Evidence map›Paper›PMID 29374208›Full record

ArticleScientific reports2018

Down-regulation of guanylate binding protein 1 causes mitochondrial dysfunction and cellular senescence in macrophages.

Xiaoxue Qiu, Hong Guo, Junshu Yang, Yinduo Ji, Chia-Shan Wu, Xiaoli Chen

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 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

6 authors at 2 institutions in 1 country.

Xiaoxue QiuDepartment of Food Science and Nutrition, College of Food, Agricultural and Natural Resource Sciences, University of Minnesota, Twin Cities, Minnesota, USA.
Hong GuoDepartment of Food Science and Nutrition, College of Food, Agricultural and Natural Resource Sciences, University of Minnesota, Twin Cities, Minnesota, USA.
Junshu YangDepartment of Veterinary Biomedical Sciences, College of Veterinary Medicine, University of Minnesota, Twin Cities, Minnesota, USA.
Yinduo JiDepartment of Veterinary Biomedical Sciences, College of Veterinary Medicine, University of Minnesota, Twin Cities, Minnesota, USA.
Chia-Shan WuDepartment of Nutrition and Food Science, Texas A&M University, College Station, TX, USA.
Xiaoli ChenDepartment of Food Science and Nutrition, College of Food, Agricultural and Natural Resource Sciences, University of Minnesota, Twin Cities, Minnesota, USA. xlchen@umn.edu.
University of Minnesota · USTexas A&M University · US

Funding

Obesity and Energy Metabolism CoreP30DK050456 · NIDDK · UNIVERSITY OF MINNESOTA TWIN CITIES · PI BERNLOHR, DAVID A · 1995 to 2015
$17.0M
NIDDK NIH HHS P30 DK050456
6 · The paper itself

Abstract

Macrophage polarization is tightly associated with its metabolic reprograming and immune dysfunction. However, the intracellular molecules/pathways that connect these alterations in inflammatory macrophages remain largely unidentified. Herein, we explored the role of guanylate binding protein 1 (Gbp1), an intracellular anti-microbial protein, in regulating polarization, metabolic reprogramming, and cellular aging of macrophages. We showed that Gbp1 expression in inguinal white adipose tissue is significantly decreased in high-fat diet -fed and aged mice. Gbp1 expression is significantly induced by IFNγ and LPS in macrophages but not adipocytes. Downregulation of Gbp1 expression causes macrophage polarization towards a pro-inflammatory phenotype. Gbp1 knockdown (Kd) macrophages have impaired mitochondrial respiratory function, which is further supported by down-regulation of genes encoding electron transport chain components and genes involved in fatty acid oxidation and mitochondrial function. Moreover, we observed Gbp1 is localized in both cytosol and mitochondrial fraction, and Gbp1 Kd macrophages display decreased mitophagy activity. More interestingly, Gbp1 Kd macrophages undergo senescence as evidenced by increased activation of AMPK-p53 pathway and positive staining of β-galactosidase. These observations suggest that Gbp1 may play an important role in protecting against mitochondrial dysfunction and preserving immune function of macrophages during inflammatory stress and aging.

Indexed as

Cell DifferentiationCellular SenescenceDown-Regulation3T3-L1 CellsAnimalsCell RespirationElectron TransportGTP-Binding ProteinsMacrophagesMiceMice, Inbred C57BLMitochondriaRAW 264.7 CellsGbp2b protein, mouseGTP-Binding Proteins

Identifiers

PMID29374208
PMCPMC5785964
OpenAlexW2806707508

What OpenQuestion holds

Textmetadata
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.