertrophy

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Georgios Kararigas ◽  
Daniela Fliegner ◽  
Vera Regitz‐Zagrosek
2011 ◽  
Vol 43 (8) ◽  
pp. 438-446 ◽  
Author(s):  
Georgios Kararigas ◽  
Daniela Fliegner ◽  
Jan-Åke Gustafsson ◽  
Vera Regitz-Zagrosek

Cardiac hypertrophy, the adaptive response of the heart to overload, is a major risk factor for heart failure and sudden death. Estrogen (E2) and estrogen receptor beta (ERbeta) offer protection against hypertrophy and in the transition to heart failure. However, the underlying pathways remain incompletely defined. We employed a publicly available microarray dataset of female wild-type (WT) and ERbeta knockout (BERKO) mice subjected to pressure overload-induced hypertrophy to perform a systematic investigation of the mechanisms involved in the protection conferred by the E2/ERbeta axis. We show that considerably more genes were modulated in response to pressure overload in BERKO mice than in WT mice. The majority of the identified candidates in BERKO mice were induced, while those in WT mice were repressed. Pathway analysis revealed a similar pattern. This study is the first to demonstrate that the lack of ERbeta led to a significant increase of inflammatory pathways. Mitochondrial bioenergetics- and oxidative stress-related pathways were also modulated. In conclusion, ERbeta acquires the role of gatekeeper of the genomic response of the heart to pressure overload-induced hypertrophy. This may offer the molecular explanation for its cardioprotective role. We consider the present study to be a useful resource and that it will contribute to downstream functional analysis and to the characterization of pathways with previously unknown role in hypertrophy.


PLoS ONE ◽  
2013 ◽  
Vol 8 (5) ◽  
Author(s):  
Carine Bossard ◽  
Muriel Busson ◽  
David Vindrieux ◽  
Françoise Gaudin ◽  
Véronique Machelon ◽  
...  

PLoS ONE ◽  
2012 ◽  
Vol 7 (9) ◽  
pp. e44787 ◽  
Author(s):  
Carine Bossard ◽  
Muriel Busson ◽  
David Vindrieux ◽  
Françoise Gaudin ◽  
Véronique Machelon ◽  
...  

2009 ◽  
Vol 136 (5) ◽  
pp. A-762
Author(s):  
Jennifer Koetsier ◽  
Ramesh K. Wali ◽  
John Hart ◽  
Dhananjay Kunte ◽  
Laura K. Bianchi ◽  
...  

2006 ◽  
Vol 103 (8) ◽  
pp. 2959-2964 ◽  
Author(s):  
O. Wada-Hiraike ◽  
O. Imamov ◽  
H. Hiraike ◽  
K. Hultenby ◽  
T. Schwend ◽  
...  

2006 ◽  
Vol 103 (48) ◽  
pp. 18350-18355 ◽  
Author(s):  
O. Wada-Hiraike ◽  
H. Hiraike ◽  
H. Okinaga ◽  
O. Imamov ◽  
R. P. A. Barros ◽  
...  

Medicine ◽  
2021 ◽  
Vol 100 (7) ◽  
pp. e24398
Author(s):  
Fangxiang Mu ◽  
Minge Shi ◽  
Li Huang ◽  
Dafen Wang ◽  
Aiqun Shen

2017 ◽  
Author(s):  
Hanliang He ◽  
Chunqing Wang ◽  
Qifeng Tang ◽  
Fan Yang ◽  
Youjia Xu

AbstractMC3T3-E1 is a clonal pre-osteoblastic cell line derived from newborn mouse calvaria, which is commonly used in osteoblast studies. To investigate the effects of estrogen on osteoblasts, we treated MC3T3-E1 cells with various concentrations of estrogen and assessed their proliferation. Next, we performed RNA deep sequencing to investigate the effects on estrogen target genes. Bmpr1a and Tgfbr1, important participants in the TGF-beta signaling pathway, were down-regulated in our deep sequencing results. Bioinformatics analysis revealed that estrogen receptor response elements (EREs) were present in the Bmpr1a and Tgfbr1 promoters. Culturing the cells with the estrogen receptor (ER) alpha or beta antagonists 1,3-bis(4-hydroxyphenyl)-4-methyl-5-[4-(2-piperidinylethoxy)phenol]-1H-pyrazole dihydrochloride (MPP) or 4-[2-phenyl-5,7-bis(trifluoromethyl) pyrazolo[1,5-alpha]pyrimidin-3-yl] phenol (PTHPP), respectively, demonstrated that ER beta is involved in the estrogen-mediated repression of Tgfbr1 and Bmpr1a.The chromatin immunoprecipitation (ChIP) results were consistent with the conclusion that E2 increased the binding of ER beta at the EREs located in the Tgfbr1 and Bmpr1a promoters. Our research provides new insight into the role of estrogen in bone metabolisms.


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