Evidence map›Paper›PMID 31698979›Full record

ArticleJournal of the American Heart Association2019

Newly Identified Peptide, Peptide Lv, Promotes Pathological Angiogenesis.

Liheng Shi, Min Zhao, Colette A Abbey, Shu-Huai Tsai, Wankun Xie, Dylan Pham, Samantha Chapman, Kayla J Bayless, Travis W Hein, Robert H Rosa and 3 more

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.3field-weighted citation impact, top 40% 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

8 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. HInternational journal of molecular sciences · 2022
    Article
  6. Article
  7. Article
  8. Newly Identified Peptide, Peptide Lv, Promotes Pathological Angiogenesis.Journal of the American Heart Association · 2019
    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

13 authors at 2 institutions in 1 country.

Liheng ShiDepartment of Veterinary Integrative Biosciences College of Veterinary Medicine and Biomedical Sciences Texas A&M University College Station TX.
Min ZhaoDepartment of Medical Physiology Ophthalmic Vascular Research Program College of Medicine Texas A&M University Health Science Center Bryan TX.
Colette A AbbeyDepartment of Molecular and Cellular Medicine College of Medicine Texas A&M University Health Science Center Bryan TX.
Shu-Huai TsaiDepartment of Medical Physiology Ophthalmic Vascular Research Program College of Medicine Texas A&M University Health Science Center Bryan TX.
Wankun XieDepartment of Medical Physiology Ophthalmic Vascular Research Program College of Medicine Texas A&M University Health Science Center Bryan TX.
Dylan PhamDepartment of Veterinary Integrative Biosciences College of Veterinary Medicine and Biomedical Sciences Texas A&M University College Station TX.
Samantha ChapmanDepartment of Veterinary Integrative Biosciences College of Veterinary Medicine and Biomedical Sciences Texas A&M University College Station TX.
Kayla J BaylessDepartment of Molecular and Cellular Medicine College of Medicine Texas A&M University Health Science Center Bryan TX.
Travis W HeinDepartment of Medical Physiology Ophthalmic Vascular Research Program College of Medicine Texas A&M University Health Science Center Bryan TX.
Robert H RosaDepartment of Medical Physiology Ophthalmic Vascular Research Program College of Medicine Texas A&M University Health Science Center Bryan TX.
Michael L KoDepartment of Veterinary Integrative Biosciences College of Veterinary Medicine and Biomedical Sciences Texas A&M University College Station TX.
Lih KuoDepartment of Medical Physiology Ophthalmic Vascular Research Program College of Medicine Texas A&M University Health Science Center Bryan TX.
Gladys Y-P KoDepartment of Veterinary Integrative Biosciences College of Veterinary Medicine and Biomedical Sciences Texas A&M University College Station TX.
Texas A&M University · USTexas A&M Health Science Center · US

Funding

Roles of LOX-1 and Stress-Activated Kinases in Retinal Dysfunction during Early DiabetesR01EY024624 · NEI · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI HEIN, TRAVIS W · 2015 to 2017
$1.4M
Vasomotor Dysfunction of Retinal Arterioles in DiabetesR01EY023335 · NEI · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI HEIN, TRAVIS W · 2014 to 2016
$1.1M
NEI NIH HHS R01 EY023335NEI NIH HHS R01 EY024624
6 · The paper itself

Abstract

Background We recently discovered a small endogenous peptide, peptide Lv, with the ability to activate vascular endothelial growth factor receptor 2 and its downstream signaling. As vascular endothelial growth factor through vascular endothelial growth factor receptor 2 contributes to normal development, vasodilation, angiogenesis, and pathogenesis of various diseases, we investigated the role of peptide Lv in vasodilation and developmental and pathological angiogenesis in this study. Methods and Results The endothelial cell proliferation, migration, and 3-dimensional sprouting assays were used to test the abilities of peptide Lv in angiogenesis in vitro. The chick chorioallantoic membranes and early postnatal mice were used to examine its impact on developmental angiogenesis. The oxygen-induced retinopathy and laser-induced choroidal neovascularization mouse models were used for in vivo pathological angiogenesis. The isolated porcine retinal and coronary arterioles were used for vasodilation assays. Peptide Lv elicited angiogenesis in vitro and in vivo. Peptide Lv and vascular endothelial growth factor acted synergistically in promoting endothelial cell proliferation. Peptide Lv-elicited vasodilation was not completely dependent on nitric oxide, indicating that peptide Lv had vascular endothelial growth factor receptor 2/nitric oxide-independent targets. An antibody against peptide Lv, anti-Lv, dampened vascular endothelial growth factor-elicited endothelial proliferation and laser-induced vascular leakage and choroidal neovascularization. While the pathological angiogenesis in mouse eyes with oxygen-induced retinopathy was enhanced by exogenous peptide Lv, anti-Lv dampened this process. Furthermore, deletion of peptide Lv in mice significantly decreased pathological neovascularization compared with their wild-type littermates. Conclusions These results demonstrate that peptide Lv plays a significant role in pathological angiogenesis but may be less critical during development. Peptide Lv is involved in pathological angiogenesis through vascular endothelial growth factor receptor 2-dependent and -independent pathways. As anti-Lv dampened the pathological angiogenesis in the eye, anti-Lv may have a therapeutic potential to treat pathological angiogenesis.

Indexed as

AnimalsArteriolesCell Migration AssaysCell MovementCell ProliferationChick EmbryoChorioallantoic MembraneChoroidal NeovascularizationCoronary VesselsDiabetic RetinopathyDisease Models, AnimalDogsHumansHuman Umbilical Vein Endothelial CellsMiceMice, KnockoutLv peptide, mousePeptidesVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2angiogenesisendothelial cellvasculogenesis

Identifiers

PMID31698979
PMCPMC6915261
OpenAlexW2988528846

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.