Evidence map›Paper›PMID 25400823›Full record

ArticleInternational journal of clinical and experimental pathology2014

MiR-378 overexpression attenuates high glucose-suppressed osteogenic differentiation through targeting CASP3 and activating PI3K/Akt signaling pathway.

Li You, Wensha Gu, Lin Chen, Ling Pan, Jinyu Chen, Yongde Peng

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

Article in International journal of clinical and experimental pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

52 citing papers in PubMed, 78 citations in OpenAlex.

  1. Review
  2. Article
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  5. Exosomes and microRNAs as mediators of the exercise.European journal of medical research · 2025
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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

6 authors at 1 institution in 1 country.

Li YouDepartment of Endocrinology and Metabolism, Shanghai First People's Hospital, Shanghai Jiao Tong University School of Medicine 100 Haining Road, Shanghai 200080, China.
Wensha GuDepartment of Endocrinology and Metabolism, Shanghai First People's Hospital, Shanghai Jiao Tong University School of Medicine 100 Haining Road, Shanghai 200080, China.
Lin ChenDepartment of Endocrinology and Metabolism, Shanghai First People's Hospital, Shanghai Jiao Tong University School of Medicine 100 Haining Road, Shanghai 200080, China.
Ling PanDepartment of Endocrinology and Metabolism, Shanghai First People's Hospital, Shanghai Jiao Tong University School of Medicine 100 Haining Road, Shanghai 200080, China.
Jinyu ChenDepartment of Endocrinology and Metabolism, Shanghai First People's Hospital, Shanghai Jiao Tong University School of Medicine 100 Haining Road, Shanghai 200080, China.
Yongde PengDepartment of Endocrinology and Metabolism, Shanghai First People's Hospital, Shanghai Jiao Tong University School of Medicine 100 Haining Road, Shanghai 200080, China.
Shanghai First People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hyperglycemia is one of the possible causes for osteoporosis and bone fracture in diabetes mellitus. Here we modeled diabetes-induced osteoporosis in vitro using preosteoblastic cell line MC3T3-E1 and a diabetic mice model for in vivo studies. We found that in addition to reducing osteoblast viability and differentiation (mineralization), culture in elevated glucose down regulated microRNA-378 (miR-378) expression but ectopic miR-378 expression reversed the effects of high glucose. We identified caspase-3 (CASP3) as a target of miR-378 and showed that miR-378 repressed CASP3 mRNA and protein expression under high glucose condition. We further showed that both miR-378 expression and CASP3 silencing independently restored alkaline phosphatase (ALP) activity and the expression of osteoblastic differentiation markers Runt-related transcription factor 2 (Runx2), osteorix (Osx), collagen I (Col I), osteocalcin (OCN), and osteonectin (ON). We also found that under high glucose conditions miR-378 activated the PI3K/Akt signaling pathway and down regulated pro-apoptotic CytC, Apaf-1 and Bax proteins via the PI3K/Akt pathway. Collectively, these results suggest that miR-378 overexpression attenuates high glucose-suppressed osteogenic differentiation through targeting CASP3 and activating the PI3K/Akt pathway.

Indexed as

Cell DifferentiationOsteogenesisSignal Transduction3T3 CellsAlkaline PhosphataseAnimalsApoptosisCalcification, PhysiologicCaspase 3Cell SurvivalCollagen Type ICore Binding Factor Alpha 1 SubunitDiabetes Mellitus, ExperimentalGlucoseMaleMiceAlkaline PhosphataseCasp3 protein, mouseCaspase 3Collagen Type ICore Binding Factor Alpha 1 SubunitGlucoseMicroRNAsMIRN378 microRNA, mouseOsteocalcinPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktRunx2 protein, mouseSp7 protein, mouseSp7 Transcription FactorTranscription FactorsCASP3high glucoseMiR-378osteogenic differentiationPI3K/Akt signaling

Identifiers

PMID25400823
PMCPMC4230144
OpenAlexW267009310

What OpenQuestion holds

Textmetadata
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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.