Evidence map›Paper›PMID 30402207›Full record

ArticleOxidative medicine and cellular longevity2018

miR-26a Potentially Contributes to the Regulation of Fatty Acid and Sterol Metabolism In Vitro Human HepG2 Cell Model of Nonalcoholic Fatty Liver Disease.

Omaima Ali, Hebatallah A Darwish, Kamal M Eldeib, Samy A Abdel Azim

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

29 citing papers in PubMed, 46 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

4 authors at 3 institutions in 2 countries.

Omaima AliMedicinal Chemistry and Molecular Pharmacology (MCMP), College of Pharmacy, Purdue University, West Lafayette, IN 47907, USA.
Hebatallah A DarwishDepartment of Biochemistry, Faculty of Pharmacy, Cairo University, Cairo 11562, Egypt.
Kamal M EldeibNational Organization of Drug Control and Research (NODCAR), Cairo 12553, Egypt.
Samy A Abdel AzimDepartment of Biochemistry, Faculty of Pharmacy, Cairo University, Cairo 11562, Egypt.ORCID 0000-0002-3371-139X
Cairo University · EGNational Organization for Drug Control and Research · EGPurdue University West Lafayette · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nonalcoholic fatty liver disease (NAFLD) is a metabolic-related disorder ranging from steatosis to steatohepatitis, which may progress to cirrhosis and hepatocellular carcinoma (HCC). This study aimed at assessing the regulatory and protective role of miR-26a on lipid metabolism and progression of NAFLD in human HepG2 cells loaded with free fatty acids (FFA). Lentivirus expressing miR-26a or negative control miR was used to transduce HepG2 cells and to establish stable cell lines. Gain or loss of function using an miR-26a inhibitor was used to compare triglyceride content (TG), total cholesterol level (CL), total antioxidant capacity (TAC), malondialdehyde (MDA) and the level of apoptosis. In addition, quantitative reverse transcription polymerase chain reaction (qPCR) was used to assess the mRNA levels of lipogenesis, TG synthesis, storage genes, inflammatory and fibrogenic markers, and autophagic besides endoplasmic reticulum (ER) stress markers after gaining or losing the function of miR-26a. miR-26a levels decreased in response to FFA in human HepG2 cells. After the establishment of a stable cell line, the upregulation of miR-26a resulted in the downregulation of TG, CL, and MDA levels, through regulating mRNA levels of genes involved in lipid homeostasis, ER stress marker, inflammatory and fibrogenic markers. Nevertheless, there was a marked increment in the mRNA expression of autophagic marker genes. Moreover, miR-26a overexpression protects the cells from apoptosis, whereas inhibition of miR-26a, using an anti-miR-26a oligonucleotide, decreased the expression of miR-26a which potentially contributes to altered lipid metabolism in HepG2 cells loaded with FFA. In conclusion, these findings suggested that miR-26a has a crucial role in regulating fatty acid and cholesterol homeostasis in HepG2 cells, along with the offered protection against the progression of NAFLD

Indexed as

Models, BiologicalApoptosisAutophagyCholesterolEndoplasmic Reticulum StressFatty AcidsGene Expression RegulationHep G2 CellsHumansLipid MetabolismMalondialdehydeMicroRNAsNon-alcoholic Fatty Liver DiseaseOxidative StressProtein Kinase C-deltaRNA, MessengerCholesterolFatty AcidsMalondialdehydeMicroRNAsMIRN26 microRNA, humanProtein Kinase C-deltaRNA, MessengerSterolsTriglycerides

Identifiers

PMID30402207
PMCPMC6196797
OpenAlexW2893025311

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.