Evidence map›Paper›PMID 30909920›Full record

ArticleLipids in health and disease2019

Lipopolysaccharide and palmitic acid synergistically induced MCP-1 production via MAPK-meditated TLR4 signaling pathway in RAW264.7 cells.

Xuehong Wang, Xin Jiang, Bin Deng, Juan Xiao, Junfei Jin, Zhaoquan Huang

Open access · goldAbstract read
In one paragraph

Article in Lipids in health and disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.0field-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

25 citing papers in PubMed, 35 citations in OpenAlex.

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  13. Pathophysiology of cellulite: Possible involvement of selective endotoxemia.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2023
    Review
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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

6 authors at 3 institutions in 1 country.

Xuehong WangDepartment of Pathology, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Xin JiangLaboratory of Hepatobiliary and Pancreatic Surgery, Affiliated Hospital of Guilin Medical University, 15 Lequn Road, Guilin, 541001, Guangxi, China.
Bin DengLaboratory of Hepatobiliary and Pancreatic Surgery, Affiliated Hospital of Guilin Medical University, 15 Lequn Road, Guilin, 541001, Guangxi, China.
Juan XiaoLaboratory of Hepatobiliary and Pancreatic Surgery, Affiliated Hospital of Guilin Medical University, 15 Lequn Road, Guilin, 541001, Guangxi, China.
Junfei JinLaboratory of Hepatobiliary and Pancreatic Surgery, Affiliated Hospital of Guilin Medical University, 15 Lequn Road, Guilin, 541001, Guangxi, China. changliangzijin@163.com.
Zhaoquan HuangDepartment of Pathology, the Affiliated Hospital of Guilin Medical University, 15 Lequn Road, Guilin, 541001, Guangxi, China. gxlzzq@163.com.
Guilin Medical University · CN181st Hospital of Chinese People's Liberation Army · CNXiangya Hospital Central South University · CN

Funding

National Natural Science Foundation of China 8156130230Natural Science Foundation of Guangxi 2015GXNSFEA139003
6 · The paper itself

Abstract

backgroundObesity increases the risk of developing diabetes mellitus. Clinical studies suggest that risk factors like palmitic acid (PA) and lipopolysaccharide (LPS) exist simultaneously in diabetes with obesity. Combination of PA and LPS even at low concentration can induce strong inflammatory reaction. Monocyte chemoattractant protein-1 (MCP-1) is an important inflammatory chemokine related to insulin resistance and type II diabetes. Our previous study using PCR array revealed that LPS and PA synergistically induce MCP-1 mRNA expression in macrophage cells RAW264.7, while the protein expression of MCP-1 in this case was not investigated. Moreover, the underling mechanism in the synergistic effect of MCP-1 expression or production induced by treatment of LPS and PA combination remains unclear.

methodsProtein secretion of MCP-1 was measured by the enzyme-linked immunosorbent assay (ELISA) and mRNA levels of MCP-1 and Toll-like receptor 4 (TLR4) were measured by real-time PCR. Statistical analysis was conducted using SPSS software.

resultsLPS could increase MCP-1 transcription as well as secretion in RAW264.7, and PA amplified this effect obviously. Meanwhile, combination of LPS with PA increased TLR4 mRNA expression while LPS alone or PA alone could not, TLR4 knockdown inhibited MCP-1 transcription/secretion induced by LPS plus PA. Moreover, not NF-κB inhibitor but inhibitors of mitogen-activated protein kinase (MAPK) signaling pathways, including c-Jun NH2-terminal kinase (JNK), extracellular signal-regulated kinase (ERK), and p38 MAPK were found to block MCP-1 generation stimulated by LPS plus PA.

conclusionLPS and PA synergistically induced MCP-1 secretion in RAW264.7 macrophage cells, in which MCP-1 transcription mediated by MAPK/TLR4 signaling pathways was involved. Combined treatment of PA and LPS in RAW264.7 cells mimics the situation of diabetes with obesity that has higher level of PA and LPS, MAPK/TLR4/ MCP-1 might be potential therapeutic targets for diabetes with obesity.

Indexed as

AnimalsChemokine CCL2Diabetes MellitusDisease Models, AnimalDrug SynergismGene Expression RegulationHumansLipopolysaccharidesMAP Kinase Kinase 1MiceObesityPalmitic AcidRAW 264.7 CellsSignal TransductionToll-Like Receptor 4Ccl2 protein, mouseChemokine CCL2LipopolysaccharidesMAP Kinase Kinase 1Palmitic AcidTlr4 protein, mouseToll-Like Receptor 4LipopolysaccharideMAPKMCP-1Palmitic acidTLR4

Identifiers

PMID30909920
PMCPMC6434618
OpenAlexW2943383731

What OpenQuestion holds

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LicenceCC BY
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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.