Evidence map›Paper›PMID 30984553›Full record

ArticleFEBS open bio2019

Vascular leakage caused by loss of Akt1 is associated with impaired mural cell coverage.

Jung Min Ha, Seo Yeon Jin, Hye Sun Lee, Farzaneh Vafaeinik, Yoo Jin Jung, Hye Jin Keum, Sang Heon Song, Dong Hyung Lee, Chi Dae Kim, Sun Sik Bae

Open access · goldAbstract read
In one paragraph

Article in FEBS open bio, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

7 citing papers in PubMed, 15 citations in OpenAlex.

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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

10 authors at 3 institutions in 1 country.

Jung Min HaBiomedical Research Institute Gene and Cell Therapy Center for Vessel Associated Disease Department of Pharmacology Pusan National University School of Medicine Yangsan Korea.
Seo Yeon JinBiomedical Research Institute Gene and Cell Therapy Center for Vessel Associated Disease Department of Pharmacology Pusan National University School of Medicine Yangsan Korea.
Hye Sun LeeBiomedical Research Institute Gene and Cell Therapy Center for Vessel Associated Disease Department of Pharmacology Pusan National University School of Medicine Yangsan Korea.
Farzaneh VafaeinikBiomedical Research Institute Gene and Cell Therapy Center for Vessel Associated Disease Department of Pharmacology Pusan National University School of Medicine Yangsan Korea.
Yoo Jin JungBiomedical Research Institute Gene and Cell Therapy Center for Vessel Associated Disease Department of Pharmacology Pusan National University School of Medicine Yangsan Korea.
Hye Jin KeumBiomedical Research Institute Gene and Cell Therapy Center for Vessel Associated Disease Department of Pharmacology Pusan National University School of Medicine Yangsan Korea.
Sang Heon SongBiomedical Research Institute Department of Internal Medicine Pusan National University Hospital Busan Korea.
Dong Hyung LeeDepartment of Gynecology and Obstetrics Pusan National University Yangsan Hospital Korea.
Chi Dae KimBiomedical Research Institute Gene and Cell Therapy Center for Vessel Associated Disease Department of Pharmacology Pusan National University School of Medicine Yangsan Korea.
Sun Sik BaeBiomedical Research Institute Gene and Cell Therapy Center for Vessel Associated Disease Department of Pharmacology Pusan National University School of Medicine Yangsan Korea.
Pusan National University · KRPusan National University Yangsan Hospital · KRPusan National University Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Angiogenesis plays a critical role in embryo development, tissue repair, tumor growth and wound healing. In the present study, we investigated the role of the serine/threonine kinase Akt in angiogenesis. Silencing of Akt1 in human umbilical vein endothelial cells significantly inhibited vascular endothelial growth factor (VEGF)-induced capillary-like tube formation. Mice lacking Akt1 exhibited impaired retinal angiogenesis with delayed endothelial cell (EC) proliferation. In addition, VEGF-induced corneal angiogenesis and tumor development were significantly inhibited in mice lacking Akt1. Loss of Akt1 resulted in reduced angiogenic sprouting, as well as the proliferation of ECs and mural cells. Addition of culture supernatant of vascular smooth muscle cells (VSMCs) in which Akt1 was silenced suppressed tube formation, the stability of preformed tubes and the proliferation of ECs. In addition, attachment of VSMCs to ECs was significantly reduced in cells in which Akt1 was silenced. Mural cell coverage of retinal vasculature was reduced in mice lacking Akt1. Finally, mice lacking Akt1 showed severe retinal hemorrhage compared to the wild-type. These results suggest that the regulation of EC function and mural cell coverage by Akt1 is important for blood vessel maturation during angiogenesis.

Indexed as

AnimalsCell ProliferationEndothelial CellsGene SilencingHumansHuman Umbilical Vein Endothelial CellsMiceNeovascularization, PhysiologicProto-Oncogene Proteins c-aktRatsVascular Endothelial Growth FactorsAKT1 protein, humanAkt1 protein, mouseProto-Oncogene Proteins c-aktVascular Endothelial Growth FactorsAktangiogenesiscoverageendotheliummural cellvascular leakage

Identifiers

PMID30984553
PMCPMC6443864
OpenAlexW2921690849

What OpenQuestion holds

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LicenceCC BY
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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.