Growth hormone directly stimulates GATA2 expression.

GATA2 Growth hormone Growth hormone receptor Signal transduction Transcription factors

Journal

Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society
ISSN: 1532-2238
Titre abrégé: Growth Horm IGF Res
Pays: Scotland
ID NLM: 9814320

Informations de publication

Date de publication:
24 Jan 2024
Historique:
received: 08 09 2023
revised: 01 01 2024
accepted: 22 01 2024
medline: 29 1 2024
pubmed: 29 1 2024
entrez: 28 1 2024
Statut: aheadofprint

Résumé

GATA2 is a key transcription factor involved in the differentiation and determination of thyrotrophs and gonadotrophs in pituitary and hematopoietic development. However, studies on the upstream ligands of the GATA2 signal transduction pathway have been limited. To identify upstream ligands, we examined growth hormone (GH) as a plausible stimulator. We evaluated GH-induced GATA2 expression in murine TtT/GF thyrotrophic pituitary tumor cells and its direct impact on the GHR/JAK/STAT5 pathway using a combination of a reporter assay, real-time quantitative polymerase chain reaction, and western blotting. GATA2 expression increased with activated STAT5B in a dose-dependent manner and was inhibited by a STAT5 specific inhibitor. Moreover, we found functional STAT5B binding site consensus sequences at -359 bp in the GATA2 promoter region. These findings suggest that GH directly stimulates GATA2 via the GHR/JAK/STAT pathway and participates in various developmental phenomena mediated by GATA2.

Identifiants

pubmed: 38281404
pii: S1096-6374(24)00002-9
doi: 10.1016/j.ghir.2024.101572
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

101572

Informations de copyright

Copyright © 2024 Elsevier Ltd. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest None.

Auteurs

Mana Mitsutani (M)

Medicine & Clinical Science, Faculty of Pharmacy and Pharmaceutical Sciences, Mukogawa Women's University, Hyogo 663-8179, Japan.

Midori Matsushita (M)

Medicine & Clinical Science, Faculty of Pharmacy and Pharmaceutical Sciences, Mukogawa Women's University, Hyogo 663-8179, Japan.

Mei Yokoyama (M)

Medicine & Clinical Science, Faculty of Pharmacy and Pharmaceutical Sciences, Mukogawa Women's University, Hyogo 663-8179, Japan.

Ayumu Morita (A)

Medicine & Clinical Science, Faculty of Pharmacy and Pharmaceutical Sciences, Mukogawa Women's University, Hyogo 663-8179, Japan.

Hiromi Hano (H)

Medicine & Clinical Science, Faculty of Pharmacy and Pharmaceutical Sciences, Mukogawa Women's University, Hyogo 663-8179, Japan.

Tomomi Fujikawa (T)

Medicine & Clinical Science, Faculty of Pharmacy and Pharmaceutical Sciences, Mukogawa Women's University, Hyogo 663-8179, Japan.

Tetsuya Tagami (T)

Clinical Research Institute for Endocrine and Metabolic Diseases, National Hospital Organization Kyoto Medical Center, Kyoto 612-8555, Japan.

Kenji Moriyama (K)

Medicine & Clinical Science, Faculty of Pharmacy and Pharmaceutical Sciences, Mukogawa Women's University, Hyogo 663-8179, Japan; Clinical Research Institute for Endocrine and Metabolic Diseases, National Hospital Organization Kyoto Medical Center, Kyoto 612-8555, Japan; Institute of Biosciences, Mukogawa Women's University, Hyogo 663-8179, Japan. Electronic address: kemori@mukogawa-u.ac.jp.

Classifications MeSH