Evidence map›Paper›PMID 26832331›Full record

ArticleDevelopmental cell2016

HDAC3-Dependent Epigenetic Pathway Controls Lung Alveolar Epithelial Cell Remodeling and Spreading via miR-17-92 and TGF-β Signaling Regulation.

Yi Wang, David B Frank, Michael P Morley, Su Zhou, Xiaoru Wang, Min Min Lu, Mitchell A Lazar, Edward E Morrisey

Open access · greenAbstract read
In one paragraph

Article in Developmental cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
7.2field-weighted citation impact, top 3% 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

64 citing papers in PubMed, 114 citations in OpenAlex.

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  13. Breathing new life into the study of COPD with genes identified from genome-wide association studies.European respiratory review : an official journal of the European Respiratory Society · 2024
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4 more citing papers are in PubMed but not listed here.

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

8 authors at 3 institutions in 2 countries.

Yi WangDepartment of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
David B FrankDepartment of Pediatrics, University of Pennsylvania, Philadelphia, PA 19104, USA.
Michael P MorleyDepartment of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
Su ZhouDepartment of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA; Penn Cardiovascular Institute, University of Pennsylvania, Philadelphia, PA 19104, USA.
Xiaoru WangDepartment of Pediatrics, Provincial Hospital Affiliated to Shandong University, Shandong University, Jinan, Shandong 250021, China.
Min Min LuDepartment of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA; Penn Cardiovascular Institute, University of Pennsylvania, Philadelphia, PA 19104, USA.
Mitchell A LazarDepartment of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA; Institute for Diabetes, Obesity, and Metabolism, University of Pennsylvania, Philadelphia, PA 19104, USA.
Edward E MorriseyDepartment of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA; Penn Cardiovascular Institute, University of Pennsylvania, Philadelphia, PA 19104, USA; Penn Center for Pulmonary Biology, University of Pennsylvania, Philadelphia, PA 19104, USA; Department of Cell and Developmental Biology, University of Pennsylvania, Philadelphia, PA 19104, USA; Penn Institute for Regenerative Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA; Translational Research Center, University of Pennsylvania, Room 11-124, 3400 Civic Center Boulevard, Building 421, Philadelphia, PA 19104-5129, USA. Electronic address: emorrise@mail.med.upenn.edu.
University of Pennsylvania · USPenn Center for AIDS Research · USShandong University · CN

Funding

VIRAL VECTOR COREP30DK019525 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI MITCHELL A. LAZAR · 1986 to 2026
$48.3M
Training in Molecular Therapeutics for Pediatric CardiologyT32HL007915 · NHLBI · CHILDREN'S HOSP OF PHILADELPHIA · PI Robert J Levy, JOSEPH W ROSSANO · 1999 to 2026
$13.4M
THYROID HORMONE RECEPTORS-REGULATION AND FUNCTIONR37DK043806 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI LAZAR, MITCHELL A. · 1998 to 2017
$8.8M
Expansion of cardiac and hematopoietic progenitors by Wnt and NotchU01HL100405 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI EPSTEIN, JONATHAN A., MORRISEY, EDWARD E · 2009 to 2015
$8.1M
Wnt signaling in the alveolar nicheR01HL087825 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI MORRISEY, EDWARD E · 2008 to 2021
$6.4M
Molecular pathways controlling alveolar epithelial remodeling in development and regenerationR01HL132999 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI MORRISEY, EDWARD E · 2016 to 2023
$4.6M
Epigenic Regulation of Lung Progenitor Repair and RegenerationU01HL110942 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI MORRISEY, EDWARD E · 2012 to 2016
$3.4M
NHLBI NIH HHS HL110942NHLBI NIH HHS NIH T32 HL007915NHLBI NIH HHS R01 HL087825NHLBI NIH HHS R01 HL132999NHLBI NIH HHS T32 HL007915NHLBI NIH HHS U01 HL100405NHLBI NIH HHS U01 HL110942NIDDK NIH HHS NIH P30 DK19525NIDDK NIH HHS NIH R37 DK43806NIDDK NIH HHS P30 DK019525NIDDK NIH HHS R37 DK043806
6 · The paper itself

Abstract

The terminal stages of pulmonary development, called sacculation and alveologenesis, involve both differentiation of distal lung endoderm progenitors and extensive cellular remodeling of the resultant epithelial lineages. These processes are coupled with dramatic expansion of distal airspace and surface area. Despite the importance of these late developmental processes and their relation to neonatal respiratory diseases, little is understood about the molecular and cellular pathways critical for their successful completion. We show that a histone deacetylase 3 (Hdac3)-mediated epigenetic pathway is critical for the proper remodeling and expansion of the distal lung saccules into primitive alveoli. Loss of Hdac3 in the developing lung epithelium leads to a reduction of alveolar type 1 cell spreading and a disruption of lung sacculation. Hdac3 represses miR-17-92 expression, a microRNA cluster that regulates transforming growth factor β (TGF-β) signaling. De-repression of miR-17-92 in Hdac3-deficient lung epithelium results in decreased TGF-β signaling activity. Importantly, inhibition of TGF-β signaling and overexpression of miR-17-92 can phenocopy the defects observed in Hdac3 null lungs. Conversely, loss of miR-17-92 expression rescues many of the defects caused by loss of Hdac3 in the lung. These studies reveal an intricate epigenetic pathway where Hdac3 is required to repress miR-17-92 expression to allow for proper TGF-β signaling during lung sacculation.

Indexed as

Epigenesis, GeneticSignal TransductionAnimalsCell DifferentiationEpithelial CellsGene Expression Regulation, DevelopmentalHistone Deacetylase 3Histone DeacetylasesLungMiceMicroRNAsTransforming Growth Factor betaHistone Deacetylase 3Histone DeacetylasesMicroRNAsMIRN17-92 microRNA, mouseTransforming Growth Factor beta

Identifiers

PMID26832331
PMCPMC4750387
OpenAlexW2263021307

What OpenQuestion holds

Textmetadata
LicenceTDM
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.