PMID- 19505996
OWN - NLM
STAT- MEDLINE
DCOM- 20091123
LR  - 20220321
IS  - 1460-2407 (Electronic)
IS  - 1360-9947 (Print)
IS  - 1360-9947 (Linking)
VI  - 15
IP  - 10
DP  - 2009 Oct
TI  - Induction of endometrial epithelial cell invasion and c-fms expression by 
      transforming growth factor beta.
PG  - 665-73
LID - 10.1093/molehr/gap043 [doi]
AB  - Transforming growth factor beta 1 (TGF-beta1) levels are increased in the 
      peritoneal fluid of endometriosis patients, and endometrial cells express 
      TGF-beta signaling components; however, little is known regarding the role of 
      TGF-beta in endometriosis. Our objective was to examine the effects of TGF-beta1 
      on (i) the expression of macrophage colony-stimulating factor receptor encoded by 
      the c-fms gene, (ii) transmesothelial invasiveness of endometrial cells, (iii) 
      cellular proliferation and (iv) attachment to peritoneal mesothelial cells 
      (PMCs). Effects of TGF-beta1 on c-fms mRNA expression were determined by 
      real-time RT-PCR and c-fms cell-surface expression by flow cytometry. Effects of 
      TGF-beta1 on the invasiveness of the immortalized endometrial epithelial cell 
      (EEC) line EM42 and primary EECs were examined using a three-dimensional in vitro 
      system modeling the peritoneum. Cellular proliferation and attachment to PMCs 
      were also examined using established techniques. TGF-beta1 had little or no 
      effect on cellular proliferation and endometrial cell attachment to PMCs. 
      TGF-beta1 significantly induced the expression of c-fms mRNA and c-fms 
      cell-surface expression. TGF-beta1 enhanced transmesothelial invasion by EM42 
      cells and EECs. Antagonists of TGF-beta1 signaling significantly inhibited both 
      the induction of c-fms expression and cellular invasiveness, suggesting that 
      additional studies are warranted to assess the therapeutic potential of TGF-beta 
      antagonists in endometriosis.
FAU - Liu, Ya-Guang
AU  - Liu YG
AD  - Department of Obstetrics and Gynecology, University of Texas Health Science 
      Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA.
FAU - Tekmal, Rajeshwar R
AU  - Tekmal RR
FAU - Binkley, Peter A
AU  - Binkley PA
FAU - Nair, Hareesh B
AU  - Nair HB
FAU - Schenken, Robert S
AU  - Schenken RS
FAU - Kirma, Nameer B
AU  - Kirma NB
LA  - eng
GR  - P30CA54174/CA/NCI NIH HHS/United States
GR  - R01 HD049637-01A2/HD/NICHD NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20090608
PL  - England
TA  - Mol Hum Reprod
JT  - Molecular human reproduction
JID - 9513710
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Imidazoles)
RN  - 0 (Pyridines)
RN  - 0 (Transforming Growth Factor beta)
RN  - EC 2.7.10.1 (Receptor, Macrophage Colony-Stimulating Factor)
RN  - OU13V1EYWQ (SB 203580)
SB  - IM
MH  - Cell Adhesion/drug effects
MH  - Cell Line
MH  - Cells, Cultured
MH  - Chromatin Immunoprecipitation
MH  - Endometrium/*cytology
MH  - Enzyme Inhibitors/pharmacology
MH  - Epithelial Cells/*cytology/drug effects
MH  - Female
MH  - Flow Cytometry
MH  - Gene Expression/drug effects
MH  - Humans
MH  - Imidazoles/pharmacology
MH  - Promoter Regions, Genetic/genetics
MH  - Pyridines/pharmacology
MH  - Receptor, Macrophage Colony-Stimulating Factor/genetics/*metabolism
MH  - Transforming Growth Factor beta/antagonists & inhibitors/*pharmacology/physiology
PMC - PMC2744470
EDAT- 2009/06/10 09:00
MHDA- 2009/12/16 06:00
PMCR- 2010/10/01
CRDT- 2009/06/10 09:00
PHST- 2009/06/10 09:00 [entrez]
PHST- 2009/06/10 09:00 [pubmed]
PHST- 2009/12/16 06:00 [medline]
PHST- 2010/10/01 00:00 [pmc-release]
AID - gap043 [pii]
AID - 10.1093/molehr/gap043 [doi]
PST - ppublish
SO  - Mol Hum Reprod. 2009 Oct;15(10):665-73. doi: 10.1093/molehr/gap043. Epub 2009 Jun 
      8.