Chemokine CCL24 promotes the growth and invasiveness of trophoblasts through ERK1/2 and PI3K signaling pathways in human early pregnancy
| العنوان: | Chemokine CCL24 promotes the growth and invasiveness of trophoblasts through ERK1/2 and PI3K signaling pathways in human early pregnancy |
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| المؤلفون: | Wen-Qing Shang, Xuan Chen, Da-Jin Li, Min-Min Yuan, Li-Ping Jin, Ming-Qing Li, Hui Li, Li-Bing Liu, Yu-Han Meng |
| المصدر: | REPRODUCTION. 150:417-427 |
| بيانات النشر: | Bioscientifica, 2015. |
| سنة النشر: | 2015 |
| مصطلحات موضوعية: | Adult, Embryology, Chemokine, Stromal cell, p38 mitogen-activated protein kinases, Apoptosis, Enzyme-Linked Immunosorbent Assay, Biology, MMP9, Immunoenzyme Techniques, Phosphatidylinositol 3-Kinases, Young Adult, Endocrinology, Cell Movement, Pregnancy, Humans, Cells, Cultured, reproductive and urinary physiology, PI3K/AKT/mTOR pathway, Cell Proliferation, Mitogen-Activated Protein Kinase 1, Mitogen-Activated Protein Kinase 3, Kinase, Cell growth, Chemokine CCL24, Obstetrics and Gynecology, Cell Biology, Flow Cytometry, Molecular biology, Trophoblasts, Cell biology, Reproductive Medicine, embryonic structures, biology.protein, Female, CCL24 |
| الوصف: | Chemokine CCL24, acting through receptor CCR3, is a potent chemoattractant for eosinophil in allergic diseases and parasitic infections. We recently reported that CCL24 and CCR3 are co-expressed by trophoblasts in human early pregnant uterus. Here we prove with evidence that steroid hormones estradiol (E), progesterone (P), and human chorionic gonadotropin (hCG), as well as decidual stromal cells (DSCs) could regulate the expression of CCL24 and CCR3 of trophoblasts. We further investigate how trophoblast-derived CCL24 mediates the function of trophoblasts in vitro, and conclude that CCL24/CCR3 promotes the proliferation, viability and invasiveness of trophoblasts. In addition, analysis of the downstream signaling pathways of CCL24/CCR3 show that extracellular signal-regulated kinases (ERK1/2) and phosphoinositide 3-kinase (PI3K) pathways may contribute to the proliferation, viability and invasiveness of trophoblasts by activating intracellular molecules Ki67 and matrix metallopeptidase 9 (MMP9). However, we did not observe any inhibitory effect on trophoblasts when blocking c-Jun N-terminal kinase (JNK) or p38 pathways. In conclusion, our data suggests that trophoblast-derived CCL24 at the maternal-fetal interface promotes trophoblasts cell growth and invasiveness by ERK1/2 and PI3K pathways. Meanwhile, pregnancy-related hormones (P and hCG), as well as DSCs could up-regulate CCL24/CCR3 expression in trophoblasts, which may indirectly influence the biological functions of trophoblasts. Thus, our results provide a possible explanation for the growth and invasion of trophoblasts in human embryo implantation. |
| تدمد: | 1741-7899 1470-1626 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::2000c8e795d5be0563655648ce91c470Test https://doi.org/10.1530/rep-15-0119Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....2000c8e795d5be0563655648ce91c470 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 17417899 14701626 |
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