Evidence map›Paper›PMID 34149651›Full record

ArticleFrontiers in microbiology2021

RIPK3-Dependent Necroptosis Limits PRV Replication in PK-15 Cells.

Hongchao Gou, Zhibiao Bian, Rujian Cai, Pinpin Chu, Shuai Song, Yan Li, Zhiyong Jiang, Kunli Zhang, Dongxia Yang, Chunling Li

Open access · goldAbstract read
In one paragraph

Article in Frontiers in microbiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 25% 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

13 citing papers in PubMed, 11 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

10 authors at 3 institutions in 1 country.

Hongchao GouInstitute of Animal Health, Guangdong Academy of Agricultural Sciences, Guangzhou, China.
Zhibiao BianInstitute of Animal Health, Guangdong Academy of Agricultural Sciences, Guangzhou, China.
Rujian CaiInstitute of Animal Health, Guangdong Academy of Agricultural Sciences, Guangzhou, China.
Pinpin ChuInstitute of Animal Health, Guangdong Academy of Agricultural Sciences, Guangzhou, China.
Shuai SongInstitute of Animal Health, Guangdong Academy of Agricultural Sciences, Guangzhou, China.
Yan LiInstitute of Animal Health, Guangdong Academy of Agricultural Sciences, Guangzhou, China.
Zhiyong JiangInstitute of Animal Health, Guangdong Academy of Agricultural Sciences, Guangzhou, China.
Kunli ZhangInstitute of Animal Health, Guangdong Academy of Agricultural Sciences, Guangzhou, China.
Dongxia YangInstitute of Animal Health, Guangdong Academy of Agricultural Sciences, Guangzhou, China.
Chunling LiInstitute of Animal Health, Guangdong Academy of Agricultural Sciences, Guangzhou, China.
Guangdong Provincial Center for Disease Control and Prevention · CNGuangdong Academy of Agricultural Sciences · CNJi Hua Laboratory · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pigs infected by pseudorabies virus (PRV) display necrotic pathology in multiple organs. The mechanism by which PRV induces cell death is still unclear. Recently, necroptosis was identified as a programmed process dependent on the receptor interacting protein kinase 3 (RIPK3) and mixed lineage kinase-like protein (MLKL). In this study, we demonstrated that PRV induced RIPK3-dependent necroptosis in PK-15 cells. The data showed that PRV infection caused cell death with Propidium Iodide (PI)-positive staining. Transmission electron microscopy analysis indicated plasma membrane disruption in PRV-infected cells. A pan-caspase inhibitor did not prevent PRV-induced necrotic cell death. Western blot analysis indicated that caspase-3 and caspase-8 were not cleaved during PRV infection. Although the transcription of tumor necrosis factor-alpha (TNF-α) was increased by PRV infection, RIPK1 was shown to be not involved in PRV-induced necrotic cell death by use of its specific inhibitor. Further experiments indicated that the phosphorylation of RIPK3 and MLKL was upregulated in PRV-infected cells. Stable shRNA knockdown of RIPK3 or MLKL had a recovery effect on PRV-induced necrotic cell death. Meanwhile, viral titers were enhanced in RIPK3 and MLKL knockdown cells. Hence, we concluded that initiation of necroptosis in host cells plays a limiting role in PRV infection. Considering that necroptosis is an inflammatory form of programmed cell death, our data may be beneficial for understanding the necrotic pathology of pigs infected by PRV.

Indexed as

mixed lineage kinase-like protein (MLKL)necroptosisPK-15 cellpseudorabies virus (PRV)receptor interacting protein kinase 3 (RIPK3)

Identifiers

PMID34149651
PMCPMC8211757
OpenAlexW3171086485

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.