Evidence map›Paper›PMID 29460267›Full record

ArticleMolecular neurobiology2018

Hypoxia-Preconditioned Human Umbilical Vein Endothelial Cells Protect Against Neurovascular Damage After Hypoxic Ischemia in Neonatal Brain.

Yi-Chao Lee, Ying-Chao Chang, Chia-Ching Wu, Chao-Ching Huang

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
7.6field-weighted citation impact, top 3% 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

19 citing papers in PubMed, 32 citations in OpenAlex.

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  12. Care of Infants Born to Women with Diabetes.Current diabetes reports · 2020
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  14. Fractalkine/CX3CL1 in Neoplastic Processes.International journal of molecular sciences · 2020
    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

4 authors at 4 institutions in 1 country.

Yi-Chao LeePh.D. Program for Neural Regenerative Medicine, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan.
Ying-Chao ChangDepartment of Pediatrics, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan.
Chia-Ching WuDepartment of Cell Biology and Anatomy, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Chao-Ching HuangDepartment of Pediatrics, College of Medicine, Taipei Medical University, Taipei City, Taiwan. huangped@tmu.edu.tw.ORCID http://orcid.org/0000-0003-2799-7181
Chang Gung University · TWNational Cheng Kung University · TWTaipei Medical University · TWTaipei Medical University Hospital · TW

Funding

Ministry of Science and Technology, Taiwan 103-2314-B-038-062-MY3Ministry of Science and Technology, Taiwan 104-2314-B-006-093-MY3
6 · The paper itself

Abstract

Therapy targeting the neurovascular unit may provide effective neuroprotection against neonatal hypoxia-ischemia (HI). We hypothesized that the peripheral injection of hypoxia-preconditioned human umbilical vein endothelial cells (HUVECs) following HI protects against neurovascular damage and provides long-term neuroprotection in a postpartum (P) day-7 rat pup model. Compared with normoxic HUVECs, hypoxic HUVECs showed enhanced migration and angiogenesis in vitro and had augmented migration effects into the brain when administered intraperitoneally in vivo after HI. Moreover, 24 and 72 h post-HI, the hypoxic HUVECs group but not the normoxic HUVECs or culture-medium groups had significantly higher preservation of microvessels and neurons, and attenuation of blood-brain barrier damage than the normal-saline group. Compared to control or normal-saline groups, only the hypoxic HUVECs group had no impaired foot steps and showed a significant reduction of brain area loss at P42. Next-generation sequencing showed hypoxia-induced upregulation and downregulation of 209 and 215 genes in HUVECs, respectively. Upstream regulator analysis by ingenuity pathway analysis (IPA) identified hypoxia-inducible factor 1-alpha as the key predicted activated transcription regulator. After hypoxia, 12 genes (ADAMTS1, EFNA1, HIF1A, LOX, MEOX2, SELE, VEGFA, VEGFC, CX3CL1, HMMR, SDC, and SERPINE) associated with migration and/or angiogenesis were regulated in HUVECs. In addition, 6 genes (VEGFA, VEGFC, NTN4, TGFA, SERPINE1, and CX3CL1) involved in the survival of endothelial and neuronal cells were also markedly altered in hypoxic HUVECs. Thus, cell therapy by using hypoxic HUVECs that enhance migration and neurovascular protection may provide an effective therapeutic strategy for treating neonatal asphyxia.

Indexed as

NeuroprotectionAnimalsAnimals, NewbornApoptosisBehavior, AnimalBrainCell HypoxiaCell MovementCell SurvivalGene Expression ProfilingHumansHuman Umbilical Vein Endothelial CellsHypoxia-Inducible Factor 1, alpha SubunitHypoxia-Ischemia, BrainMaleNeovascularization, PhysiologicHypoxia-Inducible Factor 1, alpha SubunitHuman umbilical vein endothelial cellsHypoxia-inducible factor 1-alphaHypoxia-preconditionedNeonatal brain injuryNeurovascular protection

Identifiers

PMID29460267
OpenAlexW2792946487

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.