Evidence map›Paper›PMID 15730854›Full record

ArticleExperimental hematology2005

Cytokine signals through STAT3 promote expression of granulocyte secondary granule proteins in 32D cells.

Lei Wang, Murat O Arcasoy, Stephanie S Watowich, Bernard G Forget

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Experimental hematology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.9field-weighted citation impact, top 27% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 15 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 1 country.

Lei WangDepartment of Medicine, Yale University School of Medicine, New Haven, CT 06520-8021, USA.
Murat O Arcasoy
Stephanie S Watowich
Bernard G Forget
Yale University · USDuke Medical Center · USThe University of Texas MD Anderson Cancer Center · US

Funding

RED BLOOD CELL DISEASES, HEMOSTASIS, AND BLOOD BANKINGT32HL007262 · NHLBI · YALE UNIVERSITY · PI DHODAPKAR, MADHAV V · 1985 to 2011
$4.0M
Molecular Genetics of the Red Cell Membrane SkeletonR01DK019482 · NIDDK · YALE UNIVERSITY · PI FORGET, BERNARD G · 1986 to 2006
$1.7M
ERYTHROPOIETIN RECEPTOR REGULATION OF ERYTHROPOIESISK08DK002566 · NIDDK · YALE UNIVERSITY · PI ARCASOY, MURAT O · 1998 to 2002
$364k
MOLECULAR MECHANISMS CYTOKINE RECEPTOR SIGNALINGR01CA077447 · NCI · UNIVERSITY OF TEXAS MD ANDERSON CAN CTR · PI WATOWICH, STEPHANIE S · 1998 to 2000
$250k
NCI NIH HHS R01 CA077447NCI NIH HHS R01-CA77447NHLBI NIH HHS T32 HL007262NHLBI NIH HHS T32-HL07262NIDDK NIH HHS K08 DK002566NIDDK NIH HHS K08-DK02566NIDDK NIH HHS R01 DK019482NIDDK NIH HHS R01-DK19482
6 · The paper itself

Abstract

objectiveIn a previous study, we showed that activation of a transfected human erythropoietin receptor (EPOR) in the murine myeloid cell line 32D resulted in the development of morphologic features of granulocytic differentiation and expression of the neutrophil primary granule protein myeloperoxidase. We now studied if EPOR signaling could also mediate secondary granule protein gene expression and investigated the signal transduction requirements for induction of secondary granule gene expression in 32D cells. MATERIALS AND

methodsWild-type and variant 32D cells expressing normal or chimeric EPORs or receptors for granulocyte colony-stimulating factor (G-CSFRs) were stimulated with EPO or G-CSF and the expression of granulocyte-specific genes was analyzed by Northern blot analysis. To determine the signaling mechanisms required for secondary granule protein gene induction, the activation of STAT pathways following growth factor stimulation was studied by Western blot analysis.

resultsWe found that EPO treatment of 32D cells engineered to express EPOR did not result in induction of the secondary granule protein genes encoding lactoferrin and 24p3 lipocalin, the mouse homolog of human N-Gal, or the myeloid transcription factor C/EBPepsilon. Replacement of the intracellular domain of EPOR with the intracellular domain of G-CSFR in a chimeric receptor was associated with EPO-mediated induction of lactoferrin, 24p3 lipocalin, and C/EBPepsilon genes. We found that STAT3 phosphorylation was mediated by the intracellular domain of G-CSFR, but not EPOR. Replacement of one or two of the STAT5 binding sites in the intracytoplasmic domain of the EPOR with STAT3 binding sites resulted in EPO-mediated STAT3 activation and a marked increase in the expression of the 24p3 lipocalin gene. Knockdown of STAT3 protein levels with siRNA caused significant decrease in 24p3 lipocalin gene induction.

conclusionThese results indicate that EPOR signaling cannot substitute for G-CSFR signaling to stimulate secondary granule protein gene expression in 32D cells. In addition, STAT3 is a critical mediator of 24p3 lipocalin gene expression in these cells.

Indexed as

AnimalsCell DifferentiationCell LineCytoplasmic GranulesDNA-Binding ProteinsErythropoietinGene Expression RegulationGranulocytesHumansMiceProtein BiosynthesisReceptors, ErythropoietinReceptors, Granulocyte Colony-Stimulating FactorRecombinant ProteinsSignal TransductionSTAT3 Transcription FactorDNA-Binding ProteinsErythropoietinReceptors, ErythropoietinReceptors, Granulocyte Colony-Stimulating FactorRecombinant ProteinsSTAT3 protein, humanStat3 protein, mouseSTAT3 Transcription FactorTrans-Activators

Identifiers

PMID15730854
PMCPMC2388245
OpenAlexW2000545175

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.