Evidence map›Paper›PMID 24973403›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2014

CCN1 secretion and cleavage regulate the lung epithelial cell functions after cigarette smoke.

Hyung-Geun Moon, Sang-Heon Kim, Jinming Gao, Taihao Quan, Zhaoping Qin, Juan C Osorio, Ivan O Rosas, Min Wu, Yohannes Tesfaigzi, Yang Jin

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

Article in American journal of physiology. Lung cellular and molecular physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 2 pooled it
3.6field-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

66 citing papers in PubMed, 2 syntheses or guidelines pooled it, 110 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Article
  6. Review
  7. Harmonising cellular conversations: decoding the vital roles of extracellular vesicles in respiratory system intercellular communications.European respiratory review : an official journal of the European Respiratory Society · 2024
    Review
  8. Review
  9. Article
  10. Exosome-encapsulated lncRNA HOTAIRM1 contributes to PMScience China. Life sciences · 2024
    Article
  11. Epigenetic regulation of pulmonary inflammation.Seminars in cell & developmental biology · 2024
    Review
  12. Review
  13. Review
  14. Article
  15. Circulating Exosomes and Ambient Air Pollution Exposure in COPD.Chronic obstructive pulmonary diseases (Miami, Fla.) · 2023
    Article
  16. Extracellular vesicles and COPD: foe or friend?Journal of nanobiotechnology · 2023
    Review
  17. Review
  18. Review
  19. Review
  20. Review

6 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

10 authors at 6 institutions in 3 countries.

Hyung-Geun MoonDivision of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts;
Sang-Heon KimDivision of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts; Department of Internal Medicine, Hanyang University College of Medicine, Seoul, Republic of Korea;
Jinming GaoDepartment of Respiratory Diseases, Peking Union Medical College Hospital, Peking Union Medical College & Chinese Academy of Medical Sciences, Beijing, China;
Taihao QuanDepartment of Dermatology, University of Michigan Medical School, Ann Arbor, Michigan;
Zhaoping QinDepartment of Dermatology, University of Michigan Medical School, Ann Arbor, Michigan;
Juan C OsorioDivision of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts;
Ivan O RosasDivision of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts; Lovelace Respiratory Research Institute, Albuquerque, New Mexico.
Min WuBiochemistry and Molecular Biology, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, North Dakota; and.
Yohannes TesfaigziLovelace Respiratory Research Institute, Albuquerque, New Mexico.
Yang JinDivision of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts; yjin@rics.bwh.harvard.edu.
Brigham and Women's Hospital · USHarvard University · USLovelace Respiratory Research Institute · USUniversity of Michigan–Ann Arbor · USChinese Academy of Medical Sciences & Peking Union Medical College · CNUniversity of North Dakota · 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
NHLBI NIH HHS R01 HL102076NHLBI NIH HHS R01-HL-102076
6 · The paper itself

Abstract

Despite extensive research, the pathogenesis of cigarette smoking (CS)-associated emphysema remains incompletely understood, thereby impeding development of novel therapeutics, diagnostics, and biomarkers. Here, we report a novel paradigm potentially involved in the development of epithelial death and tissue loss in CS-associated emphysema. After prolonged exposure of CS, CCN1 cleavage was detected both in vitro and in vivo. Full-length CCN1 (flCCN1) was secreted in an exosome-shuttled manner, and secreted plasmin converted flCCN1 to cleaved CCN1 (cCCN1) in extracellular matrix. Interestingly, exosome-shuttled flCCN1 facilitated the interleukin (IL)-8 and vascular endothelial growth factor (VEGF) release in response to cigarette smoke extract (CSE). Therefore, flCCN1 potentially promoted CS-induced inflammation via IL-8-mediated neutrophil recruitment and also maintained the lung homeostasis via VEGF secretion. Interestingly, cCCN1 abolished these functions. Furthermore, cCCN1 promoted protease and matrix metalloproteinase (MMP)-1 production after CSE. These effects were mainly mediated by the COOH-terminal fragments of CCN1 after cleavage. Both the decrease of VEGF and the elevation of MMPs favor the development of emphysema. cCCN1, therefore, likely contributes to the epithelial cell damage after CS. Additionally, CSE and cCCN1 both stimulated integrin-α7 expressions in lung epithelial cells. The integrin-α7 appeared to be the binding receptors of cCCN1 and, subsequently, mediated its cellular function by promoting MMP1. Consistent with our observation on the functional roles of cCCN1 in vitro, elevated cCCN1 level was found in the bronchoalveolar lavage fluid from mice with emphysematous changes after 6 mo CS exposure. Taken together, we hypothesize that cCCN1 promoted the epithelial cell death and tissue loss after prolonged CS exposure.

Indexed as

AnimalsBronchoalveolar Lavage FluidCysteine-Rich Protein 61EmphysemaEpithelial CellsFibrinolysinHumansIntegrin alpha ChainsInterleukin-8LungMaleMatrix Metalloproteinase 1MiceNeutrophil InfiltrationSmokingVascular Endothelial Growth Factor ACCN1 protein, humanCCN1 protein, mouseCysteine-Rich Protein 61FibrinolysinIntegrin alpha ChainsInterleukin-8Matrix Metalloproteinase 1Vascular Endothelial Growth Factor Acigarette smokingcleaved ccn1full-length CCN1matrix metalloproteinase-1

Identifiers

PMID24973403
PMCPMC4137167
OpenAlexW2322031379

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.