scholarly journals Effects of Trichostatin A, a Histone Deacetylase Inhibitor, on Mouse Gonadal Development In Vitro

2004 ◽  
Vol 50 (2) ◽  
pp. 227-235 ◽  
Author(s):  
Takuo MIZUKAMI ◽  
Masahiko FUJISAWA ◽  
Yoshiakira KANAI ◽  
Masamichi KUROHMARU ◽  
Yoshihiro HAYASHI
2004 ◽  
Vol 32 (5) ◽  
pp. 840-842 ◽  
Author(s):  
V.C. Emmans ◽  
H.A. Rodway ◽  
A.N. Hunt ◽  
K.A. Lillycrop

Neuroblastoma is a childhood cancer, which spontaneously regresses. This has led to a search for agents that mimic this process. We show that both natural and synthetic ligands of PPARγ (peroxisome-proliferator-activated receptor γ) inhibit the growth of neuroblastoma cells in vitro. The degree of PPAR activation was attenuated however in the presence of the retinoblastoma protein. Addition of trichostatin A, a histone deacetylase inhibitor, abolished retinoblastoma protein repression of PPAR activity. Moreover, enhanced growth inhibition was observed when neuroblastoma cells were treated with a PPARγ ligand and a histone deacetylase inhibitor, suggesting a combination therapy to treat neuroblastoma might prove more effective than using either agent alone.


2006 ◽  
Vol 93 (2) ◽  
pp. 341-347 ◽  
Author(s):  
Andrew J. Olaharski ◽  
Zhiying Ji ◽  
Ji-Young Woo ◽  
Sophia Lim ◽  
Alan E. Hubbard ◽  
...  

Zygote ◽  
2011 ◽  
Vol 21 (1) ◽  
pp. 59-63 ◽  
Author(s):  
Clara Slade Oliveira ◽  
Naiara Zoccal Saraiva ◽  
Marcela Maria de Souza ◽  
Tatiane de Almeida Drummond Tetzner ◽  
Marina Ragagnin de Lima ◽  
...  

SummaryTrichostatin A (TSA) is a histone deacetylase inhibitor that induces histone hyperacetylation and increases gene expression levels. The aim of the present study was to establish a suitable condition for the use of TSA in in vitro cultures of bovine embryos, and to determine whether TSA would increase blastocyst rates by improvement of chromatin remodelling during embryonic genome activation and by increasing the expression of crucial genes during early development. To test this hypothesis, 8-cell embryos were exposed to four concentrations of TSA for different periods of time to establish adequate protocols. In a second experiment, three experimental groups were selected for the evaluation of embryo quality based on the following parameters: apoptosis, total cell number and blastocyst hatching. TSA promoted embryonic arrest and degeneration at concentrations of 15, 25 and 50 nM. All treated groups presented lower blastocyst rates. Exposure of embryos to 5 nM for 144 h and to 15 nM for 48 h decreased blastocyst hatching. However, the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay (TUNEL) assay revealed similar apoptosis rates and total cell numbers in all groups studied. Although, in the present study, TSA treatment did not improve the parameters studied, the results provided background information on TSA supplementation during in vitro culture of bovine embryos and showed that embryo quality was apparently not affected, despite a decrease in blastocyst rate after exposure to TSA.


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