Evidence map›Paper›PMID 33387198›Full record

ArticleMolecular biology reports2021

Microglia induce neurogenic protein expression in primary cortical cells by stimulating PI3K/AKT intracellular signaling in vitro.

Kristi Lorenzen, Nicholas W Mathy, Erin R Whiteford, Alex Eischeid, Jing Chen, Matthew Behrens, Xian-Ming Chen, Annemarie Shibata

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

Article in Molecular biology reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.5field-weighted citation impact, top 39% 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

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
  2. Recent progresses in novelFrontiers in bioengineering and biotechnology · 2022
    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

8 authors at 1 institution in 2 countries.

Kristi LorenzenBiology Department, Creighton University, Omaha, NE, USA.
Nicholas W MathyBiology Department, Creighton University, Omaha, NE, USA.
Erin R WhitefordBiology Department, Creighton University, Omaha, NE, USA.
Alex EischeidBiology Department, Creighton University, Omaha, NE, USA.
Jing ChenBiology Department, Creighton University, Omaha, NE, USA.
Matthew BehrensBiology Department, Creighton University, Omaha, NE, USA.
Xian-Ming ChenDepartment of Medical Microbiology and Immunology, Creighton University School of Medicine, Creighton University, Omaha, NE, USA.
Annemarie ShibataBiology Department, Creighton University, Omaha, NE, USA. annemarieshibata@creighton.edu.ORCID http://orcid.org/0000-0003-2451-3065
Creighton University · US

Funding

UNMC Structural Biology CoreP20GM103427 · NIGMS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI Heather Colleen Jensen-Smith · 2012 to 2026
$59.2M
ZINC FINGER-INSPIRED FLUORESCENT CHEMOSENSORSP20RR016469 · NCRR · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI TURPEN, JAMES B · 2001 to 2011
$36.2M
Creighton University HSSIFNCRR NIH HHS P20 RR016469NIGMS NIH HHS P20 GM103427
6 · The paper itself

Abstract

Emerging evidence suggests that microglia can support neurogenesis. Little is known about the mechanisms by which microglia regulate the cortical environment and stimulate cortical neurogenesis. We used an in vitro co-culture model system to investigate the hypothesis that microglia respond to soluble signals from cortical cells, particularly following mechanical injury, to alter the cortical environment and promote cortical cell proliferation, differentiation, and survival. Analyses of cortical cell proliferation, cell death, neurogenic protein expression, and intracellular signaling were performed on uninjured and injured cortical cells in co-culture with microglial cell lines. Microglia soluble cues enhanced cortical cell viability and proliferation cortical cells. Co-culture of injured cortical cells with microglia significantly reduced cell death of cortical cells. Microglial co-culture significantly increased Nestin + and α-internexin + cortical cells. Multiplex ELISA and RT-PCR showed decreased pro-inflammatory cytokine production by microglia co-cultured with injured cortical cells. Inhibition of AKT phosphorylation in cortical cells blocked microglial-enhanced cortical cell viability and expression of neurogenic markers in vitro. This in vitro model system allows for assessment of the effect of microglial-derived soluble signals on cortical cell viability, proliferation, and stages of differentiation during homeostasis or following mechanical injury. These data suggest that microglia cells can downregulate inflammatory cytokine production following activation by mechanical injury to enhance proliferation of new cells capable of neurogenesis via activation of AKT intracellular signaling. Increasing our understanding of the mechanisms that drive microglial-enhanced cortical neurogenesis during homeostasis and following injury in vitro will provide useful information for future primary cell and in vivo studies.

Indexed as

AnimalsCell DifferentiationCell ProliferationCells, CulturedCell SurvivalCerebral CortexCoculture TechniquesGene Expression Regulation, DevelopmentalIntermediate Filament ProteinsMicrogliaNestinNeurogenesisNeuronsPhosphatidylinositol 3-KinasesPrimary Cell CultureProto-Oncogene Proteins c-aktalpha-internexinIntermediate Filament ProteinsNes protein, ratNestinPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktMicrogliaNestinNeurogenesisPI3K/AKTα-internexin

Identifiers

PMID33387198
PMCPMC7884585
OpenAlexW3116189970

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.