NLRP3 inflammasome-mediated Pyroptosis induce Notch signal activation in endometriosis angiogenesis
Endometriosis is characterized by the presence of endometrial tissue outside the uterus that not only causes severe pelvic pain and infertility but also increased risk for ovarian carcinogenesis in women of reproductive age. Here, we found that angiogenesis was increased and accompanied with up-regu...
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| Published in | Molecular and cellular endocrinology Vol. 574; p. 111952 |
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| Main Authors | , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Ireland
Elsevier B.V
20.08.2023
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0303-7207 1872-8057 1872-8057 |
| DOI | 10.1016/j.mce.2023.111952 |
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| Abstract | Endometriosis is characterized by the presence of endometrial tissue outside the uterus that not only causes severe pelvic pain and infertility but also increased risk for ovarian carcinogenesis in women of reproductive age. Here, we found that angiogenesis was increased and accompanied with up-regulation of Notch1 in human endometriotic tissue sample, which is associated with pyroptosis induced by activation of endothelial NLRP3 inflammasome. Further, in endometriosis model induced in wild type and NLRP3-deficient (NLRP3-KO) mice, we found that deficiency of NLRP3 suppressing the development of endometriosis. In vitro, inhibiting the activation of NLRP3 inflammasome prevents LPS/ATP-induced tube formation in endothelial cells. Meanwhile, knockdown NLRP3 expression by gRNA disrupt the interaction between Notch1 and HIF-1α under the inflammatory microenvironment. This study demonstrates that activation of NLRP3 inflammasome-mediated pyroptosis affects angiogenesis in endometriosis via Notch1-dependent manner.
•Activation of NLRP3 inflammasome played a central role in the development of endometriosis angiogenesis.•NLRP3 inflammasome induced angiogenesis through Notch1 signaling.•NLRP3 inflammasome regulated the interaction between Notch1 and HIF-1α. |
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| AbstractList | Endometriosis is characterized by the presence of endometrial tissue outside the uterus that not only causes severe pelvic pain and infertility but also increased risk for ovarian carcinogenesis in women of reproductive age. Here, we found that angiogenesis was increased and accompanied with up-regulation of Notch1 in human endometriotic tissue sample, which is associated with pyroptosis induced by activation of endothelial NLRP3 inflammasome. Further, in endometriosis model induced in wild type and NLRP3-deficient (NLRP3-KO) mice, we found that deficiency of NLRP3 suppressing the development of endometriosis. In vitro, inhibiting the activation of NLRP3 inflammasome prevents LPS/ATP-induced tube formation in endothelial cells. Meanwhile, knockdown NLRP3 expression by gRNA disrupt the interaction between Notch1 and HIF-1α under the inflammatory microenvironment. This study demonstrates that activation of NLRP3 inflammasome-mediated pyroptosis affects angiogenesis in endometriosis via Notch1-dependent manner.Endometriosis is characterized by the presence of endometrial tissue outside the uterus that not only causes severe pelvic pain and infertility but also increased risk for ovarian carcinogenesis in women of reproductive age. Here, we found that angiogenesis was increased and accompanied with up-regulation of Notch1 in human endometriotic tissue sample, which is associated with pyroptosis induced by activation of endothelial NLRP3 inflammasome. Further, in endometriosis model induced in wild type and NLRP3-deficient (NLRP3-KO) mice, we found that deficiency of NLRP3 suppressing the development of endometriosis. In vitro, inhibiting the activation of NLRP3 inflammasome prevents LPS/ATP-induced tube formation in endothelial cells. Meanwhile, knockdown NLRP3 expression by gRNA disrupt the interaction between Notch1 and HIF-1α under the inflammatory microenvironment. This study demonstrates that activation of NLRP3 inflammasome-mediated pyroptosis affects angiogenesis in endometriosis via Notch1-dependent manner. Endometriosis is characterized by the presence of endometrial tissue outside the uterus that not only causes severe pelvic pain and infertility but also increased risk for ovarian carcinogenesis in women of reproductive age. Here, we found that angiogenesis was increased and accompanied with up-regulation of Notch1 in human endometriotic tissue sample, which is associated with pyroptosis induced by activation of endothelial NLRP3 inflammasome. Further, in endometriosis model induced in wild type and NLRP3-deficient (NLRP3-KO) mice, we found that deficiency of NLRP3 suppressing the development of endometriosis. In vitro, inhibiting the activation of NLRP3 inflammasome prevents LPS/ATP-induced tube formation in endothelial cells. Meanwhile, knockdown NLRP3 expression by gRNA disrupt the interaction between Notch1 and HIF-1α under the inflammatory microenvironment. This study demonstrates that activation of NLRP3 inflammasome-mediated pyroptosis affects angiogenesis in endometriosis via Notch1-dependent manner. Endometriosis is characterized by the presence of endometrial tissue outside the uterus that not only causes severe pelvic pain and infertility but also increased risk for ovarian carcinogenesis in women of reproductive age. Here, we found that angiogenesis was increased and accompanied with up-regulation of Notch1 in human endometriotic tissue sample, which is associated with pyroptosis induced by activation of endothelial NLRP3 inflammasome. Further, in endometriosis model induced in wild type and NLRP3-deficient (NLRP3-KO) mice, we found that deficiency of NLRP3 suppressing the development of endometriosis. In vitro, inhibiting the activation of NLRP3 inflammasome prevents LPS/ATP-induced tube formation in endothelial cells. Meanwhile, knockdown NLRP3 expression by gRNA disrupt the interaction between NICD and HIF-1α under the inflammatory microenvironment. This study demonstrates that activation of NLRP3 inflammasome-mediated pyroptosis affects angiogenesis in endometriosis via Notch1-dependent manner. Endometriosis is characterized by the presence of endometrial tissue outside the uterus that not only causes severe pelvic pain and infertility but also increased risk for ovarian carcinogenesis in women of reproductive age. Here, we found that angiogenesis was increased and accompanied with up-regulation of Notch1 in human endometriotic tissue sample, which is associated with pyroptosis induced by activation of endothelial NLRP3 inflammasome. Further, in endometriosis model induced in wild type and NLRP3-deficient (NLRP3-KO) mice, we found that deficiency of NLRP3 suppressing the development of endometriosis. In vitro, inhibiting the activation of NLRP3 inflammasome prevents LPS/ATP-induced tube formation in endothelial cells. Meanwhile, knockdown NLRP3 expression by gRNA disrupt the interaction between Notch1 and HIF-1α under the inflammatory microenvironment. This study demonstrates that activation of NLRP3 inflammasome-mediated pyroptosis affects angiogenesis in endometriosis via Notch1-dependent manner. •Activation of NLRP3 inflammasome played a central role in the development of endometriosis angiogenesis.•NLRP3 inflammasome induced angiogenesis through Notch1 signaling.•NLRP3 inflammasome regulated the interaction between Notch1 and HIF-1α. |
| ArticleNumber | 111952 |
| Author | Peng, Rui Dong, Su Wang, Wei Chen, Yang Dai, Linfeng Zhang, Minyi Chen, Yulin Shi, Zhimian Peng, Xianglan Lin, Yike He, Hong Li, Jieyi Xiao, Jing Cai, Dongpeng |
| Author_xml | – sequence: 1 givenname: Minyi surname: Zhang fullname: Zhang, Minyi organization: Department of Pharmacology, School of Chinese Pharmaceutical Science, Guangzhou University of Chinese Medicine, Guangzhou, 510006, China – sequence: 2 givenname: Zhimian surname: Shi fullname: Shi, Zhimian organization: Department of Pharmacology, School of Chinese Pharmaceutical Science, Guangzhou University of Chinese Medicine, Guangzhou, 510006, China – sequence: 3 givenname: Xianglan surname: Peng fullname: Peng, Xianglan organization: Department of Obstetrics and Gynecology, Department of Gynecologic Oncology Research Office, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510150, Guangdong, China – sequence: 4 givenname: Dongpeng surname: Cai fullname: Cai, Dongpeng organization: Department of Pharmacology, School of Chinese Pharmaceutical Science, Guangzhou University of Chinese Medicine, Guangzhou, 510006, China – sequence: 5 givenname: Rui surname: Peng fullname: Peng, Rui organization: Department of Obstetrics and Gynecology, Department of Gynecologic Oncology Research Office, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510150, Guangdong, China – sequence: 6 givenname: Yike surname: Lin fullname: Lin, Yike organization: Department of Pharmacology, School of Chinese Pharmaceutical Science, Guangzhou University of Chinese Medicine, Guangzhou, 510006, China – sequence: 7 givenname: Linfeng surname: Dai fullname: Dai, Linfeng organization: Department of Pharmacology, School of Chinese Pharmaceutical Science, Guangzhou University of Chinese Medicine, Guangzhou, 510006, China – sequence: 8 givenname: Jieyi surname: Li fullname: Li, Jieyi organization: Department of Pharmacology, School of Chinese Pharmaceutical Science, Guangzhou University of Chinese Medicine, Guangzhou, 510006, China – sequence: 9 givenname: Yulin surname: Chen fullname: Chen, Yulin organization: Department of Pharmacology, School of Chinese Pharmaceutical Science, Guangzhou University of Chinese Medicine, Guangzhou, 510006, China – sequence: 10 givenname: Jing surname: Xiao fullname: Xiao, Jing organization: The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510120, Guangdong, China – sequence: 11 givenname: Su surname: Dong fullname: Dong, Su organization: Department of Pharmacy, People's Hospital of Dongxihu District, Wuhan, 430040, Hubei, China – sequence: 12 givenname: Wei surname: Wang fullname: Wang, Wei email: wangwei26960@126.com organization: Department of Pharmacology, School of Chinese Pharmaceutical Science, Guangzhou University of Chinese Medicine, Guangzhou, 510006, China – sequence: 13 givenname: Yang surname: Chen fullname: Chen, Yang email: ychen8@gzucm.edu.cn organization: Department of Pharmacology, School of Chinese Pharmaceutical Science, Guangzhou University of Chinese Medicine, Guangzhou, 510006, China – sequence: 14 givenname: Hong surname: He fullname: He, Hong email: hehe200010@gzhmu.edu.cn organization: Department of Obstetrics and Gynecology, Department of Gynecologic Oncology Research Office, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510150, Guangdong, China |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/37268099$$D View this record in MEDLINE/PubMed |
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| Keywords | Angiogenesis Endometriosis Notch1 signal Pyroptosis NLRP3 inflammasome |
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| SubjectTerms | Angiogenesis Animals carcinogenesis endocrinology Endometriosis endometrium Endothelial Cells - metabolism Female Humans inflammasomes Inflammasomes - metabolism Mice NLR Family, Pyrin Domain-Containing 3 Protein - metabolism NLRP3 inflammasome Notch1 signal pain Pyroptosis risk Signal Transduction |
| Title | NLRP3 inflammasome-mediated Pyroptosis induce Notch signal activation in endometriosis angiogenesis |
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