Evidence map›Paper›PMID 29746502›Full record

ArticlePloS one2018

Potential involvement of the 18 kDa translocator protein and reactive oxygen species in apoptosis of THP-1 macrophages induced by sonodynamic therapy.

Xin Sun, Shuyuan Guo, Wei Wang, Zhengyu Cao, Juhua Dan, Jiali Cheng, Wei Cao, Fang Tian, Wenwu Cao, Ye Tian

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.7field-weighted citation impact, top 33% 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

7 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Sonodynamic therapy for the treatment of atherosclerosis.Journal of pharmaceutical analysis · 2024
    Review
  3. Recent Advances for Dynamic-Based Therapy of Atherosclerosis.International journal of nanomedicine · 2023
    Review
  4. Review
  5. Article
  6. Article
  7. 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

10 authors at 3 institutions in 2 countries.

Xin SunLaboratory of Photo- and Sono-theranostic Technologies, Harbin Institute of Technology, Harbin, Heilongjiang, China.
Shuyuan GuoDepartment of Cardiology, the First Affiliated Hospital, Cardiovascular Institute, Harbin Medical University, Harbin, Heilongjiang, China.
Wei WangDepartment of Cardiology, the First Affiliated Hospital, Cardiovascular Institute, Harbin Medical University, Harbin, Heilongjiang, China.
Zhengyu CaoDepartment of Cardiology, the First Affiliated Hospital, Cardiovascular Institute, Harbin Medical University, Harbin, Heilongjiang, China.
Juhua DanDepartment of Pathophysiology, the State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education, Harbin, Heilongjiang, China.
Jiali ChengDepartment of Cardiology, the First Affiliated Hospital, Cardiovascular Institute, Harbin Medical University, Harbin, Heilongjiang, China.
Wei CaoDepartment of Cardiology, the First Affiliated Hospital, Cardiovascular Institute, Harbin Medical University, Harbin, Heilongjiang, China.
Fang TianDepartment of Cardiology, the First Affiliated Hospital, Cardiovascular Institute, Harbin Medical University, Harbin, Heilongjiang, China.
Wenwu CaoLaboratory of Photo- and Sono-theranostic Technologies, Harbin Institute of Technology, Harbin, Heilongjiang, China.
Ye TianDepartment of Cardiology, the First Affiliated Hospital, Cardiovascular Institute, Harbin Medical University, Harbin, Heilongjiang, China.ORCID 0000-0003-3726-7270
Ministry of Education of the People's Republic of China · CNPennsylvania State University · USHarbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sonodynamic therapy (SDT) with exogenous protoporphyrin IX (PpIX) or endogenous PpIX derived from 5-aminolevulinic acid (ALA) has been carried out to produce apoptotic effects on macrophages, indicating a potential treatment methodology for atherosclerosis. Our previous studies have found that mitochondria damage by reactive oxygen species (ROS) plays a major role in the SDT-induced apoptosis. This study aimed at investigating the potential involvement of the mitochondrial 18 kDa translocator protein (TSPO) and ROS in the pro-apoptotic effects of SDT on THP-1 macrophages. THP-1 macrophages were divided into control and SDT groups, and went through pretreatment of the specific TSPO ligand PK11195 and ROS scavengers N-Acetyl Cysteine (NAC), then compared with groups without pretreatment. Application of PK11195 reduced intracellular accumulation of endogenous PpIX. PK11195 and NAC reduced the generation of intracellular ROS and oxidation of cardiolipin induced by SDT, respectively. PK11195 and NAC also reduced SDT-induced mitochondrial membrane potential (ΔΨm) loss, the translocation of cytochrome c and cell apoptosis. PpIX accumulation, ROS generation and cell apoptosis were also attenuated by siTSPO. Our findings indicate the pivotal role of TSPO and ROS in SDT-induced cardiolipin oxidation, ΔΨm collapse, cytochrome c translocation and apoptosis in THP-1 macrophages.

Indexed as

Aminolevulinic AcidApoptosisCell SurvivalCytochromes cHumansMacrophagesMembrane Potential, MitochondrialMitochondriaProtoporphyrinsReactive Oxygen SpeciesReceptors, GABATHP-1 CellsUltrasonic TherapyAminolevulinic AcidCytochromes cprotoporphyrin IXProtoporphyrinsReactive Oxygen SpeciesReceptors, GABATSPO protein, human

Identifiers

PMID29746502
PMCPMC5944937
OpenAlexW2802111665

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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.