The Roles of TNF-α in the Pathogenesis of Endometriosis

• Main Authors: Yu-Wei Chiou, 邱昱維
• Other Authors: Nancy M. Wang
• Format: Others
• Language: en_US
• Published: 2014
• Online Access: http://ndltd.ncl.edu.tw/handle/22rnfy

碩士 === 國立彰化師範大學 === 生物技術研究所 === 102 === Endometriosis is a common gynecological disease and the main clinical feature involving infertility, inflammation, chronic pelvic pain and dysmenorrhoea. TNF-α, one of the major inflammatory cytokine, was found increased in peritoneal fluid of women with endometriosis. In baboons, TNF-α blockade resulted in inhibition of the development and growth of endometriosis implants. However, the roles of TNF-α in the pathogenesis of endometriosis were not understood. Thus the aim of this experiment is to study TNF-α in endometriotic cells to examine : migration, proliferation ectopic growth and inflammation. Migration abilities of endometriotic cells were assessed using in vitro wound healing assay. The effects of TNF-α was examined by adding (10ng/ml) TNF-α and (10ng/ml) anti-TNF-α antibody for 12hr before migration assay. Hormone receptor related gene expressions were determined by real-time PCR analysis. TNF-α stimulated endometriotic cell migration by 1.45 fold. Adding TNF-α antibody inhibited migration by 0.64 fold. Migration rate of endometriotic cell is 1.74 fold faster than fibroblast by TNF-α treatment and decreased 0.86 fold by adding TNF-α antibody. There were no correlations between migration rates and expressions of hormone receptor genes (ESR1, ESR2, PGR). Endometriotic cells were able to ectopic growth, TNF-α also stimulated 26 fold large coverage, and up-regulated of VCAM1 expression for 7.44 fold. Thus, increased TNF-α is a major factor caused endometriotic cell migration and ectopic growth. Stimulatory effects are independent of hormonal status. Inhibition of TNF-α using anti-TNF-α antibody abolished the stimulation effect. However, endometriosis is a hormone dependent disease; thus, we suggest that using anti-inflammatory and hormone receptor inhibitor in a same time to treat of endometriosis.