Growth differentiation factor-15 stimulates the synthesis of corticotropin-releasing factor in hypothalamic 4B cells

Growth differentiation factor-15 (GDF15) is a stress-activated cytokine that regulates cell growth and inflammatory and stress responses. We previously reported the role and regulation of GDF15 in pituitary corticotrophs. Dexamethasone increases Gdf15 gene expression levels and production. GDF15 sup...

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Veröffentlicht in:Peptides (New York, N.Y. : 1980) N.Y. : 1980), 2023-12, Vol.170, p.171112-171112, Article 171112
Hauptverfasser: Tasso, Mizuki, Kageyama, Kazunori, Iwasaki, Yasumasa, Watanuki, Yutaka, Niioka, Kanako, Takayasu, Shinobu, Daimon, Makoto
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container_title Peptides (New York, N.Y. : 1980)
container_volume 170
creator Tasso, Mizuki
Kageyama, Kazunori
Iwasaki, Yasumasa
Watanuki, Yutaka
Niioka, Kanako
Takayasu, Shinobu
Daimon, Makoto
description Growth differentiation factor-15 (GDF15) is a stress-activated cytokine that regulates cell growth and inflammatory and stress responses. We previously reported the role and regulation of GDF15 in pituitary corticotrophs. Dexamethasone increases Gdf15 gene expression levels and production. GDF15 suppresses adrenocorticotropic hormone synthesis in pituitary corticotrophs and subsequently mediates the negative feedback effect of glucocorticoids. Here, we analyzed corticotropin-releasing factor (Crf) promoter activity in hypothalamic 4B cells transfected with promoter-driven luciferase reporter constructs. The effects of time and GDF15 concentration on Crf mRNA levels were analyzed using quantitative real-time polymerase chain reaction. Glial cell-derived neurotrophic factor family receptor α-like (GFRAL) protein is expressed in 4B cells. GDF15 increased Crf promoter activity and Crf mRNA levels in 4B cells. The protein kinase A and C pathways also contributed to the GDF15-induced increase in Crf gene expression. GDF15 stimulates GFRAL, subsequently increasing the phosphorylation of AKT, an extracellular signal-related kinase, and the cAMP response element-binding protein. Therefore, GDF15-dependent pathways may be involved in regulating Crf expression under stressful conditions in hypothalamic cells.
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GDF15 stimulates GFRAL, subsequently increasing the phosphorylation of AKT, an extracellular signal-related kinase, and the cAMP response element-binding protein. 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subjects cAMP-dependent protein kinase
cell growth
corticotropin
corticotropin-releasing hormone
Corticotropin-Releasing Hormone - genetics
Corticotropin-Releasing Hormone - metabolism
cytokines
dexamethasone
family
gene expression
glucocorticoids
Growth Differentiation Factors - genetics
Growth Differentiation Factors - metabolism
Growth Differentiation Factors - pharmacology
Hypothalamus - metabolism
luciferase
phosphorylation
Promoter Regions, Genetic
quantitative polymerase chain reaction
Receptors, Corticotropin-Releasing Hormone - genetics
Receptors, Corticotropin-Releasing Hormone - metabolism
RNA, Messenger - metabolism
title Growth differentiation factor-15 stimulates the synthesis of corticotropin-releasing factor in hypothalamic 4B cells
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