Evidence map›Paper›PMID 28433632›Full record

ArticleBiochemical and biophysical research communications2017

Role of microRNA-130b in placental PGC-1α/TFAM mitochondrial biogenesis pathway.

Shaoning Jiang, April M Teague, Jeanie B Tryggestad, Steven D Chernausek

Abstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing 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

30 citing papers in PubMed, 43 citations in OpenAlex.

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  15. MicroRNAs: key regulators of the trophoblast function in pregnancy disorders.Journal of assisted reproduction and genetics · 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

4 authors at 1 institution in 1 country.

Shaoning JiangDepartment of Pediatrics, Section of Diabetes and Endocrinology, Harold Hamm Diabetes Center, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA. Electronic address: shaoning-jiang@ouhsc.edu.
April M TeagueDepartment of Pediatrics, Section of Diabetes and Endocrinology, Harold Hamm Diabetes Center, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
Jeanie B TryggestadDepartment of Pediatrics, Section of Diabetes and Endocrinology, Harold Hamm Diabetes Center, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
Steven D ChernausekDepartment of Pediatrics, Section of Diabetes and Endocrinology, Harold Hamm Diabetes Center, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
University of Oklahoma Health Sciences Center · US

Funding

Tracking and Evaluation CoreU54GM104938 · NIGMS · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI Janis E Campbell · 2013 to 2026
$68.2M
TRAINING COREP20MD000528 · NIMHD · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI COPELAND, KENNETH C · 2003 to 2016
$17.8M
Prenatal Conditions and the Pathway to Obesity and Diabetes in ChildrenR01DK089034 · NIDDK · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI CHERNAUSEK, STEVEN D · 2010 to 2014
$1.4M
NIDDK NIH HHS R01 DK089034NIGMS NIH HHS U54 GM104938NIMHD NIH HHS P20 MD000528
6 · The paper itself

Abstract

Diabetes during pregnancy is associated with abnormal placenta mitochondrial function and increased oxidative stress, which affect fetal development and offspring long-term health. Peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) is a master regulator of mitochondrial biogenesis and energy metabolism. The molecular mechanisms underlying the regulation of PGC-1α in placenta in the context of diabetes remain unclear. The present study examined the role of microRNA 130b (miR-130b-3p) in regulating PGC-1α expression and oxidative stress in a placental trophoblastic cell line (BeWo). Prolonged exposure of BeWo cells to high glucose mimicking hyperglycemia resulted in decreased protein abundance of PGC-1α and its downstream factor, mitochondrial transcription factor A (TFAM). High glucose treatment increased the expression of miR-130b-3p in BeWo cells, as well as exosomal secretion of miR-130b-3p. Transfection of BeWo cells with miR-130b-3p mimic reduced the abundance of PGC-1α, whereas inhibition of miR-130b-3p increased PGC-1α expression in response to high glucose, suggesting a role for miR-130b-3p in mediating high glucose-induced down regulation of PGC-1α expression. In addition, miR-130b-3p anti-sense inhibitor increased TFAM expression and reduced 4-hydroxynonenal (4-HNE)-induced production of reactive oxygen species (ROS). Taken together, these findings reveal that miR-130b-3p down-regulates PGC-1α expression in placental trophoblasts, and inhibition of miR-130b-3p appears to improve mitochondrial biogenesis signaling and protect placental trophoblast cells from oxidative stress.

Indexed as

Organelle BiogenesisDNA-Binding ProteinsHumansMicroRNAsMitochondriaMitochondrial ProteinsOxidative StressPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaReactive Oxygen SpeciesTranscription FactorsTumor Cells, CulturedDNA-Binding ProteinsMicroRNAsMIRN130 microRNA, humanMitochondrial Proteinsmitochondrial transcription factor APeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPARGC1A protein, humanReactive Oxygen SpeciesTranscription FactorsHyperglycemiamiR-130bOxidative stressPGC-1αPlacental trophoblast

Identifiers

PMID28433632
PMCPMC5522006
OpenAlexW2606557661

What OpenQuestion holds

Textmetadata
LicenceTDM
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.