Evidence map›Paper›PMID 32258168›Full record

ArticleJournal of diabetes research2020

miR-210 in Exosomes Derived from Macrophages under High Glucose Promotes Mouse Diabetic Obesity Pathogenesis by Suppressing NDUFA4 Expression.

Feng Tian, Ping Tang, Zhilian Sun, Ruifen Zhang, Danhua Zhu, Junying He, Jixing Liao, Qinghua Wan, Jie Shen

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of diabetes research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 5% 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

62 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.

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2 more citing papers are in PubMed but not listed here.

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

9 authors at 2 institutions in 1 country.

Feng TianDepartment of Endocrinology and Metabolism, The Third Affiliated Hospital of Shenzhen University, Shenzhen, Guangdong, China.
Ping TangDepartment of Endocrinology and Metabolism, The Third Affiliated Hospital of Shenzhen University, Shenzhen, Guangdong, China.
Zhilian SunDepartment of Endocrinology and Metabolism, The Third Affiliated Hospital of Shenzhen University, Shenzhen, Guangdong, China.
Ruifen ZhangDepartment of Endocrinology and Metabolism, The Third Affiliated Hospital of Shenzhen University, Shenzhen, Guangdong, China.
Danhua ZhuDepartment of Endocrinology and Metabolism, The Third Affiliated Hospital of Shenzhen University, Shenzhen, Guangdong, China.
Junying HeDepartment of Endocrinology and Metabolism, The Third Affiliated Hospital of Shenzhen University, Shenzhen, Guangdong, China.
Jixing LiaoDepartment of Endocrinology and Metabolism, The Third Affiliated Hospital of Shenzhen University, Shenzhen, Guangdong, China.
Qinghua WanDepartment of Endocrinology and Metabolism, The Third Affiliated Hospital of Shenzhen University, Shenzhen, Guangdong, China.
Jie ShenDepartment of Endocrinology and Metabolism, The Third Affiliated Hospital of Southern Medical University, Guangzhou, Guangdong, China.ORCID https://orcid.org/0000-0001-7236-2068
Shenzhen University · CNThird Affiliated Hospital of Southern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveType 2 diabetes mellitus (T2DM) is featured by insulin resistance and lipid metabolism dysregulation. A large number of miRNAs were identified in exosomes derived from adipose tissue macrophages associated with T2DM pathogenesis, but its pathogenic roles remain unknown. This study is aimed at investigating the function of miR-210 in diabetic obesity.

methodsExosomes from mouse macrophage RAW264.7 cells were characterized by electron microscopy, combined with biomarker expression by western blot. Expression of miR-210 was determined by quantitative RT-PCR. Glucose uptake was measured by a fluorometric method, and the mitochondrial respiratory chain activity was evaluated by ELISA. The target gene of miR-210 was validated by dual-luciferase reporter and pull-down assays. A mouse obese diabetic model was established by a high-fat diet and streptozocin treatment.

resultsmiR-210 was highly expressed in exosomes derived from high glucose-induced macrophage RAW264.7 cells. Macrophage-derived exosomes impaired glucose uptake and mitochondrial CIV complex activity and suppressed NADH dehydrogenase ubiquinone 1 alpha subcomplex 4 (NDUFA4) expression in 3T3-L1 adipocytes. miR-210 directly bind with mRNA sequences of NDUFA4 gene. Inhibition of miR-210 mitigated the effects of macrophage-derived exosomes on the glucose uptake and complex IV (CIV) activity in 3T3-L1 adipocytes, and NDUFA4 overexpression offset the inhibition of glucose uptake and CIV activity by macrophage-derived exosomes. Furthermore, mice with miR-210 knockout showed greatly repressed diabetic obesity development.

conclusionmiR-210 derived from adipose tissue macrophages promotes mouse obese diabetes pathogenesis by regulating glucose uptake and mitochondrial CIV activity through targeting NDUFA4 gene expression.

Indexed as

3T3-L1 CellsAdipose TissueAnimalsDiabetes Mellitus, Type 2Electron Transport Complex IVExosomesGlucoseMacrophagesMiceMicroRNAsObesityRAW 264.7 CellsElectron Transport Complex IVGlucoseMicroRNAsMIRN210 microRNA, mouse

Identifiers

PMID32258168
PMCPMC7106924
OpenAlexW3012079695

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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.