Evidence map›Paper›PMID 27461363›Full record

ArticleThe American journal of pathology2016

Lung Epithelial Cell-Specific Expression of Human Lysosomal Acid Lipase Ameliorates Lung Inflammation and Tumor Metastasis in Lipa(-/-) Mice.

Ting Zhao, Xinchun Ding, Hong Du, Cong Yan

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.9field-weighted citation impact, top 22% 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

18 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
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  4. Article
  5. Article
  6. Review
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  8. Review
  9. Review
  10. Article
  11. Review
  12. Biogenesis and Breakdown of Lipid Droplets in Pathological Conditions.Frontiers in cell and developmental biology · 2021
    Review
  13. Article
  14. Review
  15. Lipid metabolism and lipophagy in cancer.Biochemical and biophysical research communications · 2018
    Review
  16. Review
  17. Review
  18. Review
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 2 institutions in 1 country.

Ting ZhaoDepartment of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, Indiana.
Xinchun DingDepartment of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, Indiana.
Hong DuDepartment of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, Indiana; Indiana University Simon Cancer Center, Indiana University School of Medicine, Indianapolis, Indiana. Electronic address: hongdu@iupui.edu.
Cong YanDepartment of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, Indiana; Indiana University Simon Cancer Center, Indiana University School of Medicine, Indianapolis, Indiana. Electronic address: coyan@iupui.edu.
Indiana University Health · USIndiana University School of Medicine

Funding

Pathophysiology of PPARgamma in the lungR01HL087001 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI DU, HONG · 2008 to 2012
$1.9M
Stat3 Downstream Genes as Lung Adenocarcinoma BiomarkersR01CA138759 · NCI · INDIANA UNIVERSITY INDIANAPOLIS · PI YAN, CONG · 2010 to 2014
$1.8M
Inflammation and Immunosuppression in Lung CancerR01CA152099 · NCI · INDIANA UNIVERSITY INDIANAPOLIS · PI YAN, CONG · 2011 to 2015
$1.5M
NCI NIH HHS R01 CA138759NCI NIH HHS R01 CA152099NHLBI NIH HHS R01 HL087001
6 · The paper itself

Abstract

Lysosomal acid lipase (LAL), a key enzyme in the metabolic pathway of neutral lipids, has a close connection with inflammation and tumor progression. One major manifestation in LAL-deficient (Lipa(-/-)) mice is an increase of tumor growth and metastasis associated with expansion of myeloid-derived suppressor cells. In the lung, LAL is highly expressed in alveolar type II epithelial cells. To assess how LAL in lung epithelial cells plays a role in this inflammation-related pathogenic process, lung alveolar type II epithelial cell-specific expression of human LAL (hLAL) in Lipa(-/-) mice was established by crossbreeding of CCSP-driven rtTA transgene and (TetO)7-CMV-hLAL transgene into Lipa(-/-) mice (CCSP-Tg/KO). hLAL expression in lung epithelial cells not only reduced tumor-promoting myeloid-derived suppressor cells in the lung, but also down-regulated the synthesis and secretion of tumor-promoting cytokines and chemokines into the bronchoalveolar lavage fluid of Lipa(-/-) mice. hLAL expression reduced the immunosuppressive functions of bronchoalveolar lavage fluid cells, inhibited bone marrow cell transendothelial migration, and inhibited endothelial cell proliferation and migration in Lipa(-/-) mice. As a result, hLAL expression in CCSP-Tg/KO mice corrected pulmonary damage, and inhibited tumor cell proliferation and migration in vitro, and tumor metastasis to the lung in vivo. These results support a concept that LAL is a critical metabolic enzyme in lung epithelial cells that regulates lung homeostasis, immune response, and tumor metastasis.

Indexed as

Alveolar Epithelial CellsAnimalsCell MovementEnzyme-Linked Immunosorbent AssayFlow CytometryHumansImmunohistochemistryMiceMice, KnockoutNeoplasm MetastasisPneumoniaReal-Time Polymerase Chain ReactionSterol EsteraseLIPA protein, humanSterol Esterase

Identifiers

PMID27461363
PMCPMC4973654
OpenAlexW2494563470

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.