Evidence map›Paper›PMID 19684198›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2009

Intermedin/adrenomedullin-2 is a hypoxia-induced endothelial peptide that stabilizes pulmonary microvascular permeability.

Uwe Pfeil, Muhammad Aslam, Renate Paddenberg, Karin Quanz, Chia L Chang, Jae-Il Park, Barbara Gries, Amir Rafiq, Petra Faulhammer, Anna Goldenberg and 5 more

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

30 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
  2. Altitude hypoxia and hypoxemia: pathogenesis and management.Signal transduction and targeted therapy · 2026
    Review
  3. Sustained Activation of CLR/RAMP Receptors by Gel-Forming Agonists.International journal of molecular sciences · 2022
    Article
  4. Article
  5. Review
  6. Purinergic Regulation of Endothelial Barrier Function.International journal of molecular sciences · 2021
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. The Cardiopulmonary Effects of theTurkish journal of pharmaceutical sciences · 2020
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
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  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

15 authors at 5 institutions in 5 countries.

Uwe PfeilInstitute for Anatomy and Cell Biology, Department of Internal Medicine, Justus Liebig University, Aulweg 123, 35385 Giessen, Germany. uwe.pfeil@anatomie.med.uni-giessen.de
Muhammad Aslam
Renate Paddenberg
Karin Quanz
Chia L Chang
Jae-Il Park
Barbara Gries
Amir Rafiq
Petra Faulhammer
Anna Goldenberg
Tamara Papadakis
Thomas Noll
Sheau Y T Hsu
Norbert Weissmann
Wolfgang Kummer
Czech Academy of Sciences, Institute of Physiology · CZUniversity of Giessen · DEChang Gung Memorial Hospital · TWPohang University of Science and Technology · KRStanford University · US

Funding

Role of RAMPs in Intermedin SignalingR01DK070652 · NIDDK · STANFORD UNIVERSITY · PI HSU, SHEAU-YU TEDDY · 2006 to 2010
$1.4M
NIDDK NIH HHS DK-70652NIDDK NIH HHS R01 DK070652
6 · The paper itself

Abstract

Accumulating evidence suggests a pivotal role of the calcitonin receptor-like receptor (CRLR) signaling pathway in preventing damage of the lung by stabilizing pulmonary barrier function. Intermedin (IMD), also termed adrenomedullin-2, is the most recently identified peptide targeting this receptor. Here we investigated the effect of hypoxia on the expression of IMD in the murine lung and cultured murine pulmonary microvascular endothelial cells (PMEC) as well as the role of IMD in regulating vascular permeability. Monoclonal IMD antibodies were generated, and transcript levels were assayed by quantitative RT-PCR. The promoter region of IMD gene was analyzed, and the effect of hypoxia-inducible factor (HIF)-1alpha on IMD expression was investigated in HEK293T cells. Isolated murine lungs and a human lung microvascular endothelial cell monolayer model were used to study the effect of IMD on vascular permeability. IMD was identified as a pulmonary endothelial peptide by immunohistochemistry and RT-PCR. Hypoxia caused an upregulation of IMD mRNA in the murine lung and PMEC. As shown by these results, HIF-1alpha enhances IMD promoter activity. Our functional studies showed that IMD abolished the increase in pressure-induced endothelial permeability. Moreover, IMD decreased basal and thrombin-induced hyperpermeability of an endothelial cell monolayer in a receptor-dependent manner and activated PKA in these cells. In conclusion, IMD is a novel hypoxia-induced gene and a potential interventional agent for the improvement of endothelial barrier function in systemic inflammatory responses and hypoxia-induced vascular leakage.

Indexed as

Capillary PermeabilityAdrenomedullinAnimalsCell Adhesion MoleculesCell HypoxiaEndothelial CellsHumansIn Vitro TechniquesLungMiceMicrofilament ProteinsNeuropeptidesNIH 3T3 CellsPeptide HormonesPeptidesPhosphoproteinsADM2 protein, humanAdrenomedullinCell Adhesion Moleculesintermedin protein, mouseMicrofilament ProteinsNeuropeptidesPeptide HormonesPeptidesPhosphoproteinsPhosphoserineVasodilator-Stimulated Phosphoprotein

Identifiers

PMID19684198
PMCPMC2777497
OpenAlexW2101929851

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.