Evidence map›Paper›PMID 24281253›Full record

ArticleCell cycle (Georgetown, Tex.)2014

Silencing of RB1 and RB2/P130 during adipogenesis of bone marrow stromal cells results in dysregulated differentiation.

Stefania Capasso, Nicola Alessio, Giovanni Di Bernardo, Marilena Cipollaro, Mariarosa Ab Melone, Gianfranco Peluso, Antonio Giordano, Umberto Galderisi

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

10 citing papers in PubMed, 22 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 5 institutions in 2 countries.

Stefania CapassoDepartment of Experimental Medicine; Biotechnology and Molecular Biology Section; Second University of Naples; Naples, Italy.
Nicola AlessioDepartment of Experimental Medicine; Biotechnology and Molecular Biology Section; Second University of Naples; Naples, Italy; Institute of Protein Biochemistry; CNR; Naples, Italy.
Giovanni Di BernardoDepartment of Experimental Medicine; Biotechnology and Molecular Biology Section; Second University of Naples; Naples, Italy.
Marilena CipollaroDepartment of Experimental Medicine; Biotechnology and Molecular Biology Section; Second University of Naples; Naples, Italy.
Mariarosa Ab MeloneDepartment of Clinical and Experimental Medicine; Second University of Naples; Naples, Italy.
Gianfranco PelusoInstitute of Protein Biochemistry; CNR; Naples, Italy; Institute of Biomedicine and Bioresources; CNR; Naples, Italy.
Antonio GiordanoSbarro Institute for Cancer Research and Molecular Medicine; Center For Biotechnology; Temple University; Philadelphia, PA USA; Department of Medicine, Surgery and Neurociences; University of Siena; Siena, Italy.
Umberto GalderisiDepartment of Experimental Medicine; Biotechnology and Molecular Biology Section; Second University of Naples; Naples, Italy; Institute of Protein Biochemistry; CNR; Naples, Italy; Sbarro Institute for Cancer Research and Molecular Medicine; Center For Biotechnology; Temple University; Philadelphia, PA USA; GENKÖK; Genome and Stem Cell Center; Erciyes University; Kayseri, Turkey.
University of Campania "Luigi Vanvitelli" · ITUniversity of Naples Federico II · ITInstitute for Experimental Endocrinology and Oncology · ITInstitute of Biosciences and Bioresources · ITTemple College · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bone marrow adipose tissue (BMAT) is different from fat found elsewhere in the body, and only recently have some of its functions been investigated. BMAT may regulate bone marrow stem cell niche and plays a role in energy storage and thermogenesis. BMAT may be involved also in obesity and osteoporosis onset. Given the paramount functions of BMAT, we decided to better clarify the human bone marrow adipogenesis by analyzing the role of the retinoblastoma gene family, which are key players in cell cycle regulation. Our data provide evidence that the inactivation of RB1 or RB2/P130 in uncommitted bone marrow stromal cells (BMSC) facilitates the first steps of adipogenesis. In cultures with silenced RB1 or RB2/P130, we observed an increase of clones with adipogenic potential and a higher percentage of cells accumulating lipid droplets. Nevertheless, the absence of RB1 or RB2/P130 impaired the terminal adipocyte differentiation and gave rise to dysregulated adipose cells, with alteration in lipid uptake and release. For the first time, we evidenced that RB2/P130 plays a role in bone marrow adipogenesis. Our data suggest that while the inactivation of retinoblastoma proteins may delay the onset of last cell division and allow more BMSC to be committed to adipocyte, it did not allow a permanent cell cycle exit, which is a prerequisite for adipocyte terminal maturation.

Indexed as

AdipogenesisAdipocytesBone MarrowCell CycleCell DifferentiationCells, CulturedGene SilencingHumansMesenchymal Stem CellsRetinoblastoma-Like Protein p130Retinoblastoma ProteinRBL2 protein, humanRetinoblastoma-Like Protein p130Retinoblastoma Proteinadipocytesbone marrowdifferentiationmarrow stromal stem cellsretinoblastoma gene family

Identifiers

PMID24281253
PMCPMC3956544
OpenAlexW1984741574

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.