Evidence map›Paper›PMID 27402674›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2016

Novel role for p56/Lck in regulation of endothelial cell survival and angiogenesis.

Venkaiah Betapudi, Meenal Shukla, Ravi Alluri, Sergei Merkulov, Keith R McCrae

Open access · bronzeAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
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  8. FHIT, a Novel Modifier Gene in Pulmonary Arterial Hypertension.American journal of respiratory and critical care medicine · 2019
    Article
  9. Gene Therapy Leaves a Vicious Cycle.Frontiers in oncology · 2019
    Review
  10. Article
  11. Review
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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

5 authors at 2 institutions in 1 country.

Venkaiah BetapudiDepartment of Cellular and Molecular Medicine Cleveland Clinic, Cleveland, Ohio, USA; Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio, USA; and.
Meenal ShuklaDepartment of Cellular and Molecular Medicine Cleveland Clinic, Cleveland, Ohio, USA.
Ravi AlluriDepartment of Cellular and Molecular Medicine Cleveland Clinic, Cleveland, Ohio, USA.
Sergei MerkulovDepartment of Cellular and Molecular Medicine Cleveland Clinic, Cleveland, Ohio, USA.
Keith R McCraeDepartment of Cellular and Molecular Medicine Cleveland Clinic, Cleveland, Ohio, USA; Taussig Cancer Institute, Cleveland Clinic, Cleveland, Ohio, USA mccraek@ccf.org.
Case Western Reserve University · USCleveland Clinic · US

Funding

Regulation of Angiogenesis by KininogenR01HL089796 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI MCCRAE, KEITH R. · 2009 to 2013
$2.0M
NHLBI NIH HHS R01 HL089796
6 · The paper itself

Abstract

Previous studies have demonstrated that cleaved high-molecular-weight kininogen (HKa) induces endothelial apoptosis and inhibits angiogenesis and have suggested that this occurs through inhibition of Src family kinases. This study assessed the role of tyrosine-protein kinase Lck (p56/Lck) in this pathway. We analyzed early events leading to apoptosis of human endothelial cells exposed to HKa. The role of p56/Lck was investigated using short interfering (si) RNA knockdown and lentivirus expression in assays of endothelial tube formation, sprouting of neovessels from murine aorta, and angiogenesis in Matrigel plugs. HKa stimulated expression and phosphorylation of p56/Lck. siRNA knockdown of p56/Lck promoted endothelial proliferation and blocked HKa-induced apoptosis and activation of p53, Bax, and Bak. Lentivirus expression of p56/Lck in endothelial cells induced apoptosis and blocked tube formation. Expression of p56/Lck in murine aortic rings blocked sprouting angiogenesis. Lentivirus expressing p56/Lck blocked angiogenesis in Matrigel plugs, while p56/Lck short hairpin RNA inhibited the antiangiogenic effect of HKa. Scrambled siRNAs and empty lentiviral vectors were used in all experiments. Apoptosis of proliferating endothelial cells and inhibition of angiogenesis by HKa requires p56/Lck. This suggests a novel role for p56/Lck in regulation of endothelial cell survival and angiogenesis.-Betapudi, V., Shukla, M., Alluri, R., Merkulov, S., McCrae, K. R. Novel role for p56/Lck in regulation of endothelial cell survival and angiogenesis.

Indexed as

Angiogenesis Inducing AgentsAnimalsApoptosisCell SurvivalEndothelial CellsGene Knockdown TechniquesHumansLymphocyte ActivationLymphocyte Specific Protein Tyrosine Kinase p56(lck)Neovascularization, PhysiologicRNA, Small InterferingSignal TransductionAngiogenesis Inducing AgentsLymphocyte Specific Protein Tyrosine Kinase p56(lck)RNA, Small Interferingapoptosiskininogenp53tyrosine protein kinase Lck

Identifiers

PMID27402674
PMCPMC5024698
OpenAlexW2467860101

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.