Evidence map›Paper›PMID 28820328›Full record

ArticleCell cycle (Georgetown, Tex.)2017

LPS-induced inflammatory response triggers cell cycle reactivation in murine neuronal cells through retinoblastoma proteins induction.

Barbara D'Angelo, Carlo Astarita, Silvia Boffo, Mina Massaro-Giordano, Carmelina Antonella Ianuzzi, Antonella Caporaso, Marcella Macaluso, Antonio Giordano

Open access · greenAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.8field-weighted citation impact, top 25% 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

17 citing papers in PubMed, 29 citations in OpenAlex.

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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

8 authors at 4 institutions in 2 countries.

Barbara D'Angeloa Sbarro Institute for Cancer Research and Molecular Medicine, Department of Biology, Center for Biotechnology, College of Science and Technology , Temple University , Philadelphia , PA , USA.
Carlo Astaritaa Sbarro Institute for Cancer Research and Molecular Medicine, Department of Biology, Center for Biotechnology, College of Science and Technology , Temple University , Philadelphia , PA , USA.
Silvia Boffoa Sbarro Institute for Cancer Research and Molecular Medicine, Department of Biology, Center for Biotechnology, College of Science and Technology , Temple University , Philadelphia , PA , USA.
Mina Massaro-Giordanoc Department of Ophthalmology, Perelman School of Medicine , University of Pennsylvania , Philadelphia , PA.
Carmelina Antonella Ianuzzib Department of Medicine, Surgery, and Neuroscience , University of Siena , Siena , Italy.
Antonella Caporasod Oncology Research Center of Mercogliano (CROM) , Istituto Nazionale Tumori-IRCCS-Fondazione G. Pascale , Naples , Italy.
Marcella Macalusoa Sbarro Institute for Cancer Research and Molecular Medicine, Department of Biology, Center for Biotechnology, College of Science and Technology , Temple University , Philadelphia , PA , USA.
Antonio Giordanoa Sbarro Institute for Cancer Research and Molecular Medicine, Department of Biology, Center for Biotechnology, College of Science and Technology , Temple University , Philadelphia , PA , USA.
Temple University · USIstituto Nazionale Tumori IRCCS "Fondazione G. Pascale" · ITUniversity of Pennsylvania · USUniversity of Siena · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cell cycle reactivation in adult neurons is an early hallmark of neurodegeneration. The lipopolysaccharide (LPS) is a well-known pro-inflammatory factor that provokes neuronal cell death via glial cells activation. The retinoblastoma (RB) family includes RB1/p105, retinoblastoma-like 1 (RBL1/p107), and retinoblastoma-like 2 (Rb2/p130). Several studies have indicated that RB proteins exhibit tumor suppressor activities, and play a central role in cell cycle regulation. In this study, we assessed LPS-mediated inflammatory effect on cell cycle reactivation and apoptosis of neuronally differentiated cells. Also, we investigated whether the LPS-mediated inflammatory response can influence the function and expression of RB proteins. Our results showed that LPS challenges triggered cell cycle reactivation of differentiated neuronal cells, indicated by an accumulation of cells in S and G2/M phase. Furthermore, we found that LPS treatment also induced apoptotic death of neurons. Interestingly, we observed that LPS-mediated inflammatory effect on cell cycle re-entry and apoptosis was concomitant with the aberrant expression of RBL1/p107 and RB1/p105. To the best of our knowledge, our study is the first to indicate a role of LPS in inducing cell cycle re-entry and/or apoptosis of differentiated neuronal cells, perhaps through mechanisms altering the expression of specific members of RB family proteins. This study provides novel information on the biology of post-mitotic neurons and could help in identifying novel therapeutic targets to prevent de novo cell cycle reactivation and/or apoptosis of neurons undergoing neurodegenerative processes.

Indexed as

AnimalsApoptosisCell Cycle CheckpointsCell DifferentiationCell LineLipopolysaccharidesMiceNeural Stem CellsRetinoblastoma-Like Protein p107Retinoblastoma ProteinLipopolysaccharidesRetinoblastoma-Like Protein p107Retinoblastoma Proteinapoptosiscell cycleinflammationneurodegenerationneuronsrb proteinsstress

Identifiers

PMID28820328
PMCPMC5788440
OpenAlexW2749935441

What OpenQuestion holds

Textmetadata
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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.