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Article ; Online: Autophagy is required for stem-cell-mediated endometrial programming and the establishment of pregnancy.

Popli, Pooja / Kommagani, Ramakrishna

2023 , Page(s) 1–3

Abstract: Autophagy plays an important role in the normal growth and morphogenesis of a variety of tissues. Its role in uterine maturation, however, is not fully characterized. Recently, we reported that BECN1 (Beclin1)-dependent autophagy, but not apoptosis, is ... ...

Abstract	Autophagy plays an important role in the normal growth and morphogenesis of a variety of tissues. Its role in uterine maturation, however, is not fully characterized. Recently, we reported that BECN1 (Beclin1)-dependent autophagy, but not apoptosis, is crucial for stem cell-mediated endometrial programming and the establishment of pregnancy in mice. Upon genetic and pharmacological inhibition of BECN1-mediated autophagy, female mice displayed severe endometrial structural and functional defects leading to infertility. Specifically, conditional loss of
Language	English
Publishing date	2023-07-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2023.2231270
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Zs.A 6741: Show issues

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Article ; Online: Female reproductive dysfunctions and the gut microbiota.

Chadchan, Sangappa B / Singh, Vertika / Kommagani, Ramakrishna

Journal of molecular endocrinology

2022 Volume 69, Issue 3, Page(s) R81–R94

Abstract: The gut microbiome is considered an endocrine organ that can influence distant organs and associated biological pathways. Recent advances suggest that gut microbial homeostasis is essential for reproductive health and that perturbations in the gut ... ...

Abstract	The gut microbiome is considered an endocrine organ that can influence distant organs and associated biological pathways. Recent advances suggest that gut microbial homeostasis is essential for reproductive health and that perturbations in the gut microbiota can lead to reproductive pathologies. This review provides an updated overview of the relationship between the gut microbiome and female reproductive diseases. Specifically, we highlight the most recent findings on the gut microbiome in gynecological pathologies including polycystic ovarian syndrome, endometriosis, and endometrial cancer. Most studies revealed associations between altered gut microbial compositions and these reproductive diseases, though few have suggested cause-effect relationships. Future studies should focus on determining the molecular mechanisms underlying associations between gut microbiota and reproductive diseases. Understanding this bidirectional relationship could lead to the development of novel and effective strategies to prevent, diagnose, and treat female reproductive organ-related diseases.
MeSH term(s)	Endometriosis ; Female ; Gastrointestinal Microbiome ; Homeostasis ; Humans ; Polycystic Ovary Syndrome/metabolism ; Reproduction
Language	English
Publishing date	2022-08-04
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	645012-x
ISSN	1479-6813 ; 0952-5041
ISSN (online)	1479-6813
ISSN	0952-5041
DOI	10.1530/JME-21-0238
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Zs.A 2406: Show issues

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Article ; Online: The gut microbiota: a double-edged sword in endometriosis†.

Talwar, Chandni / Singh, Vertika / Kommagani, Ramakrishna

Biology of reproduction

2022 Volume 107, Issue 4, Page(s) 881–901

Abstract: Endometriosis that afflicts one in 10 women of reproductive age is characterized by growth of endometrial tissue in the extra-uterine sites and encompasses metabolic-, immunologic-, and endocrine-disruption. Importantly, several comorbidities are ... ...

Abstract	Endometriosis that afflicts one in 10 women of reproductive age is characterized by growth of endometrial tissue in the extra-uterine sites and encompasses metabolic-, immunologic-, and endocrine-disruption. Importantly, several comorbidities are associated with endometriosis, especially autoimmune disorders such as inflammatory bowel disease. Primarily thought of as a condition arising from retrograde menstruation, emerging evidence uncovered a functional link between the gut microbiota and endometriosis. Specifically, recent findings revealed altered gut microbiota profiles in endometriosis and in turn this altered microbiota appears to be causal in the disease progression, implying a bidirectional crosstalk. In this review, we discuss the complex etiology and pathogenesis of endometriosis, emphasizing on this recently recognized role of gut microbiome. We review the gut microbiome structure and functions and its complex network of interactions with the host for maintenance of homeostasis that is crucial for disease prevention. We highlight the underlying mechanisms on how some bacteria promote disease progression and others protect against endometriosis. Furthermore, we highlight the areas that require future emphases in the gut microbiome-endometriosis nexus and the potential microbiome-based therapies for amelioration of endometriosis.
MeSH term(s)	Disease Progression ; Endometriosis/pathology ; Female ; Gastrointestinal Microbiome ; Homeostasis ; Humans ; Microbiota
Language	English
Publishing date	2022-07-25
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1118-6
ISSN	1529-7268 ; 0006-3363
ISSN (online)	1529-7268
ISSN	0006-3363
DOI	10.1093/biolre/ioac147
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Zs.A 551: Show issues

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Article ; Online: The Multifaceted Role of Autophagy in Endometrium Homeostasis and Disease.

Popli, Pooja / Sun, Ally J / Kommagani, Ramakrishna

Reproductive sciences (Thousand Oaks, Calif.)

2021 Volume 29, Issue 4, Page(s) 1054–1067

Abstract: Autophagy is a conserved fundamental cellular process with a primary function of catabolizing harmful or surplus cellular contents such as protein aggregates, dysfunctional/long-lived organelles, intracellular pathogens, and storage nutrients. An ... ...

Abstract	Autophagy is a conserved fundamental cellular process with a primary function of catabolizing harmful or surplus cellular contents such as protein aggregates, dysfunctional/long-lived organelles, intracellular pathogens, and storage nutrients. An increasing body of evidence reveals that basal autophagy is essential for maintaining endometrial homeostasis and mediating endometrial-specific functions, including menstrual cycle, embryo implantation, and decidualization. However, perturbed levels of autophagy can lead to severe endometrial pathologies, including endometriosis, endometrial hyperplasia, endometrial cancer, adenomyosis, and leiomyoma. This review highlights the most recent findings on the activity, regulation, and function of autophagy in endometrium physiology and pathology. Understanding the mechanistic roles of autophagy in endometrium homeostasis and disease is key to developing novel therapeutic strategies for endometrium-related infertility and malignancies.
MeSH term(s)	Adenomyosis/metabolism ; Autophagy ; Endometriosis/metabolism ; Endometrium/metabolism ; Female ; Homeostasis ; Humans ; Leiomyoma/metabolism
Language	English
Publishing date	2021-04-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2276411-2
ISSN	1933-7205 ; 1933-7191
ISSN (online)	1933-7205
ISSN	1933-7191
DOI	10.1007/s43032-021-00587-2
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Zs.A 4113: Show issues

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Article: High-fat diets promote peritoneal inflammation and augment endometriosis-associated abdominal hyperalgesia.

Herup-Wheeler, Tristin / Shi, Mingxin / Harvey, Madeleine E / Talwar, Chandni / Kommagani, Ramakrishna / MacLean, James A / Hayashi, Kanako

Frontiers in endocrinology

2024 Volume 15, Page(s) 1336496

Abstract: Immune dysfunction is one of the central components in the development and progression of endometriosis by establishing a chronic inflammatory environment. Western-style high-fat diets (HFD) have been linked to greater systemic inflammation to cause ... ...

Abstract	Immune dysfunction is one of the central components in the development and progression of endometriosis by establishing a chronic inflammatory environment. Western-style high-fat diets (HFD) have been linked to greater systemic inflammation to cause metabolic and chronic inflammatory diseases, and are also considered an environmental risk factor for gynecologic diseases. Here, we aimed to examine how HFD cause an inflammatory environment in endometriosis and discern their contribution to endometriotic-associated hyperalgesia. Our results showed that HFD-induced obesity enhanced abdominal hyperalgesia that was induced by endometriotic lesions. Peritoneal inflammatory macrophages and cytokine levels increased by lesion induction were elevated by chronic exposure to HFD. Increased expression of pain-related mediators in the dorsal root ganglia was observed after lesion induction under the HFD condition. Although HFD did not affect inflammatory macrophages in the peritoneal cavity without lesion induction, the diversity and composition of the gut microbiota were clearly altered by HFD as a sign of low-grade systemic inflammation. Thus, HFD alone might not establish a local inflammatory environment in the pelvic cavity, but it can contribute to further enhancing chronic inflammation, leading to the exacerbation of endometriosis-associated abdominal hyperalgesia following the establishment and progression of the disease.
MeSH term(s)	Female ; Humans ; Endometriosis/complications ; Endometriosis/metabolism ; Hyperalgesia/etiology ; Diet, High-Fat/adverse effects ; Inflammation/metabolism ; Abdomen
Language	English
Publishing date	2024-03-15
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2024.1336496
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Article: The SARS-CoV-2 receptor, Angiotensin converting enzyme 2 (ACE2) is required for human endometrial stromal cell decidualization

Chadchan, S. B. / Maurya, V. K. / Popli, P. / Kommagani, R.

BioRxiv : the Preprint Server for Biology

Abstract: STUDY QUESTION: Is SARS-CoV-2 receptor, angiotensin-converting enzyme 2 (ACE 2) expressed in the human endometrium during the menstrual cycle, and does it participate in endometrial decidualization? SUMMARY ANSWER: ACE2 protein is highly expressed in ... ...

Abstract	STUDY QUESTION: Is SARS-CoV-2 receptor, angiotensin-converting enzyme 2 (ACE 2) expressed in the human endometrium during the menstrual cycle, and does it participate in endometrial decidualization? SUMMARY ANSWER: ACE2 protein is highly expressed in human endometrial stromal cells during the secretory phase and is essential for human endometrial stromal cell decidualization WHAT IS KNOWN ALREADY: ACE2 is expressed in numerous human tissues including the lungs, heart, intestine, kidneys and placenta ACE2 is also the receptor by which SARS-CoV-2 enters human cells STUDY DESIGN SIZE DURATION: Proliferative (n = 9) and secretory (n = 6) phase endometrium biopsies from healthy reproductive-age women and primary human endometrial stromal cells from proliferative phase endometrium were used in the study PARTICIPANTS/MATERIALS SETTING METHODS: ACE2 expression and localization were examined by qRT-PCR, Western blot, and immunofluorescence in both human endometrial samples and mouse uterine tissue The effect of ACE2 knockdown on morphological and molecular changes of human endometrial stromal cell decidualization were assessed Ovariectomized mice were treated with estrogen or progesterone to determine the effects of these hormones on ACE2 expression MAIN RESULTS AND THE ROLE OF CHANCE: In human tissue, ACE2 protein is expressed in both endometrial epithelial and stromal cells in the proliferative phase of the menstrual cycle, and expression increases in stromal cells in the secretory phase The ACE2 mRNA ( P < 0 0001) and protein abundance increased during primary human endometrial stromal cell (HESC) decidualization HESCs transfected with ACE2 -targeting siRNA were less able to decidualize than controls, as evidenced by a lack of morphology change and lower expression of the decidualization markers PRL and IGFBP1 ( P < 0 05) In mice during pregnancy, ACE2 protein was expressed in uterine epithelial and stromal cells increased through day six of pregnancy Finally, progesterone induced expression of Ace2 mRNA in mouse uteri more than vehicle or estrogen ( P < 0 05) Large scale data: N/a LIMITATIONS REASONS FOR CAUTION: Experiments assessing the function of ACE2 in human endometrial stromal cell decidualization were in vitro Whether SARS-CoV-2 can enter human endometrial stromal cells and affect decidualization have not been assessed WIDER IMPLICATIONS OF THE FINDINGS: Expression of ACE2 in the endometrium allow SARS-CoV-2 to enter endometrial epithelial and stromal cells, which could impair in vivo decidualization, embryo implantation, and placentation If so, women with COVID-19 may be at increased risk of early pregnancy loss STUDY FUNDINGS/COMPETING INTERESTS: This study was supported by National Institutes of Health / National Institute of Child Health and Human Development grants R01HD065435 and R00HD080742 to RK and Washington University School of Medicine start-up funds to RK The authors declare that they have no conflicts of interest
Keywords	covid19
Publisher	WHO
Document type	Article
Note	WHO #Covidence: #900739
Database	COVID19

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Article: SF3B1-dependent alternative splicing is critical for maintaining endometrial homeostasis and the establishment of pregnancy.

Popli, Pooja / Chadchan, Sangappa B / Dias, Michelle / Deng, Xinchao / Gunderson, Stephanie J / Jimenez, Patricia / Yalamanchili, Hari / Kommagani, Ramakrishna

bioRxiv : the preprint server for biology

2023

Abstract: The remarkable potential of human endometrium to undergo spontaneous remodeling is shaped by controlled spatiotemporal gene expression patterns. Although hormone-driven transcription shown to govern these patterns, the post-transcriptional processing of ... ...

Abstract	The remarkable potential of human endometrium to undergo spontaneous remodeling is shaped by controlled spatiotemporal gene expression patterns. Although hormone-driven transcription shown to govern these patterns, the post-transcriptional processing of these mRNA transcripts, including the mRNA splicing in the endometrium is not studied yet. Here, we report that the splicing factor, SF3B1 is central in driving alternative splicing (AS) events that are vital for physiological responses of the endometrium. We show that loss of SF3B1 splicing activity impairs stromal cell decidualization as well as embryo implantation. Transcriptomic analysis revealed that SF3B1 depletion decidualizing stromal cells led to differential mRNA splicing. Specifically, a significant upregulation in mutually exclusive AS events (MXEs) with SF3B1 loss resulted in the generation of aberrant transcripts. Further, we found that some of these candidate genes phenocopy SF3B1 function in decidualization. Importantly, we identify progesterone as a potential upstream regulator of SF3B1-mediated functions in endometrium possibly via maintaining its persistently high levels, in coordination with deubiquitinating enzymes. Collectively, our data suggest that SF3B1-driven alternative splicing plays a critical role in mediating the endometrial-specific transcriptional paradigms. Thus, the identification of novel mRNA variants associated with successful pregnancy establishment may help to develop new strategies to diagnose or prevent early pregnancy loss.
Language	English
Publishing date	2023-05-20
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.05.20.541590
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Article: High-fat diets promote peritoneal inflammation and augment endometriosis-associated abdominal hyperalgesia.

Herup-Wheeler, Tristin / Shi, Mingxin / Harvey, Madeleine E / Talwar, Chandni / Kommagani, Ramakrishna / MacLean, James A / Hayashi, Kanako

bioRxiv : the preprint server for biology

2023

Abstract	Immune dysfunction is one of the central components in the development and progression of endometriosis by establishing a chronic inflammatory environment. Western-style high-fat diets (HFD) have been linked to greater systemic inflammation to cause metabolic and chronic inflammatory diseases, and are also considered an environmental risk factor for gynecologic diseases. Here, we aimed to examine how HFD alter an inflammatory environment in endometriosis and discern their contribution to endometriotic-associated hyperalgesia. Our results showed that HFD-induced obesity enhanced abdominal mechanical allodynia that was induced by endometriotic lesions. Peritoneal inflammatory macrophages and cytokine levels increased by lesion induction were elevated by chronic exposure to HFD. Pain-related mediators in the dorsal root ganglia were further stimulated after lesion induction under the HFD condition. Although HFD did not affect inflammatory macrophages in the peritoneal cavity without lesion induction, the diversity and composition of the gut microbiota were clearly altered by HFD as a sign of low-grade systemic inflammation. Thus, HFD alone might not establish a local inflammatory environment in the pelvic cavity, but it can contribute to further enhancing chronic inflammation, leading to the exacerbation of endometriosis-associated abdominal hyperalgesia following the establishment and progression of the disease.
Language	English
Publishing date	2023-11-13
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.11.09.566474
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Article: The autophagy protein, ATG14 safeguards against unscheduled pyroptosis activation to enable embryo transport during early pregnancy.

Popli, Pooja / Oestreich, Arin K / Maurya, Vineet K / Rowen, Marina N / Masand, Ramya / Holtzman, Michael J / Zhang, Yong / Lydon, John / Akira, Shizuo / Moley, Kelle H / Kommagani, Ramakrishna

bioRxiv : the preprint server for biology

2024

Abstract: Recurrent pregnancy loss (RPL), characterized by two or more failed clinical pregnancies, poses a significant challenge to reproductive health. In addition to embryo quality and endometrial function, proper oviduct function is also essential for ... ...

Abstract	Recurrent pregnancy loss (RPL), characterized by two or more failed clinical pregnancies, poses a significant challenge to reproductive health. In addition to embryo quality and endometrial function, proper oviduct function is also essential for successful pregnancy establishment. Therefore, structural abnormalities or inflammation resulting from infection in the oviduct may impede the transport of embryos to the endometrium, thereby increasing the risk of miscarriage. However, the precise cellular mechanisms that maintain the structural and functional integrity of the oviduct are not studied yet. Here, we report that autophagy is critical for maintaining the oviduct homeostasis and keeping the inflammation under check to enable embryo transport. Specifically, the loss of the autophagy-related gene,
Language	English
Publishing date	2024-03-20
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.03.19.585812
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: The SARS-CoV-2 receptor, Angiotensin converting enzyme 2 (ACE2) is required for human endometrial stromal cell decidualization.

Chadchan, Sangappa B / Maurya, Vineet K / Popli, Pooja / Kommagani, Ramakrishna

bioRxiv : the preprint server for biology

2020

Abstract: Study question: Is SARS-CoV-2 receptor, angiotensin-converting enzyme 2 (ACE 2) expressed in the human endometrium during the menstrual cycle, and does it participate in endometrial decidualization?: Summary answer: ACE2 protein is highly expressed ... ...

Abstract	Study question: Is SARS-CoV-2 receptor, angiotensin-converting enzyme 2 (ACE 2) expressed in the human endometrium during the menstrual cycle, and does it participate in endometrial decidualization? Summary answer: ACE2 protein is highly expressed in human endometrial stromal cells during the secretory phase and is essential for human endometrial stromal cell decidualization. What is known already: ACE2 is expressed in numerous human tissues including the lungs, heart, intestine, kidneys and placenta. ACE2 is also the receptor by which SARS-CoV-2 enters human cells. Study design size duration: Proliferative (n = 9) and secretory (n = 6) phase endometrium biopsies from healthy reproductive-age women and primary human endometrial stromal cells from proliferative phase endometrium were used in the study. Participants/materials setting methods: ACE2 expression and localization were examined by qRT-PCR, Western blot, and immunofluorescence in both human endometrial samples and mouse uterine tissue. The effect of Main results and the role of chance: In human tissue, ACE2 protein is expressed in both endometrial epithelial and stromal cells in the proliferative phase of the menstrual cycle, and expression increases in stromal cells in the secretory phase. The Large scale data: N/A. Limitations reasons for caution: Experiments assessing the function of ACE2 in human endometrial stromal cell decidualization were Wider implications of the findings: Expression of ACE2 in the endometrium allow SARS-CoV-2 to enter endometrial epithelial and stromal cells, which could impair Study fundings/competing interests: This study was supported by National Institutes of Health / National Institute of Child Health and Human Development grants R01HD065435 and R00HD080742 to RK and Washington University School of Medicine start-up funds to RK. The authors declare that they have no conflicts of interest.
Keywords	covid19
Language	English
Publishing date	2020-06-24
Publishing country	United States
Document type	Preprint
DOI	10.1101/2020.06.23.168252
Database	MEDical Literature Analysis and Retrieval System OnLINE

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