Evidence map›Paper›PMID 33294172›Full record

ArticlePulmonary circulation

Endothelial platelet-derived growth factor-mediated activation of smooth muscle platelet-derived growth factor receptors in pulmonary arterial hypertension.

Kang Wu, Haiyang Tang, Ruizhu Lin, Shane G Carr, Ziyi Wang, Aleksandra Babicheva, Ramon J Ayon, Pritesh P Jain, Mingmei Xiong, Marisela Rodriguez and 12 more

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

Article in Pulmonary circulation. 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
1.6field-weighted citation impact, top 13% 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, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Receptor Tyrosine Kinase: Still an Interesting Target to Inhibit the Proliferation of Vascular Smooth Muscle Cells.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2023
    Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
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  14. 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

22 authors at 3 institutions in 2 countries.

Kang WuDepartments of Medicine and Physiology, The University of Arizona, Tucson, USA.
Haiyang TangDepartments of Medicine and Physiology, The University of Arizona, Tucson, USA.
Ruizhu LinDepartments of Medicine and Physiology, The University of Arizona, Tucson, USA.
Shane G CarrDepartments of Medicine and Physiology, The University of Arizona, Tucson, USA.
Ziyi WangDepartments of Medicine and Physiology, The University of Arizona, Tucson, USA.
Aleksandra BabichevaDepartments of Medicine and Physiology, The University of Arizona, Tucson, USA.
Ramon J AyonDepartments of Medicine and Physiology, The University of Arizona, Tucson, USA.
Pritesh P JainDepartments of Medicine and Physiology, The University of Arizona, Tucson, USA.
Mingmei XiongDepartments of Medicine and Physiology, The University of Arizona, Tucson, USA.
Marisela RodriguezDepartments of Medicine and Physiology, The University of Arizona, Tucson, USA.
Shamin RahimiDivision of Pulmonary, Critical Care and Sleep Medicine (Section of Physiology), University of California, San Diego, La Jolla, USA.
Francesca BalistrieriDivision of Pulmonary, Critical Care and Sleep Medicine (Section of Physiology), University of California, San Diego, La Jolla, USA.
Shayan RahimiDivision of Pulmonary, Critical Care and Sleep Medicine (Section of Physiology), University of California, San Diego, La Jolla, USA.
Daniela Valdez-JassoDepartment of Bioengineering, University of California, San Diego, La Jolla, USA.
Tatum S SimonsonDivision of Pulmonary, Critical Care and Sleep Medicine (Section of Physiology), University of California, San Diego, La Jolla, USA.
Ankit A DesaiDepartments of Medicine and Physiology, The University of Arizona, Tucson, USA.
Joe G N GarciaDepartments of Medicine and Physiology, The University of Arizona, Tucson, USA.ORCID https://orcid.org/0000-0002-6934-0420
John Y-J ShyyDivision of Cardiovascular Medicine, University of California, San Diego, La Jolla, USA.
Patricia A ThistlethwaiteDepartment of Surgery, University of California, San Diego, La Jolla, USA.
Jian WangDepartments of Medicine and Physiology, The University of Arizona, Tucson, USA.
Ayako MakinoDepartments of Medicine and Physiology, The University of Arizona, Tucson, USA.ORCID https://orcid.org/0000-0003-1259-8604
Jason X-J YuanDepartments of Medicine and Physiology, The University of Arizona, Tucson, USA.
University of Arizona · USUniversity of California System · USUniversity of California San Diego · US

Funding

Ion Channels and Membrane Receptors in Pulmonary Arterial HypertensionR35HL135807 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI YUAN, JASON X J · 2017 to 2023
$5.6M
Novel Involvement of NAMPT and TLR4 in PAH Vascular RemodelingR01HL141387 · NHLBI · UNIVERSITY OF FLORIDA · PI Joe G. N. Garcia, Ayako Makino · 2019 to 2026
$3.8M
Molecular Mechanisms of Pulmonary HypertensionR01HL070852 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI THISTLETHWAITE, PATRICIA A · 2002 to 2011
$3.1M
Pathogenic Role of IL-18 in Sickle Cell Cardiomyopathy and Inducible Ventricular TachycardiaR01HL136603 · NHLBI · UNIVERSITY OF ARIZONA · PI DESAI, ANKIT A · 2017 to 2021
$2.4M
Role of Gap Junction in Hypoxia-induced Pulmonary HypertensionR01HL146764 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MAKINO, AYAKO · 2019 to 2022
$1.6M
NHLBI NIH HHS R01 HL070852NHLBI NIH HHS R01 HL136603NHLBI NIH HHS R01 HL141387NHLBI NIH HHS R01 HL146764NHLBI NIH HHS R35 HL135807
6 · The paper itself

Abstract

Platelet-derived growth factor is one of the major growth factors found in human and mammalian serum and tissues. Abnormal activation of platelet-derived growth factor signaling pathway through platelet-derived growth factor receptors may contribute to the development and progression of pulmonary vascular remodeling and obliterative vascular lesions in patients with pulmonary arterial hypertension. In this study, we examined the expression of platelet-derived growth factor receptor isoforms in pulmonary arterial smooth muscle and pulmonary arterial endothelial cells and investigated whether platelet-derived growth factor secreted from pulmonary arterial smooth muscle cell or pulmonary arterial endothelial cell promotes pulmonary arterial smooth muscle cell proliferation. Our results showed that the protein expression of platelet-derived growth factor receptor α and platelet-derived growth factor receptor β in pulmonary arterial smooth muscle cell was upregulated in patients with idiopathic pulmonary arterial hypertension compared to normal subjects. Platelet-derived growth factor activated platelet-derived growth factor receptor α and platelet-derived growth factor receptor β in pulmonary arterial smooth muscle cell, as determined by phosphorylation of platelet-derived growth factor receptor α and platelet-derived growth factor receptor β. The platelet-derived growth factor-mediated activation of platelet-derived growth factor receptor α/platelet-derived growth factor receptor β was enhanced in idiopathic pulmonary arterial hypertension-pulmonary arterial smooth muscle cell compared to normal cells. Expression level of platelet-derived growth factor-AA and platelet-derived growth factor-BB was greater in the conditioned media collected from idiopathic pulmonary arterial hypertension-pulmonary arterial endothelial cell than from normal pulmonary arterial endothelial cell. Furthermore, incubation of idiopathic pulmonary arterial hypertension-pulmonary arterial smooth muscle cell with conditioned culture media from normal pulmonary arterial endothelial cell induced more platelet-derived growth factor receptor α activation than in normal pulmonary arterial smooth muscle cell. Accordingly, the conditioned media from idiopathic pulmonary arterial hypertension-pulmonary arterial endothelial cell resulted in more pulmonary arterial smooth muscle cell proliferation than the media from normal pulmonary arterial endothelial cell. These data indicate that (a) the expression and activity of platelet-derived growth factor receptor are increased in idiopathic pulmonary arterial hypertension-pulmonary arterial smooth muscle cell compared to normal pulmonary arterial smooth muscle cell, and (b) pulmonary arterial endothelial cell from idiopathic pulmonary arterial hypertension patients secretes higher level of platelet-derived growth factor than pulmonary arterial endothelial cell from normal subjects. The enhanced secretion (and production) of platelet-derived growth factor from idiopathic pulmonary arterial hypertension-pulmonary arterial endothelial cell and upregulated platelet-derived growth factor receptor expression (and function) in idiopathic pulmonary arterial hypertension-pulmonary arterial smooth muscle cell may contribute to enhancing platelet-derived growth factor/platelet-derived growth factor receptor-associated pulmonary vascular remodeling in pulmonary arterial hypertension.

Indexed as

endothelial cellplatelet-derived growth factorplatelet-derived growth factorreceptorsmooth muscle cell

Identifiers

PMID33294172
PMCPMC7707860
OpenAlexW3045457999

What Socratic 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 Socratic graph.