Evidence map›Paper›PMID 18314539›Full record

ArticleAmerican journal of respiratory cell and molecular biology2008

Cyclic stretch affects pulmonary endothelial cell control of pulmonary smooth muscle cell growth.

Cristhiaan D Ochoa, Haven Baker, Stephen Hasak, Robina Matyal, Aleya Salam, Charles A Hales, William Hancock, Deborah A Quinn

Abstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

14 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
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  7. Remodeling of anAPL bioengineering · 2021
    Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Adrenomedullin and adrenotensin regulate collagen synthesis and proliferation in pulmonary arterial smooth muscle cells.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2013
    Article
  13. Loss-of-function thrombospondin-1 mutations in familial pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2012
    Article
  14. 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

8 authors at 3 institutions in 1 country.

Cristhiaan D OchoaPulmonary and Critical Care Unit, Massachusetts General Hospital, Bullfinch 148, 55 Fruit Street, Boston, MA 02114, USA. cdo701@jaguar1.usouthal.edu
Haven Baker
Stephen Hasak
Robina Matyal
Aleya Salam
Charles A Hales
William Hancock
Deborah A Quinn
Harvard University Press · USNortheastern University · USMassachusetts General Hospital · US

Funding

HEPARIN ON HYPOXIC PULMONARY HYPERTENSION AND REMODELINGR01HL039150 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI HALES, CHARLES A · 1987 to 2011
$4.3M
NHLBI NIH HHS HL39150
6 · The paper itself

Abstract

Endothelial cells are subjected to mechanical forces in the form of cyclic stretch resulting from blood pulsatility. Pulmonary artery endothelial cells (PAECs) produce factors that stimulate and inhibit pulmonary artery smooth muscle cell (PASMC) growth. We hypothesized that PAECs exposed to cyclic stretch secrete proteins that inhibit PASMC growth. Media from PAECs exposed to cyclic stretch significantly inhibited PASMC growth in a time-dependent manner. Lyophilized material isolated from stretched PAEC-conditioned media significantly inhibited PASMC growth in a dose-dependent manner. This inhibition was reversed by trypsin inactivation, which is consistent with the relevant factor being a protein(s). To identify proteins that inhibited cell growth in conditioned media from stretched PAECs, we used proteomic techniques and found that thrombospondin (TSP)-1, a natural antiangiogenic factor, was up-regulated by stretch. In vitro, exogenous TSP-1 inhibited PASMC growth. TSP-1-blocking antibodies reversed conditioned media-induced inhibition of PASMC growth. Cyclic stretched PAECs secrete protein(s) that inhibit PASMC proliferation. TSP-1 may be, at least in part, responsible for this inhibition. The complete identification and understanding of the secreted proteome of stretched PAECs may lead to new insights into the pathophysiology of pulmonary vascular remodeling.

Indexed as

ActinsAnimalsCattleCell DivisionCells, CulturedCryopreservationCulture Media, ConditionedEndothelium, VascularHomeostasisMuscle, SmoothMuscle, Smooth, VascularPatch-Clamp TechniquesPulmonary ArteryRespiratory Mucosavon Willebrand FactorActinsCulture Media, Conditionedvon Willebrand Factor

Identifiers

PMID18314539
PMCPMC2438445
OpenAlexW1978578299

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.