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Cited by 53Growth Hormone and Insulin-like Growth FactorsGenomics and Chromatin DynamicsCytokine Signaling Pathways and Interactions

C/EBPβ Mediates Growth Hormone-Regulated Expression of Multiple Target Genes

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Cui, Tracy X., Lin, Grace, LaPensee, Christopher R., Calinescu, Anda-Alexandra, Rathore, Maanjot, Streeter, Cale, Piwien-Pilipuk, Graciela, Lanning, Nathan +4 more·2011·Molecular Endocrinology
DOI 10.1210/me.2010-0232PMC PMC3063086
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Abstract

Regulation of c-Fos transcription by GH is mediated by CCAAT/enhancer binding protein β (C/EBPβ). This study examines the role of C/EBPβ in mediating GH activation of other early response genes, including Cyr61, Btg2, Socs3, Zfp36, and Socs1. C/EBPβ depletion using short hairpin RNA impaired responsiveness of these genes to GH, as seen for c-Fos. Rescue with wild-type C/EBPβ led to GH-dependent recruitment of the coactivator p300 to the c-Fos promoter. In contrast, rescue with C/EBPβ mutated at the ERK phosphorylation site at T188 failed to induce GH-dependent recruitment of p300, indicating that ERK-mediated phosphorylation of C/EBPβ at T188 is required for GH-induced recruitment of p300 to c-Fos. GH also induced the occupancy of phosphorylated C/EBPβ and p300 on Cyr61, Btg2, and Socs3 at predicted C/EBP-cAMP response element-binding protein motifs in their promoters. Consistent with a role for ERKs in GH-induced expression of these genes, treatment with U0126 to block ERK phosphorylation inhibited their GH-induced expression. In contrast, GH-dependent expression of Zfp36 and Socs1 was not inhibited by U0126. Thus, induction of multiple early response genes by GH in 3T3-F442A cells is mediated by C/EBPβ. A subset of these genes is regulated similarly to c-Fos, through a mechanism involving GH-stimulated ERK 1/2 activation, phosphorylation of C/EBPβ, and recruitment of p300. Overall, these studies suggest that C/EBPβ, like the signal transducer and activator of transcription proteins, regulates multiple genes in response to GH.

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  • CCN1 is transcriptionally activated by a wide range of extracellular stimuli, including PDGF, FGF2, TGF-β1, growth hormone, phorbol ester, cAMP, vitamin D3, estrogen, tamoxifen, angiotensin II, hypoxia, UV light, and mechanical stretch.

    “Exquisitely sensitive to a wide range of extracellular stimuli, CCN1 is transcriptionally activated by platelet-derived growth factor and fibroblast growth factor 2 [8], transforming growth factor β1 (TGF-β1) [19], growth hormone [20]”

    From CCN1/CYR61: the very model of a modern matricellular protein (2011) · cites this paper as [20]

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Authors
Cui, T. X., Lin, G., LaPensee, C. R., Calinescu, A.-A., Rathore, M., Streeter, C., Piwien-Pilipuk, G., Lanning, N., Jin, H., Carter-Su, C., Qin, Z. S., & Schwartz, J.
Affiliations
  • University of Michigan (US)
  • Department of Molecular and Integrative Physiology (T.X.C., G.L., C.R.L., A.-A.C., M.R., C.S., G.P.-P., H.J., C.C.-S,. J.S.)University of Michigan, Ann Arbor, Michigan 48109
  • Graduate Program in Cellular and Molecular Biology (G.L., N.L., C.C.-S., J.S.)University of Michigan, Ann Arbor, Michigan 48109
Corresponding author
Schwartz, Jessica
ORCID
Venue
Molecular Endocrinology
Publisher
The Endocrine Society
Published
2011-04-01
Volume
25
Issue
4
Pages
681-693
ISSN
  • 0888-8809 (ISSN-L)
  • 1944-9917
DOI
10.1210/me.2010-0232
PMC
PMC3063086
OpenAlex
W1976124139
Cited by
53
References
72
Citations by year
2025: 2 · 2024: 1 · 2023: 3 · 2022: 3 · 2021: 3 · 2019: 4 · 2017: 2 · 2016: 3 · 2015: 3 · 2014: 3 · 2013: 4 · 2012: 4
FWCI
4.45
Type
journal article
Language
en
Open access
Locations
  • Molecular Endocrinology (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • CONICET Digital (CONICET) (submittedVersion, cc-by-nc-sa)
Funders
  • National Science Foundation (T32 HD007505)
  • American Diabetes Association (7-09-BS-168)
  • Emory University
  • University of Michigan (48109)
  • National Institutes of Health (NIH T32)
  • College of Pharmacy, University of Michigan
  • Medical School, University of Michigan
  • Biomedical Research Council
  • National Human Genome Research Institute (R01HG005119, HG05119)
  • National Institute of General Medical Sciences (T32GM07315, T32GM007315)
  • National Institute of Diabetes and Digestive and Kidney Diseases (DK 46072, R01DK034171, K01 DK07791, DK 34171, T32DK007791, R37DK034171, R01DK046072)
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development (T32HD007505)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Growth Hormone and Insulin-like Growth Factors
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
  • Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
Keywords
C/EBPβ, growth hormone, c-fos, P300, ERK1/2 phosphorylation, early response genes, CYR61, BTG2, SOCS3, ZFP36, SOCS1, transcriptional regulation, 3T3-F442A cells
MeSH terms
Animals, Butadienes, Cell Line, Cricetulus, Gene Expression Regulation, Cricetinae, Mutation, Nitriles, Phosphorylation, Promoter Regions, Genetic, Growth Hormone, Immunoblotting, Signal Transduction, Transcriptional Activation, Polymerase Chain Reaction, Genes, fos, Response Elements, CCAAT-Enhancer-Binding Protein-beta, RNA, Small Interfering, Chromatin Immunoprecipitation, Extracellular Signal-Regulated MAP Kinases, p300-CBP Transcription Factors, Mice

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