Evidence map›Paper›PMID 30024097›Full record

ArticleJournal of cellular and molecular medicine2018

BMSCs and miR-124a ameliorated diabetic nephropathy via inhibiting notch signalling pathway.

Jiping Sun, Fei Zhao, Wenjing Zhang, Jia Lv, Jing Lv, Aiping Yin

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

Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

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  17. METTL3-mediated mMolecular therapy : the journal of the American Society of Gene Therapy · 2022
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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.

Jiping SunDepartment of Nephrology, the First Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an, China.
Fei ZhaoDepartment of Obstetrics and Gynecology, the First Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an, China.
Wenjing ZhangDepartment of Nephrology, the First Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an, China.
Jia LvDepartment of Nephrology, the First Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an, China.
Jing LvDepartment of Nephrology, the First Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an, China.
Aiping YinDepartment of Nephrology, the First Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an, China.ORCID 0000-0003-0175-6806
First Affiliated Hospital of Xi'an Jiaotong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BMSCs are important in replacement therapy of diabetic nephropathy (DN). MiR-124a exerts effect on the differentiation capability of pancreatic progenitor cells. The objective of this study was to explore the molecular mechanisms, the functions of miR-124a and bone marrow mesenchymal stem cells (BMSCs) in the treatment of DN. Characterizations of BMSCs were identified using the inverted microscope and flow cytometer. The differentiations of BMSCs were analysed by immunofluorescence assay and DTZ staining. The expression levels of islet cell-specific transcription factors, apoptosis-related genes, podocytes-related genes and Notch signalling components were detected using quantitative real-time reverse transcription PCR (qRT-PCR) and Western blot assays. The production of insulin secretion was detected by adopting radioimmunoassay. Cell proliferation and apoptosis abilities were detected by CCK-8, flow cytometry and TUNEL assays. We found that BMSCs was induced into islet-like cells and that miR-124a could promote the BMSCs to differentiate into islet-like cells. BMSCs in combination with miR-124a regulated islet cell-specific transcription factors, apoptosis-related genes, podocytes-related genes as well as the activity of Notch signalling pathway. However, BMSCs in combination with miR-124a relieved renal lesion caused by DN and decreased podocyte apoptosis caused by HG. The protective effect of BMSCs in combination with miR-124a was closely related to the inactivation of Notch signalling pathway. MSCs in combination with miR-124a protected kidney tissue from impairment and inhibited nephrocyte apoptosis in DN.

Indexed as

Acute Kidney InjuryAnimalsApoptosisCell ProliferationDiabetic NephropathiesDisease Models, AnimalFlow CytometryGene Expression RegulationHumansInsulinMesenchymal Stem CellsMesenchymal Stem Cell TransplantationMicroRNAsPodocytesRatsReceptors, NotchInsulinMicroRNAsMIRN124 microRNA, ratReceptors, NotchTranscription Factorsapoptosisdiabetic nephropathykidney injurymiR-124aNotchpodocyte

Identifiers

PMID30024097
PMCPMC6156290
OpenAlexW2883250287

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.