PMID- 9839358
OWN - NLM
STAT- MEDLINE
DCOM- 19990217
LR  - 20131121
IS  - 0040-3709 (Print)
IS  - 0040-3709 (Linking)
VI  - 58
IP  - 5
DP  - 1998 Nov
TI  - Role of TGF-beta in RA-induced cleft palate in CD-1 mice.
PG  - 197-204
AB  - Retinoic acid (RA) plays an important role in embryogenesis, by regulating 
      morphogenesis, cell proliferation, differentiation, and extracellular matrix 
      production. RA exposure on gestational day (GD) 12 in CD-1 mice results in 
      delayed palatal shelf elevation and subsequent clefts in the secondary palate. 
      Given the dynamic and complex nature of palate development, it is not surprising 
      that this system is susceptible to changes in retinoid levels. There is evidence 
      that experimental manipulation of retinoid status during development alters 
      normal transforming growth factor-beta (TGF-beta) status. To study the role of 
      perturbation in TGF-beta levels in RA-induced cleft palate, gravid CD-1 mice were 
      treated with 70 mg/kg RA on GD 12. We examined changes in TGF-beta proteins and 
      the steady-state level of TGF-beta mRNA within the first 24 hr after exposure. 
      The interactions between RA and TGF-beta s were very complex. RA differentially 
      regulated the mRNA and protein levels of TGF-beta 1. Changes in mRNA steady-state 
      levels were rapid and transient in nature, indicating a direct mediation by RA. 
      Differential regulation was evident, because RA treatment resulted in an increase 
      in TGF-beta 1 mRNA steady levels followed by a decrease in the intracellular and 
      extracellular forms of TGF-beta 1 protein. Moreover, the patterns of localization 
      and levels of TGF-beta 2 and TGF-beta 3 proteins were not dramatically affected, 
      although there was an increase in TGF-beta 3 mRNA steady-state levels. The 
      increases in mRNA steady-state levels for TGF-beta 2 and TGF-beta 3, as for 
      TGF-beta 1, were rapid and transient in nature, again arguing for direct 
      mediation by RA. These data provide evidence for interactions between RA and 
      TGF-beta s, and indicate that RA is capable of differentially regulating TGF-beta 
      isoforms through processes involving different stages of TGF-beta synthesis and 
      secretion. Further, changes in TGF-beta isoforms were observed prior to changes 
      in mesenchyme morphology and must be considered as mediators of RA's effects on 
      mesenchyme development.
FAU - Degitz, S J
AU  - Degitz SJ
AD  - Department of Veterinary Biosciences, University of Illinois at Urbana-Champaign 
      61801, USA.
FAU - Morris, D
AU  - Morris D
FAU - Foley, G L
AU  - Foley GL
FAU - Francis, B M
AU  - Francis BM
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Teratology
JT  - Teratology
JID - 0153257
RN  - 0 (RNA, Messenger)
RN  - 0 (Transforming Growth Factor beta)
RN  - 5688UTC01R (Tretinoin)
SB  - IM
MH  - Animals
MH  - Cleft Palate/*chemically induced/metabolism
MH  - Gestational Age
MH  - Immunohistochemistry
MH  - Mice
MH  - Palate/embryology/metabolism
MH  - RNA, Messenger/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Transforming Growth Factor beta/*metabolism
MH  - Tretinoin/*adverse effects
EDAT- 1998/12/05 03:44
MHDA- 2000/06/20 09:00
CRDT- 1998/12/05 03:44
PHST- 1998/12/05 03:44 [pubmed]
PHST- 2000/06/20 09:00 [medline]
PHST- 1998/12/05 03:44 [entrez]
AID - 10.1002/(SICI)1096-9926(199811)58:5<197::AID-TERA6>3.0.CO;2-8 [pii]
AID - 10.1002/(SICI)1096-9926(199811)58:5<197::AID-TERA6>3.0.CO;2-8 [doi]
PST - ppublish
SO  - Teratology. 1998 Nov;58(5):197-204. doi: 
      10.1002/(SICI)1096-9926(199811)58:5<197::AID-TERA6>3.0.CO;2-8.