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rhTNFR: Fc Suppresses the Development of Endometriosis in a Mouse Model by Downregulating Cell Proliferation and Invasiveness

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Abstract

Tumor necrosis factor α (TNF-α), a proinflammatory cytokine, may play an important role in the pathogenesis of endometriosis; therefore, TNF-α inhibitors potentially have an effect on endometriosis. To investigate the effect of anti–TNF-α treatment on endometriosis, 2 TNF-α inhibitors: recombinant human TNF receptor: Fc fusion protein (rhTNFR: Fc) and TNF-α monoclonal antibody (TNF-α mAb) were used to treat human eutopic endometrial stromal cells (hESCs), and the effects on cell survival, cell cycle, and invasiveness were compared. It was found that rhTNFR: Fc suppressed the TNF-α–induced hESC survival and invasiveness but not TNF-α mAb. Recombinant human TNF receptor: Fc fusion protein decreased the S phase of hESC compared with the TNF-α–treated group. Then, we used a surgically induced mouse model of endometriosis to study the effect of rhTNFR: Fc treatment in vivo. The fluorescence intensity and the size of implanted endometriotic lesions in the mouse model were decreased by rhTNFR: Fc. In conclusion, rhTNFR: Fc suppresses hESC survival and invasiveness and decreases the fluorescence intensity and implant size in the mouse model of endometriosis.

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Liu, Y., Sun, L., Hou, Z. et al. rhTNFR: Fc Suppresses the Development of Endometriosis in a Mouse Model by Downregulating Cell Proliferation and Invasiveness. Reprod. Sci. 23, 847–857 (2016). https://doi.org/10.1177/1933719115620495

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