Evidence map›Paper›PMID 31964358›Full record

ArticleBMC pulmonary medicine2020

Inhibition of connexin 43 attenuates oxidative stress and apoptosis in human umbilical vein endothelial cells.

Jia-Wei Ma, Dan-Dan Ji, Qian-Qian Li, Ting Zhang, Liang Luo

Open access · goldAbstract read
In one paragraph

Article in BMC pulmonary medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

21 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
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  4. Review
  5. Hemichannels contribute to mitochondrial CaFrontiers in cell and developmental biology · 2024
    Article
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  7. Review
  8. Review
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  12. Review
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  15. Article
  16. Article
  17. Review
  18. An Update on Connexin Gap Junction and Hemichannels in Diabetic Retinopathy.International journal of molecular sciences · 2021
    Review
  19. Review
  20. 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 1 country.

Jia-Wei MaDepartment of Critical Care Medicine, The Affiliated Wuxi No.2 People's Hospital of Nanjing Medical University, Wuxi, 214002, China.
Dan-Dan JiDepartment of Critical Care Medicine, The Affiliated Wuxi No.2 People's Hospital of Nanjing Medical University, Wuxi, 214002, China.
Qian-Qian LiDepartment of Critical Care Medicine, The Affiliated Wuxi No.2 People's Hospital of Nanjing Medical University, Wuxi, 214002, China.
Ting ZhangDepartment of Clinical Laboratory, The Affiliated Wuxi Matemity and Child Health Care Hospital of Nanjing Medical University, Wuxi, 214002, China. zhangting040715@163.com.
Liang LuoDepartment of Critical Care Medicine, The Affiliated Wuxi No.2 People's Hospital of Nanjing Medical University, Wuxi, 214002, China. luoliang2117@163.com.
Nanjing Medical University · CNWuxi No.2 People's Hospital · CN

Funding

Major Project of Wuxi Municipal Commission For Health and Family Planning Z201601Nanjing Medical University Key Research Project Fund 2016NJMUZD077The13th"Top six talent peaks" project of jiangsu WSN-184
6 · The paper itself

Abstract

backgroundPrevious studies demonstrated an important role for connexin 43 (Cx43) in the regulation of apoptosis by influencing mitochondrial functions. This study aimed to investigate the relationship between Cx43 and lipopolysaccharide (LPS)-induced oxidative stress and apoptosis in human umbilical vein endothelial cells (HUVECs).

methodsWestern blot was performed to determine mitochondrial Cx43 (MtCx43) protein level and phosphorylation (p-MtCx43). Gap19, a selective Cx43 inhibitor, was used to examine the effects of Cx43 on LPS-induced oxidative stress and apoptosis in HUVECs. Expression of regulatory genes associated with oxidative stress was examined by quantitative polymerase chain reaction (qPCR) and Western blot. Apoptosis was assessed by flow cytometry.

resultsLPS stimulation resulted in increased levels of MtCx43 and p-MtCx43. Interestingly, Gap19 antagonized the upregulation of glutathione S-transferase Zeta 1 (GSTZ1) and cytochrome b alpha beta (CYBB), and the downregulation of antioxidant 1 (ATOX1), glutathione synthetase (GSS) and heme oxygenase 1 (HMOX1) induced by LPS or Cx43 overexpression. Moreover, the increased production of reactive oxygen species (ROS) and apoptosis elicited by LPS or Cx43 overexpression were reduced following treatment with Gap19.

conclusionsSelective inhibition of Cx43 hemichannels protects HUVECs from LPS-induced apoptosis and this may be via a reduction in oxidative stress production.

Indexed as

ApoptosisConnexin 43Copper Transport ProteinsDown-RegulationGene Knock-In TechniquesGlutathione SynthaseGlutathione TransferaseHeme Oxygenase-1HumansHuman Umbilical Vein Endothelial CellsLipopolysaccharidesMitochondriaMolecular ChaperonesNADPH Oxidase 2Oxidative StressReactive Oxygen SpeciesATOX1 protein, humanConnexin 43Copper Transport ProteinsCYBB protein, humanGJA1 protein, humanGlutathione SynthaseGlutathione TransferaseGSTZ1 protein, humanHeme Oxygenase-1HMOX1 protein, humanLipopolysaccharidesMolecular ChaperonesNADPH Oxidase 2Reactive Oxygen SpeciesAcute respiratory distress syndromeApoptosisConnexin 43Endothelial cellLipopolysaccharidesMitochondrionOxidative stress

Identifiers

PMID31964358
PMCPMC6975083
OpenAlexW3006467912

What OpenQuestion holds

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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.