Stimulatory effects of interleukin-1 beta on development of porcine uterine epithelial cell are mediated by activation of the ERK1/2 MAPK cell signaling cascade
- Authors
- Jeong, Wooyoung; Kim, Jinhyeon; Bazer, Fuller W.; Song, Gwonhwa; Kim, Jinyoung
- Issue Date
- 5-1월-2016
- Publisher
- ELSEVIER IRELAND LTD
- Keywords
- Pig; IL-1 beta; Ped-implantation; Uterine luminal epithelium; ERK1/2 MAPK
- Citation
- MOLECULAR AND CELLULAR ENDOCRINOLOGY, v.419, no.C, pp.225 - 234
- Indexed
- SCIE
SCOPUS
- Journal Title
- MOLECULAR AND CELLULAR ENDOCRINOLOGY
- Volume
- 419
- Number
- C
- Start Page
- 225
- End Page
- 234
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/89834
- DOI
- 10.1016/j.mce.2015.10.022
- ISSN
- 0303-7207
- Abstract
- Successful establishment of pregnancy depends on timely changes in the conceptus (embryo and associated extra-embryonic membranes) and uterine endometrium orchestrated by molecules from both the conceptus and uterus. Interleukin-1 beta (IL-1 beta) is an important mediator of that communication regulating development of the peri-implantation conceptus and opening the window of implantation during early pregnancy. However, little is known about IL-1 beta-mediated intracellular signaling cascades and functional effects in uterine luminal epithelium (LE) during the peri-implantation period of pregnancy in pigs. Therefore, this study determined, using an immortalized porcine LE (pLE) cell line from day 12 pregnant gilts: 1) the intracellular signaling cascade responsible for activities of IL-1 beta in pLE cells, and 2) the changes in cellular activities induced by IL-1 beta. IL-1 beta stimulated phosphorylation of ERK1/2 proteins in pLE cells in a dose-dependent manner. Ten ng/ml IL-1 beta increased levels of phosphorylated (p)-ERK1/2 proteins in pLE cells within 15 min post-treatment, and this IL-1 beta-induced phosphorylated status was inhibited by increasing doses of U0126 (ERK1/2 inhibitor). In addition IL-10 increased p-P7056K, pP90S6K, p-S6, and p-P38 proteins in a time-dependent manner, but IL-1 beta-induced activation of P70S6K and S6 proteins was significantly decreased in the presence of pharmacological inhibitors for ERK1/2 (U0126), MTOR (rapamycin), and P38 (SB203580). Moreover, IL-1 beta treatment potently increased the abundance of p-ERK1/2 proteins in the nucleus and cytoplasm. Similarly cytoplasmic p-S6 proteins were localized abundantly in the pLE cells treated with IL-1 beta. Furthermore, IL-10 increased proliferation of pLE cells by approximately 200%, and pretreatment of pLE cells with U0126 significantly inhibited this stimulatory effect. Collectively, results of this study indicate that IL-1 beta plays an important role in development of uterine LE by stimulating cell proliferation, and that these effects are coordinately regulated by activation of the ERK1/2 and P38 MAPK cell signaling cascades. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
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