Evidence map›Paper›PMID 26388235›Full record

ArticleCellular & molecular immunology2017

RhoB regulates the function of macrophages in the hypoxia-induced inflammatory response.

Gaoxiang Huang, Jie Su, Mingzhuo Zhang, Yiduo Jin, Yan Wang, Peng Zhou, Jian Lu

Open access · bronzeAbstract read
In one paragraph

Article in Cellular & molecular immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

22 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
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  11. The Immunogenetics of Systemic Sclerosis.Advances in experimental medicine and biology · 2022
    Article
  12. Review
  13. Article
  14. Glucocorticoid-Dependent Mechanisms of Brain Tolerance to Hypoxia.International journal of molecular sciences · 2021
    Review
  15. Article
  16. 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

7 authors at 1 institution in 1 country.

Gaoxiang HuangDepartment of Pathophysiology, Second Military Medical University, Shanghai 200433, People's Republic of China.
Jie SuDepartment of Pathophysiology, Second Military Medical University, Shanghai 200433, People's Republic of China.
Mingzhuo ZhangDepartment of Pathophysiology, Second Military Medical University, Shanghai 200433, People's Republic of China.
Yiduo JinDepartment of Pathophysiology, Second Military Medical University, Shanghai 200433, People's Republic of China.
Yan WangDepartment of Pathophysiology, Second Military Medical University, Shanghai 200433, People's Republic of China.
Peng ZhouDepartment of Pathophysiology, Second Military Medical University, Shanghai 200433, People's Republic of China.
Jian LuDepartment of Pathophysiology, Second Military Medical University, Shanghai 200433, People's Republic of China.
Second Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immune cells, particularly macrophages, play critical roles in the hypoxia-induced inflammatory response. The small GTPase RhoB is usually rapidly induced by a variety of stimuli and has been described as an important regulator of cytoskeletal organization and vesicle and membrane receptor trafficking. However, it is unknown whether RhoB is involved in the hypoxia-induced inflammatory response. Here, we investigated the effect of hypoxia on the expression of RhoB and the mechanism and significance of RhoB expression in macrophages. We found that hypoxia significantly upregulated the expression of RhoB in RAW264.7 cells, mouse peritoneal macrophages, and the spleen of rats. Hypoxia-induced expression of RhoB was significantly blocked by a specific inhibitor of hypoxia-inducible factor-1α (HIF-1α), c-Jun N-terminal kinase (JNK), or extracellular-signal regulated protein kinase (ERK), indicating that hypoxia-activated HIF-1α, JNK, and ERK are involved in the upregulation of RhoB by hypoxia. Knockdown of RhoB expression not only significantly suppressed basal production of interleukin-1 beta (IL-1β), interleukin 6 (IL-6), and tumor necrosis factor alpha (TNF-α) in normoxia but also more markedly decreased the hypoxia-stimulated production of these cytokines. Furthermore, we showed that RhoB increased nuclear factor-kappa B (NF-κB) activity, and the inhibition of NF-κB transcriptional activity significantly decreased the RhoB-increased mRNA levels of IL-1β, IL-6, and TNF-α. Finally, we demonstrated that RhoB enhanced cell adhesion and inhibited cell migration in normoxia and hypoxia. Taken together, these results suggest that RhoB plays an important role in the hypoxia-induced activation of macrophages and the inflammatory response.Cellular & Molecular Immunology advance online publication, 21 September 2015; doi:10.1038/cmi.2015.78.

Indexed as

AnimalsCell AdhesionCell HypoxiaCell MovementCytokinesGene Knockdown TechniquesGene SilencingHypoxia-Inducible Factor 1, alpha SubunitInflammationInflammation MediatorsMacrophagesMaleMAP Kinase Signaling SystemMiceMice, Inbred BALB CModels, BiologicalCytokinesHypoxia-Inducible Factor 1, alpha SubunitInflammation MediatorsNF-kappa BrhoB GTP-Binding Protein

Identifiers

PMID26388235
PMCPMC5360878
OpenAlexW2344078301

What OpenQuestion holds

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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.