open access

Vol 90, No 6 (2019)
Research paper
Published online: 2019-06-28
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GATA-3 Stimulates Proliferation of Endometriotic Cells

Peng Chen1, Fang Ren1, Dan-Bo Wang12
·
Pubmed: 31276181
·
Ginekol Pol 2019;90(6):308-313.
Affiliations
  1. Department of Obstetrics and Gynecology, Shengjing Hospital of China Medical University, Shenyang, China
  2. Department of Gynecology, Cancer Hospital of China Medical University, Shenyang, China

open access

Vol 90, No 6 (2019)
ORIGINAL PAPERS Gynecology
Published online: 2019-06-28

Abstract

Objectives: This study aimed to investigate whether there was a correlation between the expression of GATA binding protein 3 (GATA-3) and the proliferation of endometrium cells from women with endometriosis. 

Material and methods: Endometrial tissue was collected from 20 women with endometriosis (experimental group) and 10 women without endometriosis (control group). The primary endometrial cells were then cultured and identified. Each group of cells were further divided into four groups. The control group was divided into control-no treatment (C-N), control-negative control (C-NC, transfected with a scrambled siRNA negative control), control-lentiviral transfection control (C-LC) and control-GATA-3 lentiviral transfection (C-G3); the experimental group was divided into experiment-no treatment (E-N), experiment-negative control (E-NC), experiment-lentiviral transfection control (E-LC) and experiment-siGATA-3 lentiviral transfection (E-siG3). RT-PCR and western blot were used respectively to detect the endometrium cells’ GATA-3 mRNA and protein expression. Further, Cell Counting Kit-8 was used to measure the endometrium cells’ proliferation. 

Results: The relative expression of GATA-3 mRNA and protein in the E-N group was significantly higher than in the D-N group and E-siG3 group (P < 0.05). The relative cell proliferation rate in the C-G3 group at 48 h, 72 h and 96 h was significantly higher than in the C-N, C-NC and C-LC groups (P < 0.05), while in the experimental group, the proliferation rate of the E-siG3 group was significantly lower than in the E-N, E-NC and E-LC groups (P < 0.05). 

Conclusions: This study suggests the role of GATA-3 in promoting proliferation of endometrial cells; therefore, GATA-3 may play an essential role in the development of endometriosis.

Abstract

Objectives: This study aimed to investigate whether there was a correlation between the expression of GATA binding protein 3 (GATA-3) and the proliferation of endometrium cells from women with endometriosis. 

Material and methods: Endometrial tissue was collected from 20 women with endometriosis (experimental group) and 10 women without endometriosis (control group). The primary endometrial cells were then cultured and identified. Each group of cells were further divided into four groups. The control group was divided into control-no treatment (C-N), control-negative control (C-NC, transfected with a scrambled siRNA negative control), control-lentiviral transfection control (C-LC) and control-GATA-3 lentiviral transfection (C-G3); the experimental group was divided into experiment-no treatment (E-N), experiment-negative control (E-NC), experiment-lentiviral transfection control (E-LC) and experiment-siGATA-3 lentiviral transfection (E-siG3). RT-PCR and western blot were used respectively to detect the endometrium cells’ GATA-3 mRNA and protein expression. Further, Cell Counting Kit-8 was used to measure the endometrium cells’ proliferation. 

Results: The relative expression of GATA-3 mRNA and protein in the E-N group was significantly higher than in the D-N group and E-siG3 group (P < 0.05). The relative cell proliferation rate in the C-G3 group at 48 h, 72 h and 96 h was significantly higher than in the C-N, C-NC and C-LC groups (P < 0.05), while in the experimental group, the proliferation rate of the E-siG3 group was significantly lower than in the E-N, E-NC and E-LC groups (P < 0.05). 

Conclusions: This study suggests the role of GATA-3 in promoting proliferation of endometrial cells; therefore, GATA-3 may play an essential role in the development of endometriosis.

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Keywords

endometriosis; GATA-3; endometriotic cell; proliferation

About this article
Title

GATA-3 Stimulates Proliferation of Endometriotic Cells

Journal

Ginekologia Polska

Issue

Vol 90, No 6 (2019)

Article type

Research paper

Pages

308-313

Published online

2019-06-28

Page views

2114

Article views/downloads

988

DOI

10.5603/GP.2019.0056

Pubmed

31276181

Bibliographic record

Ginekol Pol 2019;90(6):308-313.

Keywords

endometriosis
GATA-3
endometriotic cell
proliferation

Authors

Peng Chen
Fang Ren
Dan-Bo Wang

References (29)
  1. Kaponis A, Kollia G, Taniguchi F, et al. Apoptosis in Endometriosis. Endometriosis. 2014: 179–190.
  2. de Ziegler D, Borghese B, Chapron C. Endometriosis and infertility: pathophysiology and management. Lancet. 2010; 376(9742): 730–738.
  3. Sampson J. Peritoneal endometriosis due to dissemination of endometrial tissue into the peritoneal cavity. American Journal of Obstetrics & Gynecology. 1927; 14: 93–94.
  4. Fauser BC, Diedrich K, Bouchard P, et al. Evian Annual Reproduction (EVAR) Workshop Group 2010. Contemporary genetic technologies and female reproduction. Hum Reprod Update. 2011; 17(6): 829–847.
  5. Chen JC, Erikson DW, Piltonen TT, et al. Coculturing human endometrial epithelial cells and stromal fibroblasts alters cell-specific gene expression and cytokine production. Fertil Steril. 2013; 100(4): 1132–1143.
  6. Qi X, Qu Y, Nan Z, et al. Caprine endometrial stromal cells modulate the effects of steroid hormones on cytokine secretion by endometrial epithelial cells in vitro. Reprod Biol. 2012; 12(3): 309–315.
  7. Lee SKi, Na BJu, Kim JY, et al. Determination of clinical cellular immune markers in women with recurrent pregnancy loss. Am J Reprod Immunol. 2013; 70(5): 398–411.
  8. Inman D, Kawana K, Schust D, et al. Cyclic regulation of T-Bet and GATA-3 in human endometrium. Reprod Sci. 2008; 15(1): 83–90.
  9. Zheng WP, Flavell RA, Zheng W, et al. The transcription factor GATA-3 is necessary and sufficient for Th2 cytokine gene expression in CD4 T cells. Cell. 1997; 89(4): 587–596.
  10. Chen P, Zhang Z, Chen Qi, et al. Expression of Th1 and Th2 cytokine-associated transcription factors, T-bet and GATA-3, in the eutopic endometrium of women with endometriosis. Acta Histochem. 2012; 114(8): 779–784.
  11. Wingfield M, Macpherson A, Healy DL, et al. Cell proliferation is increased in the endometrium of women with endometriosis. Fertil Steril. 1995; 64(2): 340–346.
  12. Wang DB, Xu YL, Chen P, et al. Silencing Cofilin-1 blocks PDGF-induced proliferation in eutopic endometrium of endometriosis patients. Cell Biol Int. 2013; 37(8): 799–804.
  13. Podgaec S, Abrao MS, Dias JA, et al. Endometriosis: an inflammatory disease with a Th2 immune response component. Hum Reprod. 2007; 22(5): 1373–1379.
  14. Chen P, Wang DB, Liang YM. Evaluation of estrogen in endometriosis patients: Regulation of GATA-3 in endometrial cells and effects on Th2 cytokines. J Obstet Gynaecol Res. 2016; 42(6): 669–677.
  15. Kouros-Mehr H, Slorach EM, Sternlicht MD, et al. GATA-3 maintains the differentiation of the luminal cell fate in the mammary gland. Cell. 2006; 127(5): 1041–1055.
  16. Grote D, Souabni A, Busslinger M, et al. Pax 2/8-regulated Gata 3 expression is necessary for morphogenesis and guidance of the nephric duct in the developing kidney. Development. 2006; 133(1): 53–61.
  17. Lim KC, Lakshmanan G, Crawford SE, et al. Gata3 loss leads to embryonic lethality due to noradrenaline deficiency of the sympathetic nervous system. Nat Genet. 2000; 25(2): 209–212.
  18. Lange M, Misfeldt M. The Importance of TLR3 Expression and Hormonal Regulation of TLR3- Induced Immune Responses in the Human Endometrium. Current Immunology Reviews. 2009; 5(3): 215–226.
  19. Rubel CA, Franco HL, Jeong JW, et al. GATA2 is expressed at critical times in the mouse uterus during pregnancy. Gene Expr Patterns. 2012; 12(5-6): 196–203.
  20. Dyson MT, Roqueiro D, Monsivais D, et al. Genome-wide DNA methylation analysis predicts an epigenetic switch for GATA factor expression in endometriosis. PLoS Genet. 2014; 10(3): e1004158.
  21. Herington JL, Bruner-Tran KL, Lucas JA, et al. Immune interactions in endometriosis. Expert Rev Clin Immunol. 2011; 7(5): 611–626.
  22. Oral E, Arici A. PATHOGENESIS OF ENDOMETRIOSIS. Obstetrics and Gynecology Clinics of North America. 1997; 24(2): 219–233.
  23. Giudice LC. Clinical practice. Endometriosis. N Engl J Med. 2010; 362(25): 2389–2398.
  24. Paul Dmowski W, Braun DP. Immunology of endometriosis. Best Pract Res Clin Obstet Gynaecol. 2004; 18(2): 245–263.
  25. Farrar JD, Asnagli H, Murphy KM. T helper subset development: roles of instruction, selection, and transcription. J Clin Invest. 2002; 109(4): 431–435.
  26. Hsu CC, Yang BC, Wu MH, et al. Enhanced interleukin-4 expression in patients with endometriosis. Fertil Steril. 1997; 67(6): 1059–1064.
  27. Antsiferova YS, Sotnikova NYu, Posiseeva LV, et al. Changes in the T-helper cytokine profile and in lymphocyte activation at the systemic and local levels in women with endometriosis. Fertil Steril. 2005; 84(6): 1705–1711.
  28. Ouyang W, Löhning M, Gao Z, et al. Stat6-independent GATA-3 autoactivation directs IL-4-independent Th2 development and commitment. Immunity. 2000; 12(1): 27–37.
  29. OuYang Z, Hirota Y, Osuga Y, et al. Interleukin-4 stimulates proliferation of endometriotic stromal cells. Am J Pathol. 2008; 173(2): 463–469.

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