Evidence map›Paper›PMID 22479600›Full record

ArticlePloS one2012

Mitochondrial dysfunction and adipogenic reduction by prohibitin silencing in 3T3-L1 cells.

Dong Liu, Yiming Lin, Ting Kang, Bo Huang, Wei Xu, Minerva Garcia-Barrio, Moshood Olatinwo, Roland Matthews, Y Eugene Chen, Winston E Thompson

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

39 citing papers in PubMed, 75 citations in OpenAlex.

  1. Article
  2. Small mitochondrial protein NERCLIN regulates cardiolipin homeostasis and mitochondrial ultrastructure.Proceedings of the National Academy of Sciences of the United States of America · 2023
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  7. The Combined Partial Knockdown ofAntioxidants (Basel, Switzerland) · 2022
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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

10 authors at 5 institutions in 2 countries.

Dong LiuCardiovascular Research Institute, Morehouse School of Medicine, Atlanta, Georgia, United States of America. dliu@msm.edu
Yiming Lin
Ting Kang
Bo Huang
Wei Xu
Minerva Garcia-Barrio
Moshood Olatinwo
Roland Matthews
Y Eugene Chen
Winston E Thompson
Morehouse School of Medicine · USEmory University · USFirst Affiliated Hospital of Nanchang University · CNSecond Affiliated Hospital of Nanchang University · CNUniversity of Michigan–Ann Arbor · US

Funding

Morehouse School of Medicine Center of Excellence Research Endowment ProgramS21MD000101 · NIMHD · MOREHOUSE SCHOOL OF MEDICINE · PI MONTGOMERY-RICE, VALERIE C. · 2001 to 2015
$74.3M
TRANSCRIPTION FACTORS AND PROSTATE CANCERG12RR003034 · NCRR · MOREHOUSE SCHOOL OF MEDICINE · PI ZHAO, XUEYING · 1986 to 2011
$32.4M
SP REGULATION OF GENE EXPRESSION IN SPERMATOGENESISU54HD041749 · NICHD · MOREHOUSE SCHOOL OF MEDICINE · PI MANN, DAVID R · 2001 to 2007
$7.4M
NCRR NIH HHS G12 RR003034NCRR NIH HHS G12RR003034NCRR NIH HHS G12RR003034-SUPPLEMENTNICHD NIH HHS U54 HD041749NICHD NIH HHS U54HD41749NIMHD NIH HHS S21 MD000101
6 · The paper itself

Abstract

Increase in mitochondrial biogenesis has been shown to accompany brown and white adipose cell differentiation. Prohibitins (PHBs), comprised of two evolutionarily conserved proteins, prohibitin-1 (PHB1) and prohibitin-2 (PHB2), are present in a high molecular-weight complex in the inner membrane of mitochondria. However, little is known about the effect of mitochondrial PHBs in adipogenesis. In the present study, we demonstrate that the levels of both PHB1 and PHB2 are significantly increased during adipogenesis of 3T3-L1 preadipocytes, especially in mitochondria. Knockdown of PHB1 or PHB2 by oligonucleotide siRNA significantly reduced the expression of adipogenic markers, the accumulation of lipids and the phosphorylation of extracellular signal-regulated kinases. In addition, fragmentation of mitochondrial reticulum, loss of mitochondrial cristae, reduction of mitochondrial content, impairment of mitochondrial complex I activity and excessive production of ROS were observed upon PHB-silencing in 3T3-L1 cells. Our results suggest that PHBs are critical mediators in promoting 3T3-L1 adipocyte differentiation and may be the potential targets for obesity therapies.

Indexed as

Gene Expression Regulation3T3-L1 CellsAdipocytesAnimalsCell DifferentiationCell LineDNA, MitochondrialGene SilencingHumansMiceMicroscopy, ConfocalMicroscopy, Electron, TransmissionMitochondriaOligonucleotidesProhibitinsReactive Oxygen SpeciesDNA, MitochondrialOligonucleotidesPHB2 protein, humanPhb2 protein, mousePHB protein, humanProhibitinsReactive Oxygen SpeciesRepressor ProteinsRNA, Small Interfering

Identifiers

PMID22479600
PMCPMC3316679
OpenAlexW2042482608

What OpenQuestion holds

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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 OpenQuestion graph.