Evidence map›Paper›PMID 25758142›Full record

ArticleBrain pathology (Zurich, Switzerland)2016

Heat Shock Protein 47 Promotes Glioma Angiogenesis.

Zhe Bao Wu, Lin Cai, Shao Jian Lin, Zhi Gen Leng, Yu Hang Guo, Wen Lei Yang, Yi Wei Chu, Shao-Hua Yang, Wei Guo Zhao

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

Article in Brain pathology (Zurich, Switzerland), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

25 citing papers in PubMed, 65 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

9 authors at 5 institutions in 2 countries.

Zhe Bao WuDepartment of Neurosurgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Lin CaiDepartment of Neurosurgery, First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Shao Jian LinDepartment of Neurosurgery, First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Zhi Gen LengDepartment of Neurosurgery, First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Yu Hang GuoDepartment of Neurosurgery, First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Wen Lei YangDepartment of Neurosurgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yi Wei ChuDepartment of Immunology and Biotherapy Research Center, Shanghai Medical College, Fudan University, Shanghai, China.
Shao-Hua YangDepartment of Pharmacology and Neuroscience, University of North Texas Health Science Center, Fort Worth, TX.
Wei Guo ZhaoDepartment of Neurosurgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Ruijin Hospital · CNFirst Affiliated Hospital of Wenzhou Medical University · CNWenzhou Medical University · CNFudan University · CNUniversity of North Texas · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heat shock protein 47 (HSP47) is a collagen-binding protein, which has been recently found to express in glioma vessels. However, the expression profile of HSP47 in glioma patients and the underlying mechanisms of HSP47 on glioma angiogenesis are not fully explored. In the current study, we found that expression of HSP47 in glioma vessels was correlated with the grades of gliomas. HSP47 knockdown by siRNAs significantly decreased cell viability in vitro and tumor volume in vivo; moreover, it reduced the microvessel density (MVD) by CD31 immunohistochemistry in vivo. HSP47 knockdown significantly inhibited tube formation, invasion and proliferation of human umbilical vein endothelial cells (HUVECs). Furthermore, conditional medium derived from HSP47 knockdown cells significantly inhibited HUVECs tube formation and migration, while it increased chemosensitivity of HUVECs cells to Avastin. Silencing of HSP47 decreased VEGF expression in glioma cells consistently, and reduced glioma vasculature. Furthermore, HSP47 promoted glioma angiogenesis through HIF1α-VEGFR2 signaling. The present study demonstrates that HSP47 promotes glioma angiogenesis and highlights the importance of HSP47 as an attractive therapeutic target of GBM.

Indexed as

Brain NeoplasmsCell MovementCell ProliferationEndothelial CellsErb-b2 Receptor Tyrosine KinasesGene Expression Regulation, NeoplasticGliomaHSP47 Heat-Shock ProteinsHumansHypoxia-Inducible Factor 1, alpha SubunitMaleMicrovesselsMiddle AgedMitogen-Activated Protein Kinase 3Neovascularization, PathologicPlatelet Endothelial Cell Adhesion Molecule-1ERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesHIF1A protein, humanHSP47 Heat-Shock ProteinsHypoxia-Inducible Factor 1, alpha SubunitKDR protein, humanMitogen-Activated Protein Kinase 3Platelet Endothelial Cell Adhesion Molecule-1RNA, Small InterferingSERPINH1 protein, humanVascular Endothelial Growth Factor Receptor-2angiogenesisglioblastomagliomaheat shock protein 47VEGFR2

Identifiers

PMID25758142
PMCPMC8029092
OpenAlexW2112449830

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.