Evidence map›Paper›PMID 27819307›Full record

ArticleScientific reports2016

Hyperglycaemia-induced reciprocal changes in miR-30c and PAI-1 expression in platelets.

Mao Luo, Rong Li, Meiping Ren, Ni Chen, Xin Deng, Xiaoyong Tan, Yongjie Li, Min Zeng, Yan Yang, Qin Wan and 1 more

Abstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
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

16 citing papers in PubMed.

  1. Review
  2. Intravenous miR-30c therapy confers dual neurovascular protection and improves long-term recovery after ischemic stroke.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Emerging Role of MicroRNA-30c in Neurological Disorders.International journal of molecular sciences · 2022
    Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
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

11 authors.

Mao LuoDrug Discovery Research Center, Southwest Medical University, Luzhou, Sichuan, China.
Rong LiDrug Discovery Research Center, Southwest Medical University, Luzhou, Sichuan, China.
Meiping RenDrug Discovery Research Center, Southwest Medical University, Luzhou, Sichuan, China.
Ni ChenDrug Discovery Research Center, Southwest Medical University, Luzhou, Sichuan, China.
Xin DengDrug Discovery Research Center, Southwest Medical University, Luzhou, Sichuan, China.
Xiaoyong TanDrug Discovery Research Center, Southwest Medical University, Luzhou, Sichuan, China.
Yongjie LiDrug Discovery Research Center, Southwest Medical University, Luzhou, Sichuan, China.
Min ZengDrug Discovery Research Center, Southwest Medical University, Luzhou, Sichuan, China.
Yan YangDalton Cardiovascular Research Center, University of Missouri, Columbia, MO, USA.
Qin WanDepartment of Endocrinology, the First Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, China.
Jianbo WuDrug Discovery Research Center, Southwest Medical University, Luzhou, Sichuan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 2 diabetic mellitus (DM2) is associated with accelerated thrombotic complications and is characterized by high levels of plasminogen activator inhibitor-1 (PAI-1). Recent studies show that human platelets have high levels of miR-30c and synthesize considerable active PAI-1. The underlying mechanism of how PAI-1 expression is upregulated in DM2 is poorly understood. We now report that hyperglycaemia-induced repression of miR-30c increases PAI-1 expression and thrombus formation in DM2. Bioinformatic analysis and identification of miRNA targets were assessed using luciferase assays, quantitative real-time PCR and western blots in vitro and in vivo. The changes in miR-30c and PAI-1 levels were identified in platelets from healthy and diabetic individuals. We found that miR-30c directly targeted the 3' UTR of PAI-1 and negatively regulated its expression. miR-30c was negatively correlated with glucose and HbA1c levels in DM2. In HFD-fed diabetic mice, increasing miR-30c expression by lenti-miR-30c significantly decreased the PAI-1 expression and prolonged the time to occlusion in an arterial thrombosis model. Platelet depletion/reinfusion experiments generating mice with selective ablation of PAI-1 demonstrate a major contribution by platelet-derived PAI-1 in the treatment of lenti-miR-30c to thrombus formation. These results provide important implications regarding the regulation of fibrinolysis by platelet miRNA under diabetic mellitus.

Indexed as

AnimalsBlood PlateletsCells, CulturedDiabetes Mellitus, Type 2HumansHyperglycemiaMaleMice, Inbred C57BLMicroRNAsPlasminogen Activator Inhibitor 1MicroRNAsMIRN30b microRNA, humanPlasminogen Activator Inhibitor 1SERPINE1 protein, human

Identifiers

PMID27819307
PMCPMC5098184

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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.