Evidence map›Paper›PMID 28499252›Full record

ArticleRedox biology2017

Crosstalk between HDAC6 and Nox2-based NADPH oxidase mediates HIV-1 Tat-induced pro-inflammatory responses in astrocytes.

Gi Soo Youn, Hyundong Cho, Donggyu Kim, Soo Young Choi, Jinseu Park

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

30 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
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  9. Role of Dysregulated Autophagy in HIV Tat, Cocaine, and cART Mediated NLRP3 Activation in Microglia.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2023
    Article
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  20. Functional impact of HIV-1 Tat on cells of the CNS and its role in HAND.Cellular and molecular life sciences : CMLS · 2020
    Review
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

5 authors at 1 institution in 1 country.

Gi Soo YounDepartment of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University, Chunchon 24252, Kangwon-Do, Republic of Korea.
Hyundong ChoDepartment of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University, Chunchon 24252, Kangwon-Do, Republic of Korea.
Donggyu KimDepartment of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University, Chunchon 24252, Kangwon-Do, Republic of Korea.
Soo Young ChoiDepartment of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University, Chunchon 24252, Kangwon-Do, Republic of Korea.
Jinseu ParkDepartment of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University, Chunchon 24252, Kangwon-Do, Republic of Korea. Electronic address: jinpark@hallym.ac.kr.
Hallym University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histone deacetylase 6 (HDAC6) likely is important in inflammatory diseases. However, how HDAC6 exerts its effect on inflammatory processes remains unclear. HIV-1 transactivator of transcription (Tat) activates NADPH oxidase resulting in generation of reactive oxygen species (ROS), leading to extensive neuro-inflammation in the central nervous system. We investigated the correlation of HDAC6 and NADPH oxidase in HIV-1 Tat-stimulated astrocytes. HDAC6 knockdown attenuated HIV-1 Tat-induced ROS generation and NADPH oxidase activation. HDAC6 knockdown suppressed HIV-1 Tat-induced expression of NADPH oxidase subunits, such as Nox2, p47phox, and p22phox. Specific inhibition of HDAC6 using tubastatin A suppressed HIV-1 Tat-induced ROS generation and activation of NADPH oxidase. N-acetyl cysteine, diphenyl iodonium, and apocynin suppressed HIV-1 Tat-induced expression of HDAC6 and the pro-inflammatory chemokines CCL2, CXCL8, and CXCL10. Nox2 knockdown attenuated HIV-1 Tat-induced HDAC6 expression and subsequent expression of chemokines. The collective results point to the potential crosstalk between HDAC6 and NADPH oxidase, which could be a combined therapeutic target for relief of HIV-1 Tat-mediated neuro-inflammation.

Indexed as

AnimalsAstrocytesCell LineChemokinesGene Knockdown TechniquesHistone Deacetylase 6HIV-1HumansHydroxamic AcidsIndolesMiceNADPH Oxidase 2Reactive Oxygen Speciestat Gene Products, Human Immunodeficiency VirusChemokinesCYBB protein, humanHDAC6 protein, humanHistone Deacetylase 6Hydroxamic AcidsIndolesNADPH Oxidase 2Reactive Oxygen Speciestat Gene Products, Human Immunodeficiency Virustubastatin AAstrocytesHDAC6HIV-1 TatInflammationNADPH oxidaseROS

Identifiers

PMID28499252
PMCPMC5429231
OpenAlexW2611766569

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.