Evidence map›Paper›PMID 27807512›Full record

ArticleFrontiers in cellular and infection microbiology2016

Lipopolysaccharide Induces Human Pulmonary Micro-Vascular Endothelial Apoptosis via the YAP Signaling Pathway.

Lei Yi, Xiaoqin Huang, Feng Guo, Zengding Zhou, Mengling Chang, Jiajun Tang, Jingning Huan

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular and infection microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 33 citations in OpenAlex.

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  13. Proregenerative Activity of IL-33 in Gastric Tissue Cells UndergoingInternational journal of molecular sciences · 2020
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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 2 institutions in 1 country.

Lei YiDepartment of Orthopedics, Shanghai Fengxian Central Hospital, Branch of The Sixth People's Hospital Affiliated to Shanghai Jiao Tong University Shanghai, China.
Xiaoqin HuangDepartment of Burn and Plastic Surgery, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University Shanghai, China.
Feng GuoDepartment of Burn and Plastic Surgery, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University Shanghai, China.
Zengding ZhouDepartment of Burn and Plastic Surgery, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University Shanghai, China.
Mengling ChangDepartment of Burn and Plastic Surgery, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University Shanghai, China.
Jiajun TangDepartment of Burn and Plastic Surgery, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University Shanghai, China.
Jingning HuanDepartment of Burn and Plastic Surgery, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University Shanghai, China.
Ruijin Hospital · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gram-negative bacterial lipopolysaccharide (LPS) induces a pathologic increase in lung vascular leakage under septic conditions. LPS-induced human pulmonary micro-vascular endothelial cell (HPMEC) apoptosis launches and aggravates micro-vascular hyper-permeability and acute lung injury (ALI). Previous studies show that the activation of intrinsic apoptotic pathway is vital for LPS-induced EC apoptosis. Yes-associated protein (YAP) has been reported to positively regulate intrinsic apoptotic pathway in tumor cells apoptosis. However, the potential role of YAP protein in LPS-induced HPMEC apoptosis has not been determined. In this study, we found that LPS-induced activation and nuclear accumulation of YAP accelerated HPMECs apoptosis. LPS-induced YAP translocation from cytoplasm to nucleus by the increased phosphorylation on Y357 resulted in the interaction between YAP and transcription factor P73. Furthermore, inhibition of YAP by small interfering RNA (siRNA) not only suppressed the LPS-induced HPMEC apoptosis but also regulated P73-mediated up-regulation of BAX and down-regulation of BCL-2. Taken together, our results demonstrated that activation of the YAP/P73/(BAX and BCL-2)/caspase-3 signaling pathway played a critical role in LPS-induced HPMEC apoptosis. Inhibition of the YAP might be a potential therapeutic strategy for lung injury under sepsis.

Indexed as

ApoptosisSignal TransductionAdaptor Proteins, Signal TransducingCell NucleusCells, CulturedCell SurvivalCytoplasmEndothelial CellsHumansLipopolysaccharidesPhosphoproteinsPhosphorylationProtein BindingProtein Processing, Post-TranslationalProtein TransportTranscription FactorsAdaptor Proteins, Signal TransducingLipopolysaccharidesPhosphoproteinsTP73 protein, humanTranscription FactorsTumor Protein p73YAP1 protein, humanYAP-Signaling Proteinsapoptosisendothelial cellslipopolysaccharideP73Yes-associated protein

Identifiers

PMID27807512
PMCPMC5069405
OpenAlexW2538080681

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.