Evidence map›Paper›PMID 20805333›Full record

ArticleInfection and immunity2010

Vascular endothelial growth factor receptor 1 contributes to Escherichia coli K1 invasion of human brain microvascular endothelial cells through the phosphatidylinositol 3-kinase/Akt signaling pathway.

Wei-Dong Zhao, Wei Liu, Wen-Gang Fang, Kwang Sik Kim, Yu-Hua Chen

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.7field-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

13 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Nicotine Reduces Human Brain Microvascular Endothelial Cell Response toFrontiers in cellular and infection microbiology · 2020
    Article
  6. Article
  7. Article
  8. Transcriptional Profiling of Host Cell Responses to VirulentInternational journal of molecular sciences · 2018
    Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. 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

5 authors at 2 institutions in 2 countries.

Wei-Dong ZhaoDepartment of Developmental Biology, Key Laboratory of Cell Biology, Ministry of Public Health, China Medical University, Shenyang, China.
Wei Liu
Wen-Gang Fang
Kwang Sik Kim
Yu-Hua Chen
China Medical University · CNJohns Hopkins Medicine · US

Funding

PATHOGENESIS OF NEONATAL MENINGITISR01NS026310 · NINDS · JOHNS HOPKINS UNIVERSITY · PI KIM, KWANG S · 1988 to 2008
$3.6M
Host factors and bacterial meningitisR01NS091102 · NINDS · JOHNS HOPKINS UNIVERSITY · PI KIM, KWANG S · 2015 to 2019
$1.8M
NINDS NIH HHS R01 NS026310NINDS NIH HHS R01 NS091102
6 · The paper itself

Abstract

Escherichia coli is the most common Gram-negative organism causing neonatal meningitis. Previous studies demonstrated that E. coli K1 invasion of brain microvascular endothelial cells (BMEC) is required for penetration into the central nervous system, but the microbe-host interactions that are involved in this process remain incompletely understood. Here we report the involvement of vascular endothelial growth factor receptor 1 (VEGFR1) expressed on human brain microvascular endothelial cells (HBMEC) in E. coli K1 invasion of HBMEC. Our results showed that treatment of confluent HBMEC with pan-VEGFR inhibitors significantly inhibited E. coli K1 invasion of HBMEC. Immunofluorescence results indicated the colocalization of VEGFR1 with E. coli K1 during bacterial invasion of HBMEC. The E. coli-induced actin cytoskeleton rearrangements in HBMEC were blocked by VEGFR inhibitors but not by VEGFR2-specific inhibitors. The small interfering RNA (siRNA) knockdown of VEGFR1 in HBMEC significantly attenuated E. coli invasion and the concomitant actin filament rearrangement. Furthermore, we found an increased association of VEGFR1 with the p85 subunit of phosphatidylinositol 3-kinase (PI3K) in HBMEC infected with E. coli K1 and that E. coli K1-triggered Akt activation in HBMEC was blocked by VEGFR1 siRNA and VEGFR inhibitors. Taken together, our results demonstrate that VEGFR1 contributes to E. coli K1 invasion of HBMEC via recruitment of the PI3K/Akt signaling pathway.

Indexed as

BrainCells, CulturedEndothelial CellsEscherichia coliHumansInfant, NewbornMicrocirculationPhosphatidylinositol 3-KinasesPhosphorylationProtein Serine-Threonine KinasesSignal TransductionVascular Endothelial Growth Factor Receptor-1Phosphatidylinositol 3-KinasesProtein Serine-Threonine KinasesVascular Endothelial Growth Factor Receptor-1

Identifiers

PMID20805333
PMCPMC2976340
OpenAlexW2163153344

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.