Effect of vascular endothelial growth factor and interleukin-1β on apoptosis in endometrial cell cultures from patients with endometriosis and controls

被引:30
作者
Bilotas, Mariela [1 ]
Meresman, Gabriela [1 ]
Buquet, Ricardo [2 ]
Sueldo, Carlos [3 ]
Ines Baranao, Rosa [1 ]
机构
[1] IBYME, Buenos Aires, DF, Argentina
[2] Hosp Clin Jose San Martin, Dept Ginecol, Buenos Aires, DF, Argentina
[3] CEGyR, Buenos Aires, DF, Argentina
关键词
VEGF; IL-1; beta; Endometriosis; Apoptosis; FAS LIGAND EXPRESSION; IN-VITRO; PERITONEAL-FLUID; STROMAL CELLS; FACTOR VEGF; HORMONE AGONIST; GNRH ANALOGS; WOMEN; RECEPTOR; BCL-2;
D O I
10.1016/j.jri.2009.12.002
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The aim of this study was to evaluate the effect of vascular endothelial growth factor (VEGF) and interleukin-1 beta (IL-1 beta) on apoptosis induced by leuprolide acetate (LA) in endometrial epithelial cell cultures from patients with endometriosis. Primary endometrial epithelial cell cultures were obtained from uterine endometrial biopsies of patients with endometriosis and control women. Endometrial epithelial cells were incubated with LA; a combination of LA and VEGF: a combination of LA and IL-1 beta; or in basal conditions. LA was added 3 h prior to addition of VEGF and IL-1 beta. After stimulation, the percentage of apoptotic cells was evaluated by the acridine orange-ethidium bromide technique and Bax expression was assessed by western blot. Treatment with LA enhanced the percentage of apoptotic cells in endometrial epithelial cells from subjects with endometriosis and control subjects. Addition of either VEGF or IL-1 beta after exposure to LA restored the percentage of apoptotic cells to basal levels. Moreover, treatment with LA increased Bax expression in endometrial epithelial cells from patients with endometriosis. This effect was reverted by the addition of either VEGF or IL-1 beta. Our results show that VEGF and IL-1 beta reduce apoptosis and decrease Bax expression in endometrial epithelial cells from patients with endometriosis. This study suggests that VEGF and IL-1 beta may protect endometriotic cells from undergoing apoptosis in addition to exerting their pro-angiogenic role. (C) 2010 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:193 / 198
页数:6
相关论文
共 47 条
[1]  
ABRAMS JM, 1993, DEVELOPMENT, V117, P29
[2]  
Andreu C, 1998, MOL REPROD DEV, V51, P287, DOI 10.1002/(SICI)1098-2795(199811)51:3<287::AID-MRD8>3.0.CO
[3]  
2-L
[4]   Hypoxia-induced VEGF enhances tumor survivability via suppression of serum deprivation-induced apoptosis [J].
Baek, JH ;
Jang, JE ;
Kang, CM ;
Chung, HY ;
Kim, ND ;
Kim, KW .
ONCOGENE, 2000, 19 (40) :4621-4631
[5]   Interleukin 1β, interleukin-6, and tumor necrosis factor-α in endometriotic tissue and in endometrium [J].
Bergqvist, A ;
Bruse, C ;
Carlberg, M ;
Carlström, K .
FERTILITY AND STERILITY, 2001, 75 (03) :489-495
[6]   Regulation of Fas ligand expression by vascular endothelial growth factor in endometrial stromal cells in vitro [J].
Berkkanoglu, M ;
Guzeloglu-Kayisli, O ;
Kayisli, UA ;
Selam, BF ;
Arici, A .
MOLECULAR HUMAN REPRODUCTION, 2004, 10 (06) :393-398
[7]   Effect of GnRH analogues on apoptosis and expression of Bcl-2, Bax, Fas and FasL proteins in endometrial epithelial cell cultures from patients with endometriosis and controls [J].
Bilotas, M. ;
Baranao, R. I. ;
Buquet, R. ;
Sueldo, C. ;
Tesone, M. ;
Meresman, G. .
HUMAN REPRODUCTION, 2007, 22 (03) :644-653
[8]   Expression of GnRH receptor gene in human ectopic endometrial cells and inhibition of their proliferation by leuprolide acetate [J].
Borroni, R ;
Di Blasio, AM ;
Gaffuri, B ;
Santorsola, R ;
Busacca, M ;
Viganò, P ;
Vignali, M .
MOLECULAR AND CELLULAR ENDOCRINOLOGY, 2000, 159 (1-2) :37-43
[9]  
BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1016/0003-2697(76)90527-3
[10]   A novel role for vascular endothelial growth factor as an autocrine survival factor for embryonic stem cells during hypoxia [J].
Brusselmans, K ;
Bono, F ;
Collen, D ;
Herbert, JM ;
Carmeliet, P ;
Dewerchin, M .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2005, 280 (05) :3493-3499