Evidence map›Paper›PMID 30820314›Full record

ArticleCell & bioscience2019

Hypoxia destroys the microstructure of microtubules and causes dysfunction of endothelial cells via the PI3K/Stathmin1 pathway.

Huaming Cao, Dongsheng Yu, Xueyun Yan, Bing Wang, Zhiming Yu, Yu Song, Liang Sheng

Open access · goldAbstract read
In one paragraph

Article in Cell & bioscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.5field-weighted citation impact, top 21% 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

28 citing papers in PubMed, 39 citations in OpenAlex.

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  13. m6A epitranscriptomic and epigenetic crosstalk in cardiac fibrosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Review
  14. Article
  15. α-lipoic acid ameliorates consequences of copper overload by up-regulating selenoproteins and decreasing redox misbalance.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
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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

7 authors at 4 institutions in 1 country.

Huaming Cao *Department of Cardiology, Shibei Hospital, 4500 Gong He Xin Road, Shanghai, 200435 China.
Dongsheng Yu *2Department of Traditional Chinese Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052 Henan China.
Xueyun YanDepartment of Cardiology, Shibei Hospital, 4500 Gong He Xin Road, Shanghai, 200435 China.
Bing WangDepartment of Cardiology, Shibei Hospital, 4500 Gong He Xin Road, Shanghai, 200435 China.
Zhiming Yu5Department of Cardiology, Wuxi People's Hospital Affiliated to Nanjing Medical University, Wuxi, 214023 Jiangsu China.
Yu Song6Pharmacy College, Xinxiang Medical University, 601 Jinsui Avenue, Hongqi District, Xinxiang, 453000 Henan China.
Liang Sheng6Pharmacy College, Xinxiang Medical University, 601 Jinsui Avenue, Hongqi District, Xinxiang, 453000 Henan China.
Shanghai Zhabei District Shibei Hospital · CNXinxiang Medical University · CNFirst Affiliated Hospital of Zhengzhou University · CNNanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEndothelial cells (EC) are sensitive to changes in the microenvironment, including hypoxia and ischemia. Disruption of the microtubular network has been reported in cases of ischemia. However, the signaling pathways involved in hypoxia-induced microtubular disruption are unknown. The purpose of this study was to investigate the molecular mechanisms involved in hypoxia-induced microtubular disassembly in human umbilical vein endothelial cells (HUVECs).

resultsHUVECs were cultured under normoxic or hypoxic conditions and pretreated with or without colchicine or paclitaxel. The MTT assay, Transwell assay, trans-endothelial permeability assay, and 5-bromo-2'-deoxy-uridine staining were used to test the survival rate, migration, permeability, and proliferation of cells, respectively. Transmission electron microscopy and phalloidin staining were used to observe the microstructure and polymerization of microtubules. The results show that the functions of HUVECs and the microtubular structure were destroyed by hypoxia, but were protected by paclitaxel and a reactive oxygen species (ROS) inhibitor. We further used western blot, a luciferase assay, and co-immunoprecipitation to describe a non-transcription-independent mechanism for PI3K activation-inhibited microtubular stability mediated by Stathmin1, a PI3K interactor that functions in microtubule depolymerization. Finally, we determined that hypoxia and ROS blocked the interaction between PI3K and Stathmin1 to activate disassembly of microtubules.

conclusionThus, our data demonstrate that hypoxia induced the production of ROS and damaged EC function by destroying the microtubular structure through the PI3K/stathmin1 pathway.

Indexed as

HUVECHypoxiaMicrotubulePI3KStathmin1

Identifiers

PMID30820314
PMCPMC6380067
OpenAlexW2921163346

What OpenQuestion holds

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LicenceCC BY
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.