A balancing act: RNA binding protein HuR/TTP axis in endometriosis patients

Yasmin Nasirzadeh, Mallikarjun Bidarimath, Kasra Khalaj, Asgerally T Fazleabas, Madhuri Koti, Bruce A. Lessey, Steven L. Young, Soo Hyun Ahn, Sukhbir S. Singh, Chandrakant Tayade
2020 · doi:10.17615/zrbc-w664 · W4300073179
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This study found that RNA binding proteins TTP and HuR are dysregulated in endometriosis lesions and their silencing affects inflammatory cytokine response in related cell lines.

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This study investigated the role of RNA binding proteins HuR and TTP in the pathogenesis of endometriosis by comparing their expression in lesions from patients versus healthy fertile controls. The researchers found that these proteins are dysregulated in endometriotic tissue, with HuR stabilizing inflammatory cytokines like TNF-α and IL-6 while TTP destabilizes them, suggesting an imbalance contributes to chronic inflammation. Using siRNA knockdown in cell lines, the authors demonstrated that silencing TTP alters the cellular response to inflammatory signals and affects other competing RNA binding proteins. This paper is centrally about endometriosis — specifically examining the molecular mechanisms of inflammation driven by the HuR/TTP axis in endometriotic lesions.

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Abstract

Endometriosis, a major reproductive pathology affecting 8-10% of women is characterized by chronic inflammation and immune dysfunction. Human antigen R (HuR) and Tristetraprolin (TTP) are RNA binding proteins that competitively bind to cytokines involved in inflammation including: tumor necrosis factor alpha (TNF-α), granulocyte macrophage colony stimulating factor (GM-CSF), interleukin 6 (IL-6) among others, and stabilize and destabilize them, respectively. The aim of this study was to examine RNA binding protein (RNABP) HuR/TTP axis in endometriosis patients compared to menstrual stage matched healthy fertile controls in hopes of better understanding their contribution to the pathogenesis of endometriosis. Additionally, using a targeted in vitro siRNA approach, we examined whether knock-down of TTP can play a functional role on other RNABPs that competitively bind to inflammatory targets of TTP in both endometriotic and endometrial epithelial cell lines. Our results suggest that RNABPs TTP and HuR are dysregulated in endometriotic lesions compared to matched eutopic patient samples as well endometrium from healthy controls. Silencing of TTP in endometriotic and endometrial epithelial cells revealed differential response to inflammatory cytokines and other RNABPs. Our results suggest potential involvement of HuR/TTP RNA binding protein axis in regulation of inflammation in endometriosis.
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A balancing act: RNA binding protein HuR/TTP axis in endometriosis patients Public DepositedAdd to collection You do not have access to any existing collections. You may create a new collection. Downloadable Content Download PDFCitation MLA Khalaj, Kasra, et al. A Balancing Act: Rna Binding Protein Hur/ttp Axis In Endometriosis Patients. 2017. https://doi.org/10.17615/zrbc-w664APA Khalaj, K., Ahn, S., Bidarimath, M., Nasirzadeh, Y., Singh, S., Fazleabas, A., Young, S., Lessey, B., Koti, M., & Tayade, C. (2017). A balancing act: RNA binding protein HuR/TTP axis in endometriosis patients. https://doi.org/10.17615/zrbc-w664Chicago Khalaj, Kasra, Soo Hyun Ahn, Mallikarjun Bidarimath, Yasmin Nasirzadeh, Sukhbir S Singh, Asgerally T Fazleabas, Steven L Young et al. 2017. A Balancing Act: Rna Binding Protein Hur/ttp Axis In Endometriosis Patients. https://doi.org/10.17615/zrbc-w664- Creator - Khalaj, Kasra - Other Affiliation: Department of Biomedical and Molecular Sciences; Queen's University - Ahn, Soo Hyun - Other Affiliation: Department of Biomedical and Molecular Sciences; Queen's University - Bidarimath, Mallikarjun - Other Affiliation: Department of Biomedical and Molecular Sciences; Queen's University - Nasirzadeh, Yasmin - Other Affiliation: Department of Biomedical and Molecular Sciences; Queen's University - Singh, Sukhbir S. - Other Affiliation: Department of Obstetrics and Gynecology; University of Ottawa - Fazleabas, Asgerally T. - Other Affiliation: Department of Obstetrics Gynecology and Reproductive Biology; Michigan State University; College of Human Medicine - Young, Steven L. - School of Medicine, Department of Obstetrics and Gynecology - Lessey, Bruce A. - Other Affiliation: Department of Obstetrics and Gynecology; Greenville Health Systems - Koti, Madhuri - Other Affiliation: Department of Biomedical and Molecular Sciences; Queen's University - Tayade, Chandrakant - Other Affiliation: Department of Biomedical and Molecular Sciences; Queen's University - Khalaj, Kasra - Abstract - Endometriosis, a major reproductive pathology affecting 8-10% of women is characterized by chronic inflammation and immune dysfunction. Human antigen R (HuR) and Tristetraprolin (TTP) are RNA binding proteins that competitively bind to cytokines involved in inflammation including: tumor necrosis factor alpha (TNF-α), granulocyte macrophage colony stimulating factor (GM-CSF), interleukin 6 (IL-6) among others, and stabilize and destabilize them, respectively. The aim of this study was to examine RNA binding protein (RNABP) HuR/TTP axis in endometriosis patients compared to menstrual stage matched healthy fertile controls in hopes of better understanding their contribution to the pathogenesis of endometriosis. Additionally, using a targeted in vitro siRNA approach, we examined whether knock-down of TTP can play a functional role on other RNABPs that competitively bind to inflammatory targets of TTP in both endometriotic and endometrial epithelial cell lines. Our results suggest that RNABPs TTP and HuR are dysregulated in endometriotic lesions compared to matched eutopic patient samples as well endometrium from healthy controls. Silencing of TTP in endometriotic and endometrial epithelial cells revealed differential response to inflammatory cytokines and other RNABPs. Our results suggest potential involvement of HuR/TTP RNA binding protein axis in regulation of inflammation in endometriosis. - Date of publication - 2017 - DOI - Identifier - Publisher DOI: https://doi.org/10.1038/s41598-017-06081-7 - Onescience id: 694d33fd7494260ad0bb9ab862be7344dbd2a178 - PMID: 28724967 - PMCID: PMC5517625 - Resource type - Article - Rights statement - In Copyright - Journal title - Scientific Reports - Journal volume - 7 - Journal issue - 1 - Language - English - ISSN - 2045-2322 Relations - Parents: This work has no parents. Items | Thumbnail | Title | Date Uploaded | Visibility | Actions | |---|---|---|---|---| | PubMedCentral-PMC5517625.pdf | 2017 | Public | Download |

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