PMID- 8013384
OWN - NLM
STAT- MEDLINE
DCOM- 19940726
LR  - 20131121
IS  - 0013-7227 (Print)
IS  - 0013-7227 (Linking)
VI  - 135
IP  - 1
DP  - 1994 Jul
TI  - Expression of transforming growth factor-beta (TGF beta) isoforms and TGF beta 
      type II receptor messenger ribonucleic acid and protein, and the effect of TGF 
      beta s on endometrial stromal cell growth and protein degradation in vitro.
PG  - 450-9
AB  - Reverse transcription-polymerase chain reaction analysis of total RNA and 
      immunocytochemical observations revealed that human endometrial glandular 
      epithelial and stromal cells in primary culture express messenger RNAs and 
      proteins for transforming growth factor-beta 1 (TGF beta 1), TGF beta 2, and TGF 
      beta 3 as well as TGF beta type II receptor. The epithelial and stromal cells 
      synthesize and secrete into their culture-conditioned medium 2.6 +/- 0.3 and 1.4 
      +/- 0.2 ng TGF beta 1/10(6) cells, respectively; after transient acidification of 
      the medium, the TGF beta 1 levels were 18.1 +/- 0.4 and 7.8 +/- 0.7 ng/10(6) 
      cells. These cells also contain specific binding sites for [125I]TGF beta 1, 
      indicated by light microscope autoradiography. TGF beta s at 0.01-10 ng/ml 
      neither stimulated or inhibited subconfluent quiescent stromal cells under 
      serum-free condition nor altered the mitogenic action of 10% fetal bovine serum. 
      However, in the presence of 2% fetal bovine serum, which induced half-maximal 
      stimulation of [3H]thymidine incorporation, TGF beta 1 and TGF beta 2 at 0.1-0.5 
      ng/ml and TGF beta 3 at 0.1-2.5 ng/ml significantly stimulated the rate of 
      [3H]thymidine incorporation into quiescent stromal cells (P < 0.005); they were 
      ineffective at higher concentrations. TGF beta s did not have any effect on cell 
      proliferation, as determined by cell counting; however, at 0.1 ng/ml and higher 
      concentrations, TGF beta s significantly reduced the metabolic activity of 
      stromal cells, as determined by colorimetric 3-(4,5-dimethylthiazol-2-yl)2, 
      5-diphenyltetrazolium bromide assay (P < 0.05). The stimulatory and inhibitory 
      actions of TGF beta s in both assays were reversible using 5-10 micrograms/ml TGF 
      beta 1- and TGF beta 2- and 3-6 micrograms/ml TGF beta 3-specific neutralizing 
      antibodies. TGF beta 1 at 1 ng/ml had no significant effect on long-lived protein 
      degradation, assayed by incorporation of [14C]valine into newly synthesized 
      protein by stromal cells, and was similar to the effect of epidermal growth 
      factor or platelet-derived growth factor-BB (10 ng/ml). The data suggest that the 
      TGF beta expression by various endometrial cell types in an autocrine/paracrine 
      manner acts as a negative regulator essential for restraining endometrial growth 
      and transition from proliferation to differentiation stages during the secretory 
      phase after mitogenic stimulation during the proliferative phase of the menstrual 
      cycle.
FAU - Tang, X M
AU  - Tang XM
AD  - Department of Obstetrics and Gynecology, University of Florida, Gainesville 
      32610.
FAU - Zhao, Y
AU  - Zhao Y
FAU - Rossi, M J
AU  - Rossi MJ
FAU - Abu-Rustum, R S
AU  - Abu-Rustum RS
FAU - Ksander, G A
AU  - Ksander GA
FAU - Chegini, N
AU  - Chegini N
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Endocrinology
JT  - Endocrinology
JID - 0375040
RN  - 0 (Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Transforming Growth Factor beta)
RN  - 0 (Transforming Growth Factor beta)
RN  - VC2W18DGKR (Thymidine)
SB  - IM
MH  - Adult
MH  - Cell Division/drug effects
MH  - Cells, Cultured
MH  - Endometrium/cytology/*drug effects
MH  - Female
MH  - Fluorescent Antibody Technique
MH  - Humans
MH  - Isomerism
MH  - Proteins/metabolism
MH  - RNA, Messenger/*metabolism
MH  - Receptors, Transforming Growth Factor beta/*genetics/*metabolism
MH  - Stromal Cells/cytology/metabolism
MH  - Thymidine/metabolism
MH  - Transforming Growth Factor beta/chemistry/*metabolism/*pharmacology
EDAT- 1994/07/01 00:00
MHDA- 1994/07/01 00:01
CRDT- 1994/07/01 00:00
PHST- 1994/07/01 00:00 [pubmed]
PHST- 1994/07/01 00:01 [medline]
PHST- 1994/07/01 00:00 [entrez]
AID - 10.1210/endo.135.1.8013384 [doi]
PST - ppublish
SO  - Endocrinology. 1994 Jul;135(1):450-9. doi: 10.1210/endo.135.1.8013384.