Evidence map›Paper›PMID 35093114›Full record

ArticleJournal of orthopaedic surgery and research2022

Thioacetamide promotes osteoclast transformation of bone marrow macrophages by influencing PI3K/AKT pathways.

XiaoLi Jin, Yang Li, Yayang Yang, Hao Shen, Jin Chen, Bin Xu, Jian Xu

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of orthopaedic surgery and research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 37% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

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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.

XiaoLi Jin *School of Medical Technology and Information Engineering, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Yang Li *School of Basic Medical Sciences, FUDAN University, Shanghai, 200433, People's Republic of China.
Yayang YangDepartment of Laboratory Medicine, The First People's Hospital of Shangqiu, Shangqiu, 476000, China.
Hao ShenSchool of Medical Technology and Information Engineering, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Jin ChenSchool of Medical Technology and Information Engineering, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Bin XuDepartment of General Surgery, School of Medicine, Sir Run Run Shaw Hospital, Zhejiang University, Hangzhou, 310016, Zhejiang, People's Republic of China. 3304089@zju.edu.cn.
Jian XuSchool of Medical Technology and Information Engineering, Zhejiang Chinese Medical University, Hangzhou, 310053, China. xujian832002@163.com.ORCID http://orcid.org/0000-0002-5039-1850
Zhejiang Chinese Medical University · CNShanghai Medical College of Fudan University · CNShangqiu First People's Hospital · CNSir Run Run Shaw Hospital · CN

Funding

Natural Science Foundation of Zhejiang Province no. LY19H060001Zhejiang Province Project of the Science Technology Department no. 2015C37113Zhejiang Traditional Chinese Medicine Science and Technology Plan Project no. 2022ZB093
6 · The paper itself

Abstract

backgroundOsteoclast cell increase is a major risk factor for osteoporosis and degenerative bone and joint diseases. At present, RANKL and M-CSF are commonly used to induce osteoclastogenesis. Thioacetamide (TAA) can lead to many types of liver and kidney damage, but less attention has been paid to the association of TAA with bone damage. In this work, we investigated the effects of TAA on the osteoclastogenesis and differentiation of bone marrow macrophages (BMMs).

methodsBMMs of SD rat suckling mice were taken for primary culture. CCK-8 was used to detect the toxic effects of TAA on BMMs, and flow cytometry was used to detect the effects of TAA on the cell cycle, cell viability, apoptosis and intracytoplasmic Ca

resultsThe results suggested that TAA inhibited the proliferation of BMMs, while enhancing osteoclastogenesis at 0.5 mg/mL and 1 mg/mL as assayed by TRAP staining. Exposed to TAA, BMMs could differentiate into osteoclast-like cells with overexpression of cathepsin K and TRAP proteins. Western blot results showed that TAA can activate the expression levels of P-PI3K, P-AKT, P-P38, and P-JNK, accompanied by apoptosis of BMMs and increase in intracellular Ca

conclusionTAA may induce osteoclast formation in BMMs by activating the expression of PI3K/AKT pathway proteins, which is comparable to the classic osteoclast differentiation inducer RANKL and M-CSF. This suggests that we may find a cheap osteoclast inducer.

Indexed as

Bone ResorptionOsteoclastsAnimalsBone MarrowBone Marrow CellsCathepsin KCell DifferentiationMacrophage Colony-Stimulating FactorMacrophagesMediator ComplexMicePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRANK LigandRatsRats, Sprague-DawleyCathepsin KMacrophage Colony-Stimulating FactorMed24 protein, mouseMediator ComplexPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRANK LigandThioacetamideCell differentiationMacrophagesOsteoclastRANKLThioacetamide

Identifiers

PMID35093114
PMCPMC8800259
OpenAlexW4210579179

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.