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RISS 인기검색어
- 검색키워드
- 저자 : Lessey, Bruce A. (검색결과 2 건)
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RBPJ mediates uterine repair in the mouse and is reduced in women with recurrent pregnancy loss
Strug, Michael R.,Su, Ren‐,Wei,Kim, Tae Hoon,Mauriello, Alessandro,Ticconi, Carlo,Lessey, Bruce A.,Young, Steven L.,Lim, Jeong Mook,Jeong, Jae‐,Wook,Fazleabas, Asgerally T. Federation of American Society for Experimental Bi 2018 The FASEB Journal Vol.32 No.5
<P>Unexplained recurrent pregnancy loss (uRPL) is associated with repeated embryo loss and endometrial repair with elevated endometrial expression of inflammatory cytokines, including IFN-gamma. Notch signaling through its transcription factor recombination signal binding protein J kappa (RBPJ) regulates mechanisms including the immune response and repair after tissue injury. Initially, null mutation of RBPJ in the mouse uterus (Pgr(cre/+)Rbpj(f/f); Rbpj c-KO) results in subfertility, but we have found that these mice become infertile after pregnancy as a result of dysfunctional postpartum uterine repair, including delayed endometrial epithelial and myometrial regeneration. RNA sequencing of postpartum uterine repair sites revealed global up-regulation of inflammatory pathways, including IFN signaling. Consistent with elevated IFN-gamma, macrophages were recruited and polarized toward an M1-cytotoxic phenotype, which is associated with preventing repair and promoting further tissue injury. Through embryo transfer experiments, we show that dysfunctional postpartum repair directly impairs future embryo implantation in Rbpj c-KO mice. Last, we clinically correlated our findings from the Rbpj c-KO mouse in women diagnosed with uRPL. Reduced RBPJ in women with uRPL was associated with increased levels of IFN-gamma. The data, taken together, indicate that RBPJ regulates inflammation during endometrial repair, which is essential for future pregnancy potential, and its dysregulation may serve as an unidentified contributor to uRPL in women.</P>
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Loss of HDAC3 results in nonreceptive endometrium and female infertility
Kim, Tae Hoon,Yoo, Jung-Yoon,Choi, Kyung-Chul,Shin, Jung-Ho,Leach, Richard E.,Fazleabas, Asgerally T.,Young, Steven L.,Lessey, Bruce A.,Yoon, Ho-Geun,Jeong, Jae-Wook American Association for the Advancement of Scienc 2019 Science translational medicine Vol.11 No.474
<P>Endometriosis is a disease in which tissue that normally grows inside the uterus grows outside the uterus and causes chronic pelvic pain and infertility. However, the exact mechanisms of the pathogenesis of endometriosis-associated infertility are unknown. Epigenetic dysregulation has recently been implicated in infertility. Here, we report a reduction of histone deacetylase 3 (HDAC3) protein amounts in eutopic endometrium of infertile women with endometriosis compared to a control group. To investigate the effect of HDAC3 loss in the uterus, we generated mice with conditional ablation of <I>Hdac3</I> in progesterone receptor (PGR)–positive cells (<I>Pgr<SUP>cre/+</SUP>Hdac3<SUP>f/f</SUP></I>; <I>Hdac3<SUP>d/d</SUP></I>). Loss of <I>Hdac3</I> in the uterus of mice results in infertility due to implantation failure and decidualization defect. Expression microarray and ChIP-seq analyses identified <I>COL1A1</I> and <I>COL1A2</I> as direct targets of HDAC3 in both mice and humans. Reduction of <I>HDAC3</I> abrogated decidualization in a primary culture of human endometrial stromal cells (hESCs) similar to that observed in infertile patients with endometriosis. Whereas attenuation of <I>HDAC3</I> resulted in p300 recruitment to <I>Col1a1</I> and <I>Col1a2</I> genes in the uterus of mice as well as hESCs, inhibition of p300 permitted hESCs to undergo decidualization. Collectively, we found attenuation of HDAC3 and overexpression of collagen type I in the eutopic endometrium of infertile patients with endometriosis. HDAC3 loss caused a defect of decidualization through the aberrant transcriptional activation of <I>Col1a1</I> and <I>Col1a2</I> genes in mice and <I>COL1A1</I> and <I>COL1A2</I> genes in humans. Our results suggest that HDAC3 is critical for endometrial receptivity and decidualization.</P>
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