PMID- 10652235
OWN - NLM
STAT- MEDLINE
DCOM- 20000301
LR  - 20220330
IS  - 0006-291X (Print)
IS  - 0006-291X (Linking)
VI  - 268
IP  - 1
DP  - 2000 Feb 5
TI  - 17beta-estradiol prevents programmed cell death in cardiac myocytes.
PG  - 192-200
AB  - The cardioprotective effects of estrogens are clearly established. However, the 
      underlying mechanisms are poorly understood. Because programmed cell death 
      (apoptosis) probably contributes to the loss of cardiac myocytes in heart failure 
      and because estrogens prevent apoptosis in breast cancer cells, we investigated 
      whether the loss of cardiac myocytes by programmed cell death could be prevented 
      by physiological doses of 17beta-estradiol. Apoptosis of cultured cardiac 
      myocytes was induced by staurosporine. 17beta-estradiol (10 nM) had an 
      antiapoptotic effect as determined by morphological analysis, vital staining 
      using the Hoechst dye 33342 and terminal transferase dUTP nick-end labeling 
      (TUNEL). As a potential mechanism for the antiapoptotic effect of 
      17beta-estradiol we found a reduced activity of the ICE-like protease caspase-3 
      in hormone-treated myocytes. Furthermore, inhibition of apoptosis by estradiol 
      was associated with a reduced activity of NF-kappaB transcription factors, 
      particularly p65/RelA and p50. To our knowledge, these data provide the first 
      indication that 17beta-estradiol in physiological concentrations inhibits 
      apoptosis in cardiac myocytes. The antiapoptotic effect of estrogens might 
      contribute to the known cardioprotective effect of estrogens and provides a 
      starting point for the development of future treatment options.
CI  - Copyright 2000 Academic Press.
FAU - Pelzer, T
AU  - Pelzer T
AD  - Department of Medicine, University of Wurzburg, Wurzburg, D-97080, Germany.
FAU - Schumann, M
AU  - Schumann M
FAU - Neumann, M
AU  - Neumann M
FAU - deJager, T
AU  - deJager T
FAU - Stimpel, M
AU  - Stimpel M
FAU - Serfling, E
AU  - Serfling E
FAU - Neyses, L
AU  - Neyses L
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (NF-kappa B)
RN  - 0 (Nucleosomes)
RN  - 0 (Oligonucleotide Probes)
RN  - 4TI98Z838E (Estradiol)
RN  - EC 3.4.22.- (Casp3 protein, rat)
RN  - EC 3.4.22.- (Caspase 3)
RN  - EC 3.4.22.- (Caspases)
RN  - H88EPA0A3N (Staurosporine)
SB  - IM
MH  - Animals
MH  - Apoptosis/*drug effects
MH  - Base Sequence
MH  - Caspase 3
MH  - Caspases/metabolism
MH  - Cells, Cultured
MH  - DNA Fragmentation/drug effects
MH  - Estradiol/*pharmacology
MH  - Heart/*drug effects
MH  - In Situ Nick-End Labeling
MH  - Microscopy, Phase-Contrast
MH  - Myocardium/*cytology/metabolism
MH  - NF-kappa B/genetics/metabolism
MH  - Nucleosomes/drug effects
MH  - Oligonucleotide Probes/genetics
MH  - Rats
MH  - Staurosporine/pharmacology
EDAT- 2000/02/01 09:00
MHDA- 2000/03/04 09:00
CRDT- 2000/02/01 09:00
PHST- 2000/02/01 09:00 [pubmed]
PHST- 2000/03/04 09:00 [medline]
PHST- 2000/02/01 09:00 [entrez]
AID - S0006-291X(00)92073-4 [pii]
AID - 10.1006/bbrc.2000.2073 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2000 Feb 5;268(1):192-200. doi: 
      10.1006/bbrc.2000.2073.