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IL-1 β Upregulates StAR and Progesterone Production Through the ERK1/2- and p38-Mediated CREB Signaling Pathways in Human Granulosa-Lutein Cells

The proinflammatory cytokine interleukin-1 β (IL-1 β ) may be involved in several ovulation-associated events, such as protease synthesis, prostaglandin production, and steroidogenesis in granulosa cells. However, the exact effect of IL-1 β on progesterone synthesis in granulosa cells and the underl... Full description

Journal Title: Endocrinology 2017, Vol. 158(10), pp.3281-3291
Main Author: Dang, Xuan
Other Authors: Zhu, Qinling , He, Yaqiong , Wang, Yuan , Lu, Yao , Li, Xiaoxue , Qi, Jia , Wu, Hasiximuke , Sun, Yun
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ID: ISSN: 0013-7227 ; E-ISSN: 1945-7170 ; DOI: 10.1210/en.2017-00029
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recordid: oxford10.1210/en.2017-00029
title: IL-1 β Upregulates StAR and Progesterone Production Through the ERK1/2- and p38-Mediated CREB Signaling Pathways in Human Granulosa-Lutein Cells
format: Article
creator:
  • Dang, Xuan
  • Zhu, Qinling
  • He, Yaqiong
  • Wang, Yuan
  • Lu, Yao
  • Li, Xiaoxue
  • Qi, Jia
  • Wu, Hasiximuke
  • Sun, Yun
subjects:
  • Medicine
  • Anatomy & Physiology
ispartof: Endocrinology, 2017, Vol. 158(10), pp.3281-3291
description: The proinflammatory cytokine interleukin-1 β (IL-1 β ) may be involved in several ovulation-associated events, such as protease synthesis, prostaglandin production, and steroidogenesis in granulosa cells. However, the exact effect of IL-1 β on progesterone synthesis in granulosa cells and the underlying mechanism remain unclear. By using cultured granulosa-lutein cells collected from women undergoing in vitro fertilization or intracytoplasmic sperm injection, we found that IL-1 β upregulated steroidogenic acute regulatory protein (StAR) expression and progesterone synthesis in granulosa-lutein cells, which was comparable with luteinizing hormone effect and could be abolished by an IL-1 receptor antagonist. Moreover, IL-1 β activated the phosphorylation of cyclic adenosine monophosphate response element-binding protein (CREB), and knockdown of CREB attenuated the induction of StAR expression and progesterone synthesis by IL-1 β in granulosa-lutein cells. Furthermore, IL-1 β activated the extracellular signal–regulated kinase (ERK)1/2 and p38 pathways and inhibition of the ERK1/2 and p38 pathways attenuated the IL-1 β –induced phosphorylation of CREB, StAR expression, and progesterone synthesis in granulosa-lutein cells. In conclusion, IL-1 β could upregulate StAR expression and stimulate progesterone biosynthesis through increase in CREB phosphorylation via activating the ERK1/2 and p38 pathways in human granulosa-lutein cells. IL-1 β upregulated StAR expression and stimulated progesterone synthesis by inducing phosphorylation of CREB via activation of the p38 and ERK1/2 MAPK signaling pathways in human granulosa-lutein cells.
language:
source:
identifier: ISSN: 0013-7227 ; E-ISSN: 1945-7170 ; DOI: 10.1210/en.2017-00029
fulltext: fulltext
issn:
  • 0013-7227
  • 00137227
  • 1945-7170
  • 19457170
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titleIL-1 β Upregulates StAR and Progesterone Production Through the ERK1/2- and p38-Mediated CREB Signaling Pathways in Human Granulosa-Lutein Cells
creatorDang, Xuan ; Zhu, Qinling ; He, Yaqiong ; Wang, Yuan ; Lu, Yao ; Li, Xiaoxue ; Qi, Jia ; Wu, Hasiximuke ; Sun, Yun
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descriptionThe proinflammatory cytokine interleukin-1 β (IL-1 β ) may be involved in several ovulation-associated events, such as protease synthesis, prostaglandin production, and steroidogenesis in granulosa cells. However, the exact effect of IL-1 β on progesterone synthesis in granulosa cells and the underlying mechanism remain unclear. By using cultured granulosa-lutein cells collected from women undergoing in vitro fertilization or intracytoplasmic sperm injection, we found that IL-1 β upregulated steroidogenic acute regulatory protein (StAR) expression and progesterone synthesis in granulosa-lutein cells, which was comparable with luteinizing hormone effect and could be abolished by an IL-1 receptor antagonist. Moreover, IL-1 β activated the phosphorylation of cyclic adenosine monophosphate response element-binding protein (CREB), and knockdown of CREB attenuated the induction of StAR expression and progesterone synthesis by IL-1 β in granulosa-lutein cells. Furthermore, IL-1 β activated the extracellular signal–regulated kinase (ERK)1/2 and p38 pathways and inhibition of the ERK1/2 and p38 pathways attenuated the IL-1 β –induced phosphorylation of CREB, StAR expression, and progesterone synthesis in granulosa-lutein cells. In conclusion, IL-1 β could upregulate StAR expression and stimulate progesterone biosynthesis through increase in CREB phosphorylation via activating the ERK1/2 and p38 pathways in human granulosa-lutein cells. IL-1 β upregulated StAR expression and stimulated progesterone synthesis by inducing phosphorylation of CREB via activation of the p38 and ERK1/2 MAPK signaling pathways in human granulosa-lutein cells.
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0The proinflammatory cytokine interleukin-1 β (IL-1 β ) may be involved in several ovulation-associated events, such as protease synthesis, prostaglandin production, and steroidogenesis in granulosa cells. However, the exact effect of IL-1 β on progesterone synthesis in granulosa cells and the underlying mechanism remain unclear. By using cultured granulosa-lutein cells collected from women undergoing in vitro fertilization or intracytoplasmic sperm injection, we found that IL-1 β upregulated steroidogenic acute regulatory protein (StAR) expression and progesterone synthesis in granulosa-lutein cells, which was comparable with luteinizing hormone effect and could be abolished by an IL-1 receptor antagonist. Moreover, IL-1 β activated the phosphorylation of cyclic adenosine monophosphate response element-binding protein (CREB), and knockdown of CREB attenuated the induction of StAR expression and progesterone synthesis by IL-1 β in granulosa-lutein cells. Furthermore, IL-1 β activated the extracellular signal–regulated kinase (ERK)1/2 and p38 pathways and inhibition of the ERK1/2 and p38 pathways attenuated the IL-1 β –induced phosphorylation of CREB, StAR expression, and progesterone synthesis in granulosa-lutein cells. In conclusion, IL-1 β could upregulate StAR expression and stimulate progesterone biosynthesis through increase in CREB phosphorylation via activating the ERK1/2 and p38 pathways in human granulosa-lutein cells.
1IL-1 β upregulated StAR expression and stimulated progesterone synthesis by inducing phosphorylation of CREB via activation of the p38 and ERK1/2 MAPK signaling pathways in human granulosa-lutein cells.
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abstractThe proinflammatory cytokine interleukin-1 β (IL-1 β ) may be involved in several ovulation-associated events, such as protease synthesis, prostaglandin production, and steroidogenesis in granulosa cells. However, the exact effect of IL-1 β on progesterone synthesis in granulosa cells and the underlying mechanism remain unclear. By using cultured granulosa-lutein cells collected from women undergoing in vitro fertilization or intracytoplasmic sperm injection, we found that IL-1 β upregulated steroidogenic acute regulatory protein (StAR) expression and progesterone synthesis in granulosa-lutein cells, which was comparable with luteinizing hormone effect and could be abolished by an IL-1 receptor antagonist. Moreover, IL-1 β activated the phosphorylation of cyclic adenosine monophosphate response element-binding protein (CREB), and knockdown of CREB attenuated the induction of StAR expression and progesterone synthesis by IL-1 β in granulosa-lutein cells. Furthermore, IL-1 β activated the extracellular signal–regulated kinase (ERK)1/2 and p38 pathways and inhibition of the ERK1/2 and p38 pathways attenuated the IL-1 β –induced phosphorylation of CREB, StAR expression, and progesterone synthesis in granulosa-lutein cells. In conclusion, IL-1 β could upregulate StAR expression and stimulate progesterone biosynthesis through increase in CREB phosphorylation via activating the ERK1/2 and p38 pathways in human granulosa-lutein cells. IL-1 β upregulated StAR expression and stimulated progesterone synthesis by inducing phosphorylation of CREB via activation of the p38 and ERK1/2 MAPK signaling pathways in human granulosa-lutein cells.
pubEndocrine Society
doi10.1210/en.2017-00029
date2017-10-01