Evidence map›Paper›PMID 23002075›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2012

Hypoxia-induced endothelial CX3CL1 triggers lung smooth muscle cell phenotypic switching and proliferative expansion.

Jianliang Zhang, Hanbo Hu, Nadia L Palma, Jeffrey K Harrison, Kamal K Mubarak, Robin D Carrie, Hassan Alnuaimat, Xiaoqiang Shen, Defang Luo, Jawaharlal M Patel

Abstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.7field-weighted citation impact, top 14% 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

25 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
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  4. Article
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  6. Review
  7. Review
  8. Are circulating endothelial cells the next target for transcriptome-level pathway analysis in ARDS?American journal of physiology. Lung cellular and molecular physiology · 2023
    Article
  9. Review
  10. Research progress on the mechanism of phenotypic transformation of pulmonary artery smooth muscle cells induced by hypoxia.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2022
    Review
  11. Article
  12. Review
  13. Article
  14. Cytokines, Chemokines, and Inflammation in Pulmonary Arterial Hypertension.Advances in experimental medicine and biology · 2021
    Article
  15. Article
  16. Article
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  18. Article
  19. Review
  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

10 authors at 2 institutions in 1 country.

Jianliang ZhangDept. of Medicine, Univ. of Florida College of Medicine, Gainesville, FL 32610-0225, USA.
Hanbo Hu
Nadia L Palma
Jeffrey K Harrison
Kamal K Mubarak
Robin D Carrie
Hassan Alnuaimat
Xiaoqiang Shen
Defang Luo
Jawaharlal M Patel
University of Florida · USVeterans Health Administration · US

Funding

Viral-based Chemokine Receptor AntagonistsR01AI058256 · NIAID · UNIVERSITY OF FLORIDA · PI HARRISON, JEFFREY K. · 2006 to 2010
$2.0M
Novel Peptide for Dynamic Regulation of Lung Endothelium NOS/cGMP FunctionsR01HL085133 · NHLBI · UNIVERSITY OF FLORIDA · PI PATEL, JAWAHARLAL M. · 2008 to 2011
$1.3M
NHLBI NIH HHS HL-085133NIAID NIH HHS AI-058256
6 · The paper itself

Abstract

Distal arterioles with limited smooth muscles help maintain the high blood flow and low pressure in the lung circulation. Chronic hypoxia induces lung distal vessel muscularization. However, the molecular events that trigger alveolar hypoxia-induced peripheral endothelium modulation of vessel wall smooth muscle cell (SMC) proliferation and filling of nonmuscular areas are unclear. Here, we investigated the role of CX3CL1/CX3CR1 system in endothelial-SMC cross talk in response to hypoxia. Human lung microvascular endothelial cells responded to alveolar oxygen deficiency by overproduction of the chemokine CX3CL1. The CX3CL1 receptor CX3CR1 is expressed by SMCs that are adjacent to the distal endothelium. Hypoxic release of endothelial CX3CL1 induced SMC phenotypic switching from the contractile to the proliferative state. Inhibition of CX3CR1 prevented CX3CL1 stimulation of SMC proliferation and monolayer expansion. Furthermore, CX3CR1 deficiency attenuated spiral muscle expansion, distal vessel muscularization, and pressure elevation in response to hypoxia. Our findings indicate that the capillary endothelium relies on the CX3CL1-CX3CR1 axis to sense alveolar hypoxia and promote peripheral vessel muscularization. These results have clinical significance in the development of novel therapeutics that target mechanisms of distal arterial remodeling associated with pulmonary hypertension induced by oxygen deficiency that is present in people living at high altitudes and patients with obstructive lung diseases.

Indexed as

Cell ProliferationAnimalsCell HypoxiaChemokine CX3CL1CX3C Chemokine Receptor 1Endothelial CellsHumansHypertension, PulmonaryMiceMice, TransgenicMyocytes, Smooth MusclePulmonary AlveoliPulmonary Disease, Chronic ObstructiveReceptors, ChemokineChemokine CX3CL1CX3C Chemokine Receptor 1CX3CL1 protein, humanCx3cl1 protein, mouseCX3CR1 protein, humanCx3cr1 protein, mouseReceptors, Chemokine

Identifiers

PMID23002075
PMCPMC3517676
OpenAlexW2098586887

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.