Evidence map›Paper›PMID 29732971›Full record

ArticleCurrent Alzheimer research2018

Upregulation of Suppressor of Cytokine Signaling 3 in Microglia by Cinnamic Acid.

Sudipta Chakrabarti, Malabendu Jana, Avik Roy, Kalipada Pahan

Abstract read
In one paragraph

Article in Current Alzheimer research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

18 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. A simple protocol for isolating microglia from adult mouse brain.NeuroImmune pharmacology and therapeutics · 2023
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Regulation of blood-brain barrier integrity by microglia in health and disease: A therapeutic opportunity.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020
    Review
  11. Article
  12. Article
  13. Can cinnamon spice down autoimmune diseases?Journal of clinical & experimental immunology · 2020
    Article
  14. Article
  15. Investigation of Anti-Inflammatory Potential ofMolecules (Basel, Switzerland) · 2019
    Article
  16. Article
  17. Review
  18. Article
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

4 authors at 1 institution in 1 country.

Sudipta ChakrabartiDivision of Research and Development, Jesse Brown Veterans Affairs Medical Center, Chicago, IL-60612, United States.
Malabendu JanaDivision of Research and Development, Jesse Brown Veterans Affairs Medical Center, Chicago, IL-60612, United States.
Avik RoyDivision of Research and Development, Jesse Brown Veterans Affairs Medical Center, Chicago, IL-60612, United States.
Kalipada PahanDivision of Research and Development, Jesse Brown Veterans Affairs Medical Center, Chicago, IL-60612, United States.
Jesse Brown VA Medical Center · US

Funding

Cinnamon, CNTF and EAER01AT006681 · NCCIH · RUSH UNIVERSITY MEDICAL CENTER · PI PAHAN, KALIPADA · 2011 to 2015
$1.8M
Cinnamon and its metabolite sodium benzoate in ParkinsonismI01BX003033 · VA · JESSE BROWN VA MEDICAL CENTER · PI PAHAN, KALIPADA · 2016 to 2020
–
BLRD VA I01 BX003033NCCIH NIH HHS R01 AT006681
6 · The paper itself

Abstract

backgroundNeuroinflammation plays an important role in the pathogenesis of various neurodegenerative diseases including Alzheimer's disease (AD). Suppressor of cytokine signaling 3 (SOCS3) is an anti-inflammatory molecule that suppresses cytokine signaling and inflammatory gene expression in different cells including microglia.

objectiveThe pathways through which SOCS3 could be upregulated are poorly described. Cinnamic acid is a metabolite of cinnamon, a natural compound that is being widely used all over the world as a spice or flavoring agent. Here, we examined if cinnamic acid could upregulate SOCS3 in microglia.

methodMicroglia and astroglia isolated from mouse brain as well as BV-2 microglial cells were treated with cinnamic acid followed by monitoring the level of SOCS3 and different proinflammatory molecules by RT-PCR and real-time PCR. To nail down the mechanism, we also performed ChIP analysis to monitore the recruitment of cAMP response element binding (CREB) to the socs3 gene promoter and carried out siRNA knockdown of CREB.

resultsCinnamic acid upregulated the expression of SOCS3 mRNA and protein in mouse BV-2 microglial cells in dose- and time-dependent manner. Accordingly, cinnamic acid also increased the level of SOCS3 and suppressed the expression of inducible nitric oxide synthase and proinflammatory cytokines (TNFα, IL-1β and IL-6) in LPSstimulated BV-2 microglial cells. Similar to BV-2 microglial cells, cinnamic acid also increased the expression of SOCS3 in primary mouse microglia and astrocytes. We have seen that cAMP response element is present in the promoter of socs3 gene, that cinnamic acid induces the activation of CREB, that siRNA knockdown of CREB abrogates cinnamic acid-mediated upregulation of SOCS3, and that cinnamic acid treatment leads to the recruitment of CREB to the socs3 gene.

conclusionsThese studies suggest that cinnamic acid upregulates the expression of SOCS3 in glial cells via CREB pathway, which may be of importance in neuroinflammatory and neurodegenerative disorders.

Indexed as

AnimalsBrainCells, CulturedCinnamatesCREB-Binding ProteinCytokinesLipopolysaccharidesMass SpectrometryMiceMicrogliaRNA, MessengerRNA, Small InterferingSignal TransductionSuppressor of Cytokine Signaling 3 ProteinTransfectionUp-RegulationCinnamatescinnamic acidCREB-Binding ProteinCytokinesLipopolysaccharidesRNA, MessengerRNA, Small InterferingSuppressor of Cytokine Signaling 3 ProteinCinnamic acidCREBglial cellsmicroglial cellsneuroinflammation.SOCS3

Identifiers

PMID29732971
PMCPMC6128770
OpenAlexW2802080295

What OpenQuestion holds

Textmetadata
LicenceTDM
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.