Evidence map›Paper›PMID 30151726›Full record

ArticleMolecular neurobiology2019

Cocaine Mediated Neuroinflammation: Role of Dysregulated Autophagy in Pericytes.

Susmita Sil, Fang Niu, Eric Tom, Ke Liao, Palsamy Periyasamy, Shilpa Buch

Open access · greenAbstract read
In one paragraph

Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

42 citing papers in PubMed, 63 citations in OpenAlex.

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  13. Role of autophagy in angiogenic potential of vascular pericytes.Frontiers in cell and developmental biology · 2024
    Review
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  16. Dysfunction of the Neurovascular Unit by Psychostimulant Drugs.International journal of molecular sciences · 2023
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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.

Susmita SilDepartment of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE, 68198-5880, USA.
Fang NiuDepartment of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE, 68198-5880, USA.
Eric TomDepartment of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE, 68198-5880, USA.
Ke LiaoDepartment of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE, 68198-5880, USA.
Palsamy PeriyasamyDepartment of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE, 68198-5880, USA.
Shilpa BuchDepartment of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE, 68198-5880, USA. sbuch@unmc.edu.ORCID http://orcid.org/0000-0002-3103-6685
University of Nebraska Medical Center · USNebraska Medical Center · US

Funding

Therapeutics Core (Page 286)P30MH062261 · NIMH · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BUCH, SHILPA J., FOX, HOWARD S · 2000 to 2021
$37.7M
The combinatorial effects of Opiates and the emerging promoter-variant strains of HIV-1 subtype C on HIV neuropathogensis and latencyR01DA041751 · NIDA · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BUCH, SHILPA J., BYRAREDDY, SIDDAPPA N · 2016 to 2020
$3.9M
HIV Tat & Morphine induce mircroglial migration & activation via release of miR-9 & 138R01DA040397 · NIDA · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BUCH, SHILPA J., FOX, HOWARD S · 2015 to 2019
$2.5M
Opiate induced SIV-Neuropathogenesis: Role of miRNA-29b in the Periphery-CNS CroR01DA035203 · NIDA · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BUCH, SHILPA J. · 2013 to 2017
$2.3M
Combinatorial effects of HIV, cART, & morphine on neuroinflammation: implications for HANDR01DA044586 · NIDA · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BUCH, SHILPA J., GUO, MINGLEI · 2017 to 2021
$1.9M
HIV Tat & cocaine-mediated alterations in microglial migration & activation involve epigenetic reulation of miRNAsR01DA043138 · NIDA · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BUCH, SHILPA J., GUO, MINGLEI · 2016 to 2020
$1.9M
National Institute of Mental Health 2P30MH062261National Institutes of Health DA035203National Institutes of Health DA040397National Institutes of Health DA041751National Institutes of Health DA043138National Institutes of Health DA044586NIDA NIH HHS R01 DA035203NIDA NIH HHS R01 DA040397NIDA NIH HHS R01 DA041751NIDA NIH HHS R01 DA043138NIDA NIH HHS R01 DA044586NIMH NIH HHS P30 MH062261
6 · The paper itself

Abstract

Cocaine, a known psychostimulant, results in oxidative stress and inflammation. Recent studies from our group have shown that cocaine induces inflammation in glial cells. Our current study was aimed at investigating whether cocaine exposure could also induce inflammation in non-glial cells such as the pericytes with a focus on the endoplasmic reticulum (ER) stress/autophagy axis. Our in vitro findings demonstrated that exposure of pericytes to cocaine resulted in upregulation of the pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6) in both the intracellular as well as extracellular compartments, thus underpinning pericytes as yet another source of neuroinflammation. Cocaine exposure of pericytes resulted in increased formation of autophagosomes as demonstrated by a time-dependent increase of autophagy markers, with a concomitant defect in the fusion of the autophagosome with the lysosomes. Pharmacological blocking of the sigma 1 receptor underscored its role in cocaine-mediated activation of pericytes. Furthermore, it was also demonstrated that cocaine-mediated dysregulation of autophagy involved upstream activation of the ER stress pathways, with a subsequent downstream production of pro-inflammatory cytokines in pericytes. These findings were also validated in an in vivo model wherein pericytes in the isolated brain microvessels of cocaine injected mice (7 days) exhibited increased expression of both the autophagy marker-LC3 as well as the pro-inflammatory cytokine, IL-6. This is the first report describing the role of pericytes in cocaine-mediated neuroinflammation. Interventions aimed at blocking either the sigma-1 receptor or the upstream ER stress mediators could likely be envisioned as promising therapeutic targets for abrogating cocaine-mediated inflammation in pericytes.

Indexed as

AnimalsAutophagyBrainCells, CulturedCocaineCytokinesEndoplasmic Reticulum StressHumansInflammationInflammation MediatorsMaleMice, Inbred C57BLMicrovesselsModels, BiologicalPericytesReceptors, sigmaCocaineCytokinesInflammation MediatorsReceptors, sigmaSigma-1 ReceptorCocaineDysregulated autophagyER stressMicrovesselsNeuroinflammationPericytes

Identifiers

PMID30151726
PMCPMC6393223
OpenAlexW2888866428

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.