Estrogen inhibits GH signaling by suppressing GH-induced JAK2 phosphorylation, an effect mediated by SOCS-2.

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MARC

Leung, K C (author)

Estrogen inhibits GH signaling by suppressing GH-induced JAK2 phosphorylation, an effect mediated by SOCS-2.

Article/chapterEnglish2003

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2003-01-27
Proceedings of the National Academy of Sciences,2003

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LIBRIS-ID:oai:gup.ub.gu.se/106984
https://gup.ub.gu.se/publication/106984URI
https://doi.org/10.1073/pnas.0337600100DOI

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Language:English

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Subject category:ref swepub-contenttype
Subject category:art swepub-publicationtype

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Oral estrogen administration attenuates the metabolic action of growth hormone (GH) in humans. To investigate the mechanism involved, we studied the effects of estrogen on GH signaling through Janus kinase (JAK)2 and the signal transducers and activators of transcription (STATs) in HEK293 cells stably expressing the GH receptor (293GHR), HuH7 (hepatoma) and T-47D (breast cancer) cells. 293GHR cells were transiently transfected with an estrogen receptor-alpha expression plasmid and luciferase reporters with binding elements for STAT3 and STAT5 or the beta-casein promoter. GH stimulated the reporter activities by four- to sixfold. Cotreatment with 17beta-estradiol (E(2)) resulted in a dose-dependent reduction in the response of all three reporters to GH to a maximum of 49-66% of control at 100 nM (P < 0.05). No reduction was seen when E(2) was added 1-2 h after GH treatment. Similar inhibitory effects were observed in HuH7 and T-47D cells. E(2) suppressed GH-induced JAK2 phosphorylation, an effect attenuated by actinomycin D, suggesting a requirement for gene expression. Next, we investigated the role of the suppressors of cytokine signaling (SOCS) in E(2) inhibition. E(2) increased the mRNA abundance of SOCS-2 but not SOCS-1 and SOCS-3 in HEK293 cells. The inhibitory effect of E(2) was absent in cells lacking SOCS-2 but not in those lacking SOCS-1 and SOCS-3. In conclusion, estrogen inhibits GH signaling, an action mediated by SOCS-2. This paper provides evidence for regulatory interaction between a sex steroid and the GHJAKSTAT pathway, in which SOCS-2 plays a central mechanistic role.

Subject headings and genre

MEDICIN OCH HÄLSOVETENSKAP Klinisk medicin Endokrinologi och diabetes hsv//swe
MEDICAL AND HEALTH SCIENCES Clinical Medicine Endocrinology and Diabetes hsv//eng
Blotting
Western
Caseins
metabolism
Cell Line
DNA-Binding Proteins
metabolism
Dactinomycin
pharmacology
Dose-Response Relationship
Drug
Estradiol
metabolism
Estrogens
metabolism
Fibroblasts
metabolism
Genes
Reporter
Human Growth Hormone
metabolism
Humans
Interleukin-6
metabolism
Janus Kinase 2
Milk Proteins
Phosphorylation
Plasmids
metabolism
Precipitin Tests
Protein-Tyrosine Kinases
metabolism
Proteins
metabolism
Proto-Oncogene Proteins
Recombinant Proteins
metabolism
Repressor Proteins
STAT3 Transcription Factor
STAT5 Transcription Factor
Signal Transduction
Suppressor of Cytokine Signaling Proteins
Trans-Activators
metabolism
Transcription Factors
Transcription
Genetic
Vanadates
pharmacology

Added entries (persons, corporate bodies, meetings, titles ...)

Doyle, N (author)
Ballesteros, M (author)
Sjögren, Klara,1970Gothenburg University,Göteborgs universitet,Institutionen för invärtesmedicin, Avdelningen för internmedicin,Institute of Internal Medicine, Dept of Medicine(Swepub:gu)xsjokl (author)
Watts, C K W (author)
Low, T H (author)
Leong, G M (author)
Ross, R J M (author)
Ho, K K Y (author)
Göteborgs universitetInstitutionen för invärtesmedicin, Avdelningen för internmedicin (creator_code:org_t)

Related titles

In:Proceedings of the National Academy of Sciences of the United States of America: Proceedings of the National Academy of Sciences100:3, s. 1016-210027-8424
In:Proceedings of the National Academy of Sciences: Proceedings of the National Academy of Sciences100:3, s. 1016-211091-6490

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