Evidence map›Paper›PMID 31907997›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2020

SHIP-1, a target of miR-155, regulates endothelial cell responses in lung fibrosis.

Haiying Tang, Jingwei Mao, Xujun Ye, Fengrui Zhang, William G Kerr, Tao Zheng, Zhou Zhu

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

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

27 citing papers in PubMed, 38 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

7 authors at 4 institutions in 2 countries.

Haiying TangSection of Allergy and Clinical Immunology, Yale University School of Medicine, New Haven, CT, USA.
Jingwei MaoSection of Allergy and Clinical Immunology, Yale University School of Medicine, New Haven, CT, USA.
Xujun YeSection of Allergy and Clinical Immunology, Yale University School of Medicine, New Haven, CT, USA.
Fengrui ZhangSection of Allergy and Clinical Immunology, Yale University School of Medicine, New Haven, CT, USA.
William G KerrDepartment of Microbiology and Immunology, SUNY Upstate Medical University, Syracuse, NY, USA.
Tao ZhengSection of Allergy and Clinical Immunology, Yale University School of Medicine, New Haven, CT, USA.
Zhou ZhuSection of Allergy and Clinical Immunology, Yale University School of Medicine, New Haven, CT, USA.
Yale University · USBrown University · USDalian Medical University · CNSUNY Upstate Medical University · US

Funding

Treating lung inflammation by targeting SiglecsP01HL107151 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI SCHNAAR, RONALD L · 2011 to 2017
$15.4M
NHLBI NIH HHS P01 HL107151
6 · The paper itself

Abstract

Src Homology 2-containing Inositol Phosphatase-1 (SHIP-1) is a target of miR-155, a pro-inflammatory factor. Deletion of the SHIP-1 gene in mice caused spontaneous lung inflammation and fibrosis. However, the role and function of endothelial miR-155 and SHIP-1 in lung fibrosis remain unknown. Using whole-body miR-155 knockout mice and endothelial cell-specific conditional miR-155 (VEC-Cre-miR-155 or VEC-miR-155) or SHIP-1 (VEC-SHIP-1) knockout mice, we assessed endothelial-mesenchymal transition (EndoMT) and fibrotic responses in bleomycin (BLM) induced lung fibrosis models. Primary mouse lung endothelial cells (MLEC) and human umbilical vein endothelial cells (HUVEC) with SHIP-1 knockdown were analyzed in TGF-β1 or BLM, respectively, induced fibrotic responses. Fibrosis and EndoMT were significantly reduced in miR-155KO mice and changes in EndoMT markers in MLEC after TGF-β1 stimulation confirmed the in vivo findings. Furthermore, lung fibrosis and EndoMT responses were reduced in VEC-miR-155 mice but significantly enhanced in VEC-SHIP-1 mice after BLM challenge. SHIP-1 knockdown in HUVEC cells resulted in enhanced EndoMT induced by BLM. Meanwhile, these changes involved the PI3K/AKT, JAK/STAT3, and SMAD/STAT signaling pathways. These studies demonstrate that endothelial miR-155 plays an important role in fibrotic responses in the lung through EndoMT. Endothelial SHIP-1 is essential in controlling fibrotic responses and SHIP-1 is a target of miR-155. Endothelial cells are an integral part in lung fibrosis.

Indexed as

MAP Kinase Signaling SystemAnimalsDisease Models, AnimalHumansHuman Umbilical Vein Endothelial CellsMiceMice, KnockoutMicroRNAsPhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesPulmonary FibrosisTransforming Growth Factor beta1INPP5D protein, humanInpp5d protein, mouseMicroRNAsMIRN155 microRNA, humanMirn155 microRNA, mousePhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesTGFB1 protein, humanTgfb1 protein, mouseTransforming Growth Factor beta1endothelial-mesenchymal transitionlung fibrosismiR-155phosphatase SHIP-1

Identifiers

PMID31907997
PMCPMC7449602
OpenAlexW2997137076

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.