Pentraxin-3 mediates prosurvival actions of interferon tau in bovine luteinized granulosa cells
| Autor: | Ketan Shrestha, Emilia Przygrodzka, Senasige Thilina Madusanka, Rina Meidan, Monika M. Kaczmarek, Raghavendra Basavaraja |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Embryology Endogeny Pregnancy Proteins Luteal phase Biology Andrology 03 medical and health sciences 0302 clinical medicine Endocrinology Corpus Luteum Pregnancy Luteal Cells medicine Animals Gene silencing Viability assay 030219 obstetrics & reproductive medicine Kinase Obstetrics and Gynecology Cell Biology PTX3 Interferon tau Serum Amyloid P-Component C-Reactive Protein 030104 developmental biology medicine.anatomical_structure Gene Expression Regulation Reproductive Medicine Interferon Type I Cattle Female Corpus luteum |
| Zdroj: | Reproduction. 160:603-612 |
| ISSN: | 1741-7899 1470-1626 |
| DOI: | 10.1530/rep-20-0200 |
| Popis: | Pentraxin 3 (PTX3), a multimeric glycoprotein, is implicated in various biological functions. PTX3 was shown to be elevated in the corpus luteum (CL) of early pregnant ewes; however, its role in sheep or other ruminants’ CL during this reproductive stage or how it is regulated remain unknown. Here we explored the role of PTX3 and its relationship with interferon-tau (IFNT; the pregnancy recognition signaling molecule during early pregnancy in domestic ruminants) in bovine luteinized granulosa cells (LGCs). IFNT robustly elevated PTX3 expression in bovine LGCs, and significantly stimulated its expression in luteal endothelial cells, along with CL slices; yet, LGCs were the most responsive and sensitive among these luteal models. ALK2/ALK3/ALK6 kinase inhibitor, dorsomorphin, dose-dependently inhibited basal and IFNT-elevated PTX3 expression in LGCs. In contrast, ALK4/5/7 inhibitor, SB431542, did not alter basal and TGFB1-induced PTX3. We found that recombinant human PTX3 itself moderately but significantly increases LGC numbers. Because PTX3 is highly expressed in bovine LGCs, we next examined the impact of lowering endogenous PTX3 levels with siRNA. PTX3 silencing decreased the viable cell numbers and reversed IFNT actions on cell viability, percentage of proliferating cells, and on two key survival/death genes: BIRC5 encoding surviving protein, and FASL – a death-inducing signal. Interestingly, thrombospondin-1, a known luteal proapoptotic factor, was inversely related to PTX3 in LGCs. Together, these findings suggest a novel role for PTX3 during early pregnancy, as mediator of IFNT prosurvival actions supporting CL maintenance during this reproductive stage. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|