Evidence map›Paper›PMID 36762637›Full record

ArticleDevelopment (Cambridge, England)2023

Sp3 is essential for normal lung morphogenesis and cell cycle progression during mouse embryonic development.

Alyssa M McCoy, Omar Lakhdari, Sayane Shome, Kaitlin Caoili, Gilberto E Hernandez, Nima Aghaeepour, Lindsay D Butcher, Kathleen Fisch, Lawrence S Prince

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Development (Cambridge, England), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
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

9 authors.

Alyssa M McCoyDepartment of Pediatrics, University of California, San Diego, La Jolla, CA 92093, USA.ORCID 0000-0001-8134-6158
Omar LakhdariDepartment of Pediatrics, University of California, San Diego, La Jolla, CA 92093, USA.ORCID 0000-0002-1104-2412
Sayane ShomeDepartment of Pediatrics, Stanford University, Palo Alto, CA 94304, USA.ORCID 0000-0001-7959-470X
Kaitlin CaoiliDepartment of Pediatrics, Stanford University, Palo Alto, CA 94304, USA.
Gilberto E HernandezDepartment of Pediatrics, University of California, San Diego, La Jolla, CA 92093, USA.ORCID 0000-0001-5738-0209
Nima AghaeepourDepartment of Pediatrics, Stanford University, Palo Alto, CA 94304, USA.ORCID 0000-0002-6117-8764
Lindsay D ButcherDepartment of Pediatrics, Stanford University, Palo Alto, CA 94304, USA.
Kathleen FischDepartment of Obstetrics, Gynecology, and Reproductive Services, University of California, San Diego, La Jolla, CA 92093, USA.ORCID 0000-0002-0117-7444
Lawrence S PrinceDepartment of Pediatrics, Stanford University, Palo Alto, CA 94304, USA.ORCID 0000-0002-7010-4548

Funding

UC San Diego Clinical and Translational Research InstituteUL1TR001442 · NCATS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FIRESTEIN, GARY S, HOGARTH, MICHAEL · 2015 to 2024
$88.3M
FGF-10 Expression in a Fetal Mouse Lung Model of Bronchopulmonary DysplasiaR01HL086324 · NHLBI · VANDERBILT UNIVERSITY · PI PRINCE, LAWRENCE S · 2008 to 2017
$3.7M
Transcriptional Control of Lung Macrophage DevelopmentR01HL126703 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI HOFFMAN, HAROLD M, PRINCE, LAWRENCE S · 2015 to 2018
$1.6M
NCATS NIH HHS UL1 TR001442NHLBI NIH HHS R01 HL086324NHLBI NIH HHS R01 HL126703
6 · The paper itself

Abstract

Members of the Sp family of transcription factors regulate gene expression via binding GC boxes within promoter regions. Unlike Sp1, which stimulates transcription, the closely related Sp3 can either repress or activate gene expression and is required for perinatal survival in mice. Here, we use RNA-seq and cellular phenotyping to show how Sp3 regulates murine fetal cell differentiation and proliferation. Homozygous Sp3-/- mice were smaller than wild-type and Sp+/- littermates, died soon after birth and had abnormal lung morphogenesis. RNA-seq of Sp3-/- fetal lung mesenchymal cells identified alterations in extracellular matrix production, developmental signaling pathways and myofibroblast/lipofibroblast differentiation. The lungs of Sp3-/- mice contained multiple structural defects, with abnormal endothelial cell morphology, lack of elastic fiber formation, and accumulation of lipid droplets within mesenchymal lipofibroblasts. Sp3-/- cells and mice also displayed cell cycle arrest, with accumulation in G0/G1 and reduced expression of numerous cell cycle regulators including Ccne1. These data detail the global impact of Sp3 on in vivo mouse gene expression and development.

Indexed as

Embryonic DevelopmentTranscription FactorsAnimalsCell DivisionLungMicePromoter Regions, GeneticSp1 Transcription FactorSp1 Transcription FactorTranscription FactorsAlveolar developmentCell proliferationLipofibroblastLung mesenchymeMyofibroblastTranscriptional regulation

Identifiers

PMID36762637
PMCPMC10110423

What OpenQuestion holds

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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.