Evidence map›Paper›PMID 19437134›Full record

ArticleMolecular biology reports2010

Arsenic trioxide induces the apoptosis in vascular smooth muscle cells via increasing intracellular calcium and ROS formation.

Jing-Xiu Li, Ya-Qi Shen, Ben-Zhi Cai, Jing Zhao, Xiaopeng Bai, Yan-Jie Lu, Xue-Qi Li

Abstract read
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In one paragraph

Article in Molecular biology reports, 2010. 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
1.1field-weighted citation impact, top 24% 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, 43 citations in OpenAlex.

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  13. Monomethylarsonous acid, but not inorganic arsenic, is a mitochondria-specific toxicant in vascular smooth muscle cells.Toxicology in vitro : an international journal published in association with BIBRA · 2016
    Article
  14. Ethylacetate extract from Tetrastigma hemsleyanum induces apoptosis via the mitochondrial caspase-dependent intrinsic pathway in HepG2 cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  15. Article
  16. Cardiovascular effects of arsenic: clinical and epidemiological findings.Environmental science and pollution research international · 2014
    Review
  17. Inhibition of As(III) and Hg(II) caused aortic hypercontraction by eugenol, linalool and carvone.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2014
    Article
  18. 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 1 institution in 1 country.

Jing-Xiu LiDepartment of Cardiology, The Fourth Affiliated Hospital of Harbin Medical University, Heilongjiang, China.
Ya-Qi Shen
Ben-Zhi Cai
Jing Zhao
Xiaopeng Bai
Yan-Jie Lu
Xue-Qi Li
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The present study was designed to investigate whether arsenic trioxide induced the apoptosis in rat mesenteric arterial smooth muscle cells (SMCs), which provides new insights into mechanisms of arsenic-related vascular diseases. Here, we found that arsenic trioxide significantly decreased the viability of SMCs in a dose-dependent manner. In addition, higher level of arsenic trioxide directly caused cellular necrosis. The Hoechst and AO/EB staining demonstrated that apoptotic morphological change was presented in SMCs exposed to arsenic trioxide. The TUNEL assay displayed that more positive apoptotic signal appeared in SMCs treated with arsenic trioxide. The following result showed that ROS formation was markedly increased in arsenic trioxide-treated SMCs. Pretreatment with N-acetylcysteine, an anti-oxidant reagent, obviously attenuated the enhancement of ROS production and the reduction of cell viability induced by arsenic trioxide in SMCs. Arsenic trioxide also enhanced free intracellular Ca(2+) level in SMCs. BAPTA also significantly prevented the increased intracellular Ca(2+) and decreased cell viability induced by arsenic trioxide in SMCs. These results suggested that arsenic trioxide obviously induced apoptosis in SMCs, and its mechanism was partially associated with intracellular ROS formation and free Ca(2+) increasing.

Indexed as

AnimalsApoptosisArsenicalsArsenic TrioxideCalciumDose-Response Relationship, DrugEgtazic AcidIn Situ Nick-End LabelingL-Lactate DehydrogenaseMicroscopy, FluorescenceMuscle, Smooth, VascularNecrosisOxidesRatsReactive Oxygen Species1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acidArsenicalsArsenic TrioxideCalciumEgtazic AcidL-Lactate DehydrogenaseOxidesReactive Oxygen Species

Identifiers

PMID19437134
OpenAlexW2059347783

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.