PMID- 17869331
OWN - NLM
STAT- MEDLINE
DCOM- 20080807
LR  - 20181211
IS  - 0093-691X (Print)
IS  - 0093-691X (Linking)
VI  - 68
IP  - 8
DP  - 2007 Nov
TI  - Retinoid receptor-specific agonists regulate bovine in vitro early embryonic 
      development, differentiation and expression of genes related to cell cycle arrest 
      and apoptosis.
PG  - 1118-27
AB  - A major goal in reproductive biotechnology is the identification of pathways that 
      regulate early embryonic development and the allocation of cells to the inner 
      cell mass (ICM) and trophectoderm (TE). Retinoids regulate the development and 
      differentiation of the bovine blastocyst in vitro, although the involvement of 
      the retinoid X receptors (RXRs) remains to be clarified. This paper compares the 
      effect of a synthetic RXR agonist (LG100268; LG) with that of the retinoic acid 
      receptor (RAR) agonist all-trans retinoic acid (ATRA) on blastulation. In 
      vitro-produced morulae were treated for 48 h with LG (0.1 microM, 1 microM and 10 
      microM), ATRA 0.7 microM, or no additives. Treatment with ATRA did not increase 
      the rate of development; however, the LG 0.1 microM treatment increased both the 
      blastocyst development and hatching rate. Cell numbers increased in the ICM with 
      LG 10 microM, while a dose-dependent reduction was observed in the TE in the 
      presence of LG. Gene expression levels of p53 and p66 did not vary with LG but 
      increased with ATRA. Both LG and ATRA activated bax, a pro-apoptotic gene and 
      H2A.Z, a cell cycle-related gene. The above effects suggest the existence of 
      active p53-dependent and -independent apoptotic pathways for ATRA and LG, 
      respectively, in the bovine embryo. The expression of p53 and H2A.Z showed a 
      strong, positive correlation (r=0.93; p<0.0001) in all experimental groups; both 
      proteins are linked through the cell cycle. Agonists of RXR could be used to 
      control blastocyst development and differentiation.
FAU - Rodriguez, A
AU  - Rodriguez A
AD  - Genetica y Reproduccion SERIDA, Asturias, Spain.
FAU - Diez, C
AU  - Diez C
FAU - Caamano, J N
AU  - Caamano JN
FAU - de Frutos, C
AU  - de Frutos C
FAU - Royo, L J
AU  - Royo LJ
FAU - Munoz, M
AU  - Munoz M
FAU - Ikeda, S
AU  - Ikeda S
FAU - Facal, N
AU  - Facal N
FAU - Alvarez-Viejo, M
AU  - Alvarez-Viejo M
FAU - Gomez, E
AU  - Gomez E
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20070917
PL  - United States
TA  - Theriogenology
JT  - Theriogenology
JID - 0421510
RN  - 0 (DNA Primers)
RN  - 0 (Histones)
RN  - 0 (Keratolytic Agents)
RN  - 0 (Nicotinic Acids)
RN  - 0 (Retinoid X Receptors)
RN  - 0 (Tetrahydronaphthalenes)
RN  - 0 (bcl-2-Associated X Protein)
RN  - 5688UTC01R (Tretinoin)
RN  - UVU4X1103P (LG 100268)
SB  - IM
MH  - Animals
MH  - Apoptosis/drug effects/genetics
MH  - Cattle
MH  - Cell Count/veterinary
MH  - Cell Cycle/genetics
MH  - DNA Primers/chemistry
MH  - Embryo, Mammalian
MH  - Embryonic Development/*drug effects
MH  - Female
MH  - Gene Expression Regulation, Developmental/*drug effects
MH  - Genes, p53/drug effects/physiology
MH  - Histones/analysis
MH  - Keratolytic Agents/pharmacology
MH  - Nicotinic Acids/administration & dosage/*pharmacology
MH  - Retinoid X Receptors/*agonists/physiology
MH  - Reverse Transcriptase Polymerase Chain Reaction/veterinary
MH  - Tetrahydronaphthalenes/administration & dosage/*pharmacology
MH  - Time Factors
MH  - Tretinoin/*pharmacology
MH  - bcl-2-Associated X Protein/analysis
EDAT- 2007/09/18 09:00
MHDA- 2008/08/08 09:00
CRDT- 2007/09/18 09:00
PHST- 2007/06/07 00:00 [received]
PHST- 2007/07/27 00:00 [revised]
PHST- 2007/08/03 00:00 [accepted]
PHST- 2007/09/18 09:00 [pubmed]
PHST- 2008/08/08 09:00 [medline]
PHST- 2007/09/18 09:00 [entrez]
AID - S0093-691X(07)00496-7 [pii]
AID - 10.1016/j.theriogenology.2007.08.007 [doi]
PST - ppublish
SO  - Theriogenology. 2007 Nov;68(8):1118-27. doi: 
      10.1016/j.theriogenology.2007.08.007. Epub 2007 Sep 17.