Evidence map›Paper›PMID 28860143›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2018

IL-8 mediates idiopathic pulmonary fibrosis mesenchymal progenitor cell fibrogenicity.

Libang Yang, Jeremy Herrera, Adam Gilbertsen, Hong Xia, Karen Smith, Alexey Benyumov, Peter B Bitterman, Craig A Henke

Open access · hybridAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

60 citing papers in PubMed, 90 citations in OpenAlex.

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  17. Brg1/PRMT5 nuclear complex epigenetically regulates FOXO1 in IPF mesenchymal progenitor cells.American journal of physiology. Lung cellular and molecular physiology · 2024
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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

8 authors at 1 institution in 1 country.

Libang YangDepartment of Medicine, University of Minnesota , Minneapolis, Minnesota.
Jeremy HerreraDepartment of Medicine, University of Minnesota , Minneapolis, Minnesota.
Adam GilbertsenDepartment of Medicine, University of Minnesota , Minneapolis, Minnesota.
Hong XiaDepartment of Medicine, University of Minnesota , Minneapolis, Minnesota.
Karen SmithDepartment of Medicine, University of Minnesota , Minneapolis, Minnesota.
Alexey BenyumovDepartment of Medicine, University of Minnesota , Minneapolis, Minnesota.
Peter B BittermanDepartment of Medicine, University of Minnesota , Minneapolis, Minnesota.
Craig A HenkeDepartment of Medicine, University of Minnesota , Minneapolis, Minnesota.
University of Minnesota · US

Funding

Women's CancerP30CA077598 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI Jeffrey S. Miller · 1998 to 2026
$100.4M
TRAINING-PULMONARY CELL &MOLECULAR BIOLOGY &PHYSIOLOGYT32HL007741 · NHLBI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI DUDLEY, R. ADAMS, INGBAR, DAVID H · 1994 to 2023
$13.9M
Role of fibrotic extracellular matrix in generating the IPF FibroblastR01HL125236 · NHLBI · UNIVERSITY OF MINNESOTA · PI BITTERMAN, PETER B · 2015 to 2018
$1.9M
Integrin-Matrix Regulation of IPF Fibroblast PhenotypeR01HL125227 · NHLBI · UNIVERSITY OF MINNESOTA · PI HENKE, CRAIG A · 2015 to 2018
$1.8M
NCI NIH HHS P30 CA077598NHLBI NIH HHS R01 HL125227NHLBI NIH HHS R01 HL125236NHLBI NIH HHS T32 HL007741
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a progressive fibrotic lung disease, but the mechanisms driving progression remain incompletely defined. We previously reported that the IPF lung harbors fibrogenic mesenchymal progenitor cells (MPCs), which serve as a cell of origin for IPF fibroblasts. Proliferating IPF MPCs are located at the periphery of fibroblastic foci in an active cellular front at the interface between the myofibroblast-rich focus core and adjacent normal alveolar structures. Among a large set of genes that distinguish IPF MPCs from their control counterparts, we identified IL-8 as a candidate mediator of IPF MPC fibrogenicity and driver of fibrotic progression. IPF MPCs and their progeny displayed increased steady-state levels of IL-8 and its cognate receptor CXCR1 and secreted more IL-8 than did controls. IL-8 functioned in an autocrine manner promoting IPF MPC self-renewal and the proliferation and motility of IPF MPC progeny. Secreted IL-8 also functioned in a paracrine manner stimulating macrophage migration. Analysis of IPF lung tissue demonstrated codistribution of IPF MPCs with activated macrophages in the active cellular front of the fibroblastic focus. These findings indicate that IPF MPC-derived IL-8 is capable of expanding the mesenchymal cell population and recruiting activated macrophages cells to actively evolving fibrotic lesions.

Indexed as

Cell MovementCell ProliferationCells, CulturedHumansIdiopathic Pulmonary FibrosisInterleukin-8Mesenchymal Stem CellsSignal TransductionCXCL8 protein, humanInterleukin-8fibrotic frontIL-8IPF mesenchymal progenitor cellmacrophage

Identifiers

PMID28860143
PMCPMC5866425
OpenAlexW2752013324

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.