Evidence map›Paper›PMID 31410089›Full record

ArticleCellular & molecular biology letters2019

MiR-135-5p promotes osteoblast differentiation by targeting HIF1AN in MC3T3-E1 cells.

Nuo Yin, Longzhang Zhu, Liang Ding, Junjie Yuan, Li Du, Mingmang Pan, Feng Xue, Haijun Xiao

Open access · goldAbstract read
In one paragraph

Article in Cellular & molecular biology letters, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
5.7field-weighted citation impact, top 2% 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

72 citing papers in PubMed, 149 citations in OpenAlex.

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  15. TP508 Promotes Bone Regeneration on Distraction OsteogenesisCurrent pharmaceutical biotechnology · 2025
    Article
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12 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

8 authors at 1 institution in 1 country.

Nuo Yin *Department of Orthopaedics, Shanghai Fengxian District Central Hospital, No. 6600, Nanfeng Highway, Shanghai, 201499 China.
Longzhang Zhu *Department of Orthopaedics, Shanghai Fengxian District Central Hospital, No. 6600, Nanfeng Highway, Shanghai, 201499 China.
Liang DingDepartment of Orthopaedics, Shanghai Fengxian District Central Hospital, No. 6600, Nanfeng Highway, Shanghai, 201499 China.
Junjie YuanDepartment of Orthopaedics, Shanghai Fengxian District Central Hospital, No. 6600, Nanfeng Highway, Shanghai, 201499 China.
Li DuDepartment of Orthopaedics, Shanghai Fengxian District Central Hospital, No. 6600, Nanfeng Highway, Shanghai, 201499 China.
Mingmang PanDepartment of Orthopaedics, Shanghai Fengxian District Central Hospital, No. 6600, Nanfeng Highway, Shanghai, 201499 China.
Feng XueDepartment of Orthopaedics, Shanghai Fengxian District Central Hospital, No. 6600, Nanfeng Highway, Shanghai, 201499 China.
Haijun XiaoDepartment of Orthopaedics, Shanghai Fengxian District Central Hospital, No. 6600, Nanfeng Highway, Shanghai, 201499 China.
Xian Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMicroRNAs (miRNAs or miRs) serve crucial roles in the progression of osteoporosis. This study investigated the role and specific molecular mechanism of miR-135-5p in regulating osteoblast differentiation and calcification.

methodsBone morphogenetic protein 2 (BMP2) was employed to interfere with the differentiation of MC3T3-E1. Then, miR-135-5p mimic or miR-135-5p inhibitor was transfected into MC3T3-E1, and quantitative RT-PCR was used to measure the expression of miR-135-5p. The expressions of runt-related transcription factor 2 (Runx2), osterix (OSX), osteopontin (OPN), and osteocalcin (OCN) were determined using western blot. Alkaline phosphatase (ALP) activity was measured using an appropriate kit assay. Calcium nodule staining was evaluated with alizarin red staining. A luciferase reporter assay was used to verify the target of miR-135-5p. Hypoxia-inducible factor 1 α inhibitor (HIF1AN) overexpression was applied to investigate its own role in the mechanism and a miR-135-5p rescue experiment was also performed.

resultsOverexpression of miR-135-5p promoted osteogenic differentiation and calcification, as shown by the increase in ALP activity, calcification and osteogenic marker levels, including Runx2, OSX, OPN and OCN. Knockdown of miR-135-5p yielded the opposite results. HIF1AN was confirmed as a direct target of miR-135-5p. HIF1AN overexpression inhibited osteogenic differentiation and calcification while miR-135-5p reversed these effects.

conclusionsThese results indicate that miR-135-5p might have a therapeutic application related to its promotion of bone formation through the targeting of HIF1AN.

Indexed as

OsteogenesisAnimalsCell DifferentiationCell LineGene Expression Regulation, DevelopmentalMiceMicroRNAsMixed Function OxygenasesOsteoblastsUp-Regulationfactor inhibiting hypoxia-inducible factor 1, mouseMicroRNAsMirn135 microRNA, mouseMixed Function OxygenasesCalcificationHypoxia-inducible factor 1 α inhibitormiR-135Osteoblast differentiation

Identifiers

PMID31410089
PMCPMC6686269
OpenAlexW2968952977

What OpenQuestion holds

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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.