Evidence map›Paper›PMID 30194633›Full record

ArticleCell stress & chaperones2018

Palmitic acid induces human osteoblast-like Saos-2 cell apoptosis via endoplasmic reticulum stress and autophagy.

Lei Yang, Gaopeng Guan, Lanjie Lei, Qizhuang Lv, Shengyuan Liu, Xiuwen Zhan, Zhenzhen Jiang, Xiang Gu

Open access · greenAbstract read
In one paragraph

Article in Cell stress & chaperones, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

42 citing papers in PubMed, 74 citations in OpenAlex.

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  19. BACE1 and SCD1 are associated with neurodegeneration.Frontiers in aging neuroscience · 2023
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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

8 authors at 3 institutions in 1 country.

Lei YangCollege of Basic Medical, Jiujiang University, Jiujiang, 332000, Jiangxi, China. yangleigeili@163.com.ORCID http://orcid.org/0000-0001-8859-9692
Gaopeng GuanKey Laboratory of System Bio-medicine of Jiangxi Province, Jiujiang University, Jiujiang, 332000, Jiangxi, China.
Lanjie LeiAffiliated Hospital of Jiujiang University, Jiujiang University, Jiujiang, 332000, Jiangxi, China.
Qizhuang LvCollege of Biology & Pharmacy, Yulin Normal University, Yulin, 537000, Guangxi, China.
Shengyuan LiuKey Laboratory of System Bio-medicine of Jiangxi Province, Jiujiang University, Jiujiang, 332000, Jiangxi, China.
Xiuwen ZhanKey Laboratory of System Bio-medicine of Jiangxi Province, Jiujiang University, Jiujiang, 332000, Jiangxi, China.
Zhenzhen JiangMedicine Graduate School, Nanchang University, Nanchang, 330006, China.
Xiang GuKey Laboratory of System Bio-medicine of Jiangxi Province, Jiujiang University, Jiujiang, 332000, Jiangxi, China. eagle0094@163.com.
Jiujiang University · CNNanchang University · CNYulin Normal University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Palmitic acid (PA) is the most common saturated long-chain fatty acid in food that causes cell apoptosis. However, little is known about the molecular mechanisms of PA toxicity. In this study, we explore the effects of PA on proliferation and apoptosis in human osteoblast-like Saos-2 cells and uncover the signaling pathways involved in the process. Our study showed that endoplasmic reticulum (ER) stress and autophagy are involved in PA-induced Saos-2 cell apoptosis. We found that PA inhibited the viability of Saos-2 cells in a dose- and time-dependent manner. At the same time, PA induced the expression of ER stress marker genes (glucose-regulated protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP)), altered autophagy-related gene expression (microtubule-associated protein 1 light chain 3 (LC3), ATG5, p62, and Beclin), promoted apoptosis-related gene expression (Caspase 3 and BAX), and affected autophagic flux. Inhibiting ER stress with 4-PBA diminished the PA-induced cell apoptosis, activated autophagy, and increased the expression of Caspase 3 and BAX. Inhibiting autophagy with 3-MA attenuated the PA and ER stress-induced cell apoptosis and the apoptosis-related gene expression (Caspase 3 and BAX), but seemed to have no obvious effects on ER stress, although the CHOP expression was downregulated. Taken together, our results suggest that PA-induced Saos-2 cell apoptosis is activated via ER stress and autophagy, and the activation of autophagy depends on the ER stress during this process.

Indexed as

ApoptosisAutophagyCell Line, TumorEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressGene Expression RegulationHumansOsteoblastsPalmitic AcidSignal TransductionEndoplasmic Reticulum Chaperone BiPHSPA5 protein, humanPalmitic AcidAutophagyEndoplasmic reticulum stressPalmitic acidSaos-2 cells

Identifiers

PMID30194633
PMCPMC6237680
OpenAlexW2890076150

What OpenQuestion holds

Textmetadata
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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.