Evidence map›Paper›PMID 21821727›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2011

Increased hyaluronan fragmentation during pulmonary ischemia.

Lindsey Eldridge, Aigul Moldobaeva, Elizabeth M Wagner

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

22 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Hyaluronan and halogen-induced airway hyperresponsiveness and lung injury.Annals of the New York Academy of Sciences · 2020
    Review
  6. Upregulation of airway smooth muscle calcium-sensing receptor by low-molecular-weight hyaluronan.American journal of physiology. Lung cellular and molecular physiology · 2020
    Article
  7. Article
  8. Article
  9. The role of hyaluronan in the pathobiology and treatment of respiratory disease.American journal of physiology. Lung cellular and molecular physiology · 2016
    Review
  10. Article
  11. Article
  12. Hyaluronan mediates airway hyperresponsiveness in oxidative lung injury.American journal of physiology. Lung cellular and molecular physiology · 2015
    Article
  13. Article
  14. Review
  15. Review
  16. The Rise and Fall of Hyaluronan in Respiratory Diseases.International journal of cell biology · 2015
    Review
  17. Article
  18. Article
  19. Article
  20. Article
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

3 authors at 1 institution in 1 country.

Lindsey EldridgeDepartment of Medicine, Johns Hopkins University, Baltimore, Maryland, USA.
Aigul Moldobaeva
Elizabeth M Wagner
Johns Hopkins Medicine · US

Funding

Angiogenesis in the LungR01HL071605 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI WAGNER, ELIZABETH · 2003 to 2010
$2.8M
NHLBI NIH HHS HL071605
6 · The paper itself

Abstract

Hyaluronan (HA), a glycosaminoglycan critical to the lung extracellular matrix, has been shown to dissociate into low-molecular-weight (LMW) HA fragments following exposure to injurious stimuli. In the present study we questioned whether lung HA changed during ischemia and whether changes had an effect on subsequent angiogenesis. After left pulmonary artery ligation (LPAL) in mice, we analyzed left lung homogenates immediately after the onset of ischemia (0 h) and intermittently for 14 days. The relative expression of HA synthase (HAS)1, HAS2, and HAS3 was determined by real-time RT-PCR, total HA in the lung was measured by an ELISA-like assay, gel electrophoresis was performed to determine changes in HA size distribution, and the activity of hyaluronidases was determined by zymography. A 50% increase in total HA was measured 16 h after the onset of ischemia and remained elevated for up to 7 days. Furthermore, a fourfold increase in LMW HA fragments (495-30 kDa) was observed by 4 h after LPAL. Both HAS1 and HAS2 showed increased expression 4-16 h after LPAL, yet no changes were seen in hyaluronidase activity. These results suggest that both HA fragmentation and activation of HA synthesis contribute to increased HA levels during lung ischemia. Delivery of LMW HA fragments in an in vitro tube formation assay or directly to the ischemic mouse lung in vivo both resulted in increased angiogenesis. We conclude that ischemic injury results in matrix fragmentation, which leads to stimulation of neovascularization.

Indexed as

AnimalsCollagenDrug CombinationsElectrophoresis, Agar GelEnzyme-Linked Immunosorbent AssayGene ExpressionGlucuronosyltransferaseHyaluronan SynthasesHyaluronic AcidIschemiaLamininLungMiceMice, Inbred C57BLMolecular WeightNeovascularization, PathologicCollagenDrug CombinationsGlucuronosyltransferaseHas2 protein, mouseHas3 protein, mouseHyaluronan SynthasesHyaluronic AcidLamininmatrigelProteoglycans

Identifiers

PMID21821727
PMCPMC3213986
OpenAlexW2172154057

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.