Evidence map›Paper›PMID 23345082›Full record

ArticleJournal of molecular neuroscience : MN2013

Cellular prion protein participates in the regulation of inflammatory response and apoptosis in BV2 microglia during infection with Mycobacterium bovis.

Tianjian Ding, Xiangmei Zhou, Mohammed Kouadir, Fushan Shi, Yang Yang, Jin Liu, Min Wang, Xiaomin Yin, Lifeng Yang, Deming Zhao

Abstract read
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In one paragraph

Article in Journal of molecular neuroscience : MN, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

15 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. The multiple functions of PrPJournal of molecular medicine (Berlin, Germany) · 2022
    Review
  3. Effect of Two Different Drug-ResistantFrontiers in veterinary science · 2022
    Article
  4. Microglia in Prion Diseases: Angels or Demons?International journal of molecular sciences · 2020
    Review
  5. Review
  6. Review
  7. Implantation of Neural Probes in the Brain Elicits Oxidative Stress.Frontiers in bioengineering and biotechnology · 2018
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. 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 1 institution in 1 country.

Tianjian DingState Key Laboratories for Agrobiotechnology, Key Lab of Animal Epidemiology and Zoonosis, Ministry of Agriculture, National Animal Transmissible Spongiform Encephalopathy Laboratory, College of Veterinary Medicine, China Agricultural University, Beijing, 100193, China. dingtianjian_1986@126.com
Xiangmei Zhou
Mohammed Kouadir
Fushan Shi
Yang Yang
Jin Liu
Min Wang
Xiaomin Yin
Lifeng Yang
Deming Zhao
China Agricultural University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cellular prion protein (PrP(C)) is a glycoprotein anchored by glycosylphosphatidylinositol to the cell surface and is abundantly expressed in the central nervous system. A previous study has shown that PrP(C) contributes to the establishment of infections with intracellular bacteria in macrophages. In the present work, we investigated the role of PrP(C) in the response of BV2 microglia to Mycobacterium bovis infection. For this purpose, we examined the mRNA expression of prion protein gene (PRNP) upon M. bovis infection and analyzed the effect of siRNA-mediated disruption of PRNP on different parameters of microglial activation and apoptosis in M. bovis-infected microglia. We found that M. bovis infection induced a gradual increase in PRNP mRNA level and that siRNA-mediated silencing of PRNP in M. bovis-infected microglia reduced M. bovis-induced upregulation of pro-inflammatory factors, increased the rate of apoptosis in infected microglia, promoted the intrinsic apoptotic pathway, and downregulated the extrinsic apoptotic pathway. We conclude that PrP(C) participates in the regulation of the response of microglia to M. bovis infection through the upregulation of pro-inflammatory cytokines and the modulation of apoptosis by interference with the intrinsic apoptotic pathway.

Indexed as

ApoptosisMycobacterium bovisAnimalsCytokinesInflammationMiceMicrogliaPrion ProteinsPrionsRNA, MessengerCytokinesPrion ProteinsPrionsPrnp protein, mouseRNA, Messenger

Identifiers

PMID23345082
OpenAlexW2064127497

What OpenQuestion holds

Textmetadata
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.