Evidence map›Paper›PMID 26747785›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2016

miR-185 mediates lung epithelial cell death after oxidative stress.

Duo Zhang, Heedoo Lee, Yong Cao, Charles S Dela Cruz, Yang Jin

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

32 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. PDGFRα-positive cell-derived TIMP-1 modulates adaptive immune responses to influenza A viral infection.American journal of physiology. Lung cellular and molecular physiology · 2025
    Article
  5. Review
  6. Review
  7. Article
  8. A proinflammatory long noncoding RNA Lncenc1 regulates inflammasome activation in macrophage.American journal of physiology. Lung cellular and molecular physiology · 2023
    Article
  9. Review
  10. Emerging role of exosomes in vascular diseases.Frontiers in cardiovascular medicine · 2023
    Review
  11. Microvesicle-Derived miRNAs Regulate Proinflammatory Macrophage Activation in the Lung Following Ozone Exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2022
    Article
  12. Article
  13. Review
  14. Article
  15. MicroRNA and ROS Crosstalk in Cardiac and Pulmonary Diseases.International journal of molecular sciences · 2020
    Review
  16. Non-coding RNA and lung cancer progression.Journal of the Chinese Medical Association : JCMA · 2020
    Review
  17. Article
  18. Article
  19. Article
  20. 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

5 authors at 2 institutions in 2 countries.

Duo ZhangDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Boston University, Boston, Massachusetts;
Heedoo LeeDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Boston University, Boston, Massachusetts;
Yong CaoDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Boston University, Boston, Massachusetts; Department of Respiratory Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China;
Charles S Dela CruzSection of Pulmonary, Critical Care and Sleep Medicine, Yale University School of Medicine, New Haven, Connecticut.
Yang JinDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Boston University, Boston, Massachusetts; yjin1@bu.edu.
Boston University · USYale University · US

Funding

Cross talk between cav-1 and flot1 in lung injuryR01HL102076 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI JIN, YANG · 2011 to 2015
$2.1M
Host-Pneumococcal Interaction in the LungR01HL126094 · NHLBI · YALE UNIVERSITY · PI DELA CRUZ, CHARLES S · 2015 to 2019
$2.1M
Mechanistic insights into the systemic inflammation and organ failure in sepsisR01GM111313 · NIGMS · BRIGHAM AND WOMEN'S HOSPITAL · PI JIN, YANG · 2014 to 2017
$1.3M
Development of the RNA molecule-enriched, cell type-specific exosomesR21AI121644 · NIAID · BOSTON UNIVERSITY MEDICAL CAMPUS · PI JIN, YANG · 2016 to 2017
$444k
NHLBI NIH HHS R01 HL102076NHLBI NIH HHS R01 HL126094NIAID NIH HHS R21 AI121644NIGMS NIH HHS R01 GM111313
6 · The paper itself

Abstract

Lung epithelial cell death is a prominent feature involved in the development of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). Hyperoxia-induced ALI is an established animal model mimicking human ARDS. Small noncoding RNAs such as microRNAs (miRNAs) have potent physiological and pathological functions involving multiple disease processes. Emerging interests focus on the potential of miRNAs to serve as novel therapeutic targets and diagnostic biomarkers. We found that hyperoxia highly induces miR-185 and its precursor in human lung epithelial cells in a time-dependent manner, and this observation is confirmed using mouse primary lung epithelial cells. The hyperoxia-induced miR-185 is mediated by reactive oxygen species. Furthermore, histone deacetylase 4 (HDAC4) locates in the promoter region of miR-185. We found that hyperoxia suppresses HDAC4 specifically in a time-dependent manner and subsequently affects histone deacetylation, resulting in an elevated miR-185 transcription. Using MC1586, an inhibitor of class IIa HDACs, we showed that inhibition of class IIa HDACs upregulates the expression of miR-185, mimicking the effects of hyperoxia. Functionally, miR-185 promotes hyperoxia-induced lung epithelial cell death through inducing DNA damage. We confirmed functional roles of miR-185 using both the loss- and gain-of-function approaches. Moreover, multiple 14-3-3δ pathway proteins are highly attenuated by miR-185 in the presence of hyperoxia. Taken together, hyperoxia-induced miR-185 in lung epithelial cells contributes to oxidative stress-associated epithelial cell death through enhanced DNA damage and modulation of 14-3-3δ pathways.

Indexed as

ApoptosisOxidative Stress14-3-3 ProteinsAcetylationAlveolar Epithelial CellsAnimalsCell LineCyclin BGene ExpressionHistone DeacetylasesHumansMice, Inbred C57BLMicroRNAsPromoter Regions, GeneticProtein Processing, Post-TranslationalRepressor Proteins14-3-3 ProteinsCCNB3 protein, humanCyclin BHDAC4 protein, humanHistone DeacetylasesMicroRNAsMIRN185 microRNA, humanRepressor Proteinscell deathepithelial cellhyperoxiamiR-185oxidative stress

Identifiers

PMID26747785
PMCPMC4824162
OpenAlexW2312477239

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.