Evidence map›Paper›PMID 28181168›Full record

ArticleJournal of physiology and biochemistry2017

ApoA-I/SR-BI modulates S1P/S1PR2-mediated inflammation through the PI3K/Akt signaling pathway in HUVECs.

Kun Ren, Yan-Ju Lu, Zhong-Cheng Mo, Xing -Liu, Zhen-Li Tang, Yue Jiang, Xiao-Shan Peng, Li Li, Qing-Hai Zhang, Guang-Hui Yi

Abstract read
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In one paragraph

Article in Journal of physiology and biochemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

23 citing papers in PubMed, 38 citations in OpenAlex.

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  8. Review
  9. Review
  10. Article
  11. HDL and Scavenger Receptor Class B Type I (SRBI).Advances in experimental medicine and biology · 2022
    Review
  12. Sphingolipid metabolism and signaling in cardiovascular diseases.Frontiers in cardiovascular medicine · 2022
    Review
  13. Review
  14. Article
  15. Article
  16. Article
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  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

10 authors at 4 institutions in 1 country.

Kun RenInstitute of Cardiovascular Disease, Key Lab for Arteriosclerology of Hunan Province, University of South China, 28 W Changsheng Road, Hengyang, Hunan, 421001, China.
Yan-Ju LuDepartment of Pathology, Maternal and Child Health Hospital of Hubei Province, Wuhan City, Hubei Province, 430072, China.
Zhong-Cheng MoDepartment of Histology and Embryology, University of South China, Hengyang, Hunan, 421001, China.
Xing -LiuNational Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, 100005, China.
Zhen-Li TangInstitute of Cardiovascular Disease, Key Lab for Arteriosclerology of Hunan Province, University of South China, 28 W Changsheng Road, Hengyang, Hunan, 421001, China.
Yue JiangInstitute of Cardiovascular Disease, Key Lab for Arteriosclerology of Hunan Province, University of South China, 28 W Changsheng Road, Hengyang, Hunan, 421001, China.
Xiao-Shan PengInstitute of Cardiovascular Disease, Key Lab for Arteriosclerology of Hunan Province, University of South China, 28 W Changsheng Road, Hengyang, Hunan, 421001, China.
Li LiDepartment of Pathology, Maternal and Child Health Hospital of Hubei Province, Wuhan City, Hubei Province, 430072, China.
Qing-Hai ZhangClinical Research Institution, The First Affiliated Hospital, University of South China, Hengyang, Hunan, 421001, China.
Guang-Hui YiInstitute of Cardiovascular Disease, Key Lab for Arteriosclerology of Hunan Province, University of South China, 28 W Changsheng Road, Hengyang, Hunan, 421001, China. ghyi6108@163.com.
University of South China · CNHubei Provincial Women and Children's Hospital · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNFirst Affiliated Hospital of University of South China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial dysfunction plays a vital role during the initial stage of atherosclerosis. Oxidized low-density lipoprotein (ox-LDL) induces vascular endothelial injury and vessel wall inflammation. Sphingosine-1-phosphate (S1P) exerts numerous vasoprotective effects by binding to diverse S1P receptors (S1PRs; S1PR1-5). A number of studies have shown that in endothelial cells (ECs), S1PR2 acts as a pro-atherosclerotic mediator by stimulating vessel wall inflammation through the phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway. Scavenger receptor class B member I (SR-BI), a high-affinity receptor for apolipoprotein A-I (apoA-I)/high-density lipoprotein (HDL), inhibits nuclear factor-κB (NF-κB) translocation and decreases the plasma levels of inflammatory mediators via the PI3K/Akt pathway. We hypothesized that the inflammatory effects of S1P/S1PR2 on ECs may be regulated by apoA-I/SR-BI. The results showed that ox-LDL, a pro-inflammatory factor, augmented the S1PR2 level in human umbilical vein endothelial cells (HUVECs) in a dose- and time-dependent manner. In addition, S1P/S1PR2 signaling influenced the levels of inflammatory factors, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-10, aggravating inflammation in HUVECs. Moreover, the pro-inflammatory effects induced by S1P/S1PR2 were attenuated by SR-BI overexpression and enhanced by an SR-BI inhibitor, BLT-1. Further experiments showed that the PI3K/Akt signaling pathway was involved in this process. Taken together, these results demonstrate that apoA-I/SR-BI negatively regulates S1P/S1PR2-mediated inflammation in HUVECs by activating the PI3K/Akt signaling pathway.

Indexed as

Signal TransductionActive Transport, Cell NucleusApolipoprotein A-ICells, CulturedCyclopentanesEndothelium, VascularGene Expression RegulationHumansHuman Umbilical Vein Endothelial CellsInterleukin-10Interleukin-1betaKineticsLipoproteins, LDLLysophospholipidsPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-akt2-hexyl-1-cyclopentanone thiosemicarbazoneAKT1 protein, humanAPOA1 protein, humanApolipoprotein A-ICyclopentanesIL10 protein, humanIL1B protein, humanInterleukin-10Interleukin-1betaLipoproteins, LDLLysophospholipidsoxidized low density lipoproteinPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktReceptors, LysosphingolipidRecombinant ProteinsS1PR2 protein, humanSCARB1 protein, humanScavenger Receptors, Class BSphingosinesphingosine 1-phosphateSphingosine-1-Phosphate ReceptorsThiosemicarbazonesTNF protein, humanTumor Necrosis Factor-alphaapoA-I/SR-BIHDLInflammationS1P/S1PR2

Identifiers

PMID28181168
OpenAlexW2586295881

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.