Evidence map›Paper›PMID 28031332›Full record

ArticleMolecular pharmacology2017

Regulator of G Protein Signaling 10 (Rgs10) Expression Is Transcriptionally Silenced in Activated Microglia by Histone Deacetylase Activity.

Mohammed Alqinyah, Nagini Maganti, Mourad W Ali, Ruchi Yadav, Mei Gao, Ercan Cacan, Han-Rong Weng, Susanna F Greer, Shelley B Hooks

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

Article in Molecular pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

24 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Review
  3. Post-translational modifications regulating microglial inflammation in central nervous system disorders: a review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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  15. Acetylation in Tumor Immune Evasion Regulation.Frontiers in pharmacology · 2021
    Review
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  17. Review
  18. Review
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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

9 authors at 2 institutions in 1 country.

Mohammed AlqinyahDepartment of Pharmaceutical and Biomedical Sciences, University of Georgia, Athens, Georgia (M.A., M.W.A., R.Y., M.G., H.-R.W., S.B.H.); and Department of Biology, Georgia State University, Atlanta, Georgia (N.M., E.C., S.F.G.).
Nagini MagantiDepartment of Pharmaceutical and Biomedical Sciences, University of Georgia, Athens, Georgia (M.A., M.W.A., R.Y., M.G., H.-R.W., S.B.H.); and Department of Biology, Georgia State University, Atlanta, Georgia (N.M., E.C., S.F.G.).
Mourad W AliDepartment of Pharmaceutical and Biomedical Sciences, University of Georgia, Athens, Georgia (M.A., M.W.A., R.Y., M.G., H.-R.W., S.B.H.); and Department of Biology, Georgia State University, Atlanta, Georgia (N.M., E.C., S.F.G.).
Ruchi YadavDepartment of Pharmaceutical and Biomedical Sciences, University of Georgia, Athens, Georgia (M.A., M.W.A., R.Y., M.G., H.-R.W., S.B.H.); and Department of Biology, Georgia State University, Atlanta, Georgia (N.M., E.C., S.F.G.).
Mei GaoDepartment of Pharmaceutical and Biomedical Sciences, University of Georgia, Athens, Georgia (M.A., M.W.A., R.Y., M.G., H.-R.W., S.B.H.); and Department of Biology, Georgia State University, Atlanta, Georgia (N.M., E.C., S.F.G.).
Ercan CacanDepartment of Pharmaceutical and Biomedical Sciences, University of Georgia, Athens, Georgia (M.A., M.W.A., R.Y., M.G., H.-R.W., S.B.H.); and Department of Biology, Georgia State University, Atlanta, Georgia (N.M., E.C., S.F.G.).
Han-Rong WengDepartment of Pharmaceutical and Biomedical Sciences, University of Georgia, Athens, Georgia (M.A., M.W.A., R.Y., M.G., H.-R.W., S.B.H.); and Department of Biology, Georgia State University, Atlanta, Georgia (N.M., E.C., S.F.G.).
Susanna F GreerDepartment of Pharmaceutical and Biomedical Sciences, University of Georgia, Athens, Georgia (M.A., M.W.A., R.Y., M.G., H.-R.W., S.B.H.); and Department of Biology, Georgia State University, Atlanta, Georgia (N.M., E.C., S.F.G.).
Shelley B HooksDepartment of Pharmaceutical and Biomedical Sciences, University of Georgia, Athens, Georgia (M.A., M.W.A., R.Y., M.G., H.-R.W., S.B.H.); and Department of Biology, Georgia State University, Atlanta, Georgia (N.M., E.C., S.F.G.) shooks@uga.edu.
Georgia State University · USUniversity of Georgia · US

Funding

Glial-cytokine-neuronal interactions in neuropathic painR01NS064289 · NINDS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI WENG, HAN-RONG · 2009 to 2012
$1.2M
Identification of Novel Nuclear RGS10 Binding PartnersR21NS101161 · NINDS · UNIVERSITY OF GEORGIA · PI HOOKS, SHELLEY B · 2017 to 2018
$413k
NINDS NIH HHS R01 NS064289NINDS NIH HHS R21 NS101161
6 · The paper itself

Abstract

RGS10 has emerged as a key regulator of proinflammatory cytokine production in microglia, functioning as an important neuroprotective factor. Although RGS10 is normally expressed in microglia at high levels, expression is silenced in vitro following activation of TLR4 receptor. Given the ability of RGS10 to regulate inflammatory signaling, dynamic regulation of RGS10 levels in microglia may be an important mechanism to tune inflammatory responses. The goals of the current study were to confirm that RGS10 is suppressed in an in vivo inflammatory model of microglial activation and to determine the mechanism for activation-dependent silencing of Rgs10 expression in microglia. We demonstrate that endogenous RGS10 is present in spinal cord microglia, and RGS10 protein levels are suppressed in the spinal cord in a nerve injury-induced neuropathic pain mouse model. We show that the histone deacetylase (HDAC) enzyme inhibitor trichostatin A blocks the ability of lipopolysaccharide (LPS) to suppress Rgs10 transcription in BV-2 and primary microglia, demonstrating that HDAC enzymes are required for LPS silencing of Rgs10 Furthermore, we used chromatin immunoprecipitation to demonstrate that H3 histones at the Rgs10 proximal promoter are deacetylated in BV-2 microglia following LPS activation, and HDAC1 association at the Rgs10 promoter is enhanced following LPS stimulation. Finally, we have shown that sphingosine 1-phosphate, an endogenous microglial signaling mediator that inhibits HDAC activity, enhances basal Rgs10 expression in BV-2 microglia, suggesting that Rgs10 expression is dynamically regulated in microglia in response to multiple signals.

Indexed as

Gene SilencingTranscription, GeneticAcetylationAnimalsAzacitidineCell LineChemokine CXCL2Disease Models, AnimalHistone Deacetylase InhibitorsHistone DeacetylasesHydroxamic AcidsInflammationLipopolysaccharidesLysophospholipidsMethyltransferasesMice, Inbred C57BLAzacitidineChemokine CXCL2Histone Deacetylase InhibitorsHistone DeacetylasesHydroxamic AcidsLipopolysaccharidesLysophospholipidsMethyltransferasesReceptors, G-Protein-CoupledRgs10 protein, mouseRGS ProteinsRNA, MessengerSphingosinesphingosine 1-phosphatetrichostatin ATumor Necrosis Factor-alpha

Identifiers

PMID28031332
PMCPMC5325084
OpenAlexW2561263202

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.