Evidence map›Paper›PMID 33393160›Full record

ArticleJournal of cellular and molecular medicine2021

Long non-coding RNA MEG3 silencing and microRNA-214 restoration elevate osteoprotegerin expression to ameliorate osteoporosis by limiting TXNIP.

ChangSheng Yang, ZhengTao Gu, Rui Ding, CaiQiang Huang, QingChu Li, DengHui Xie, RongKai Zhang, YiYan Qiu

RetractedOpen access · goldAbstract readRetracted Publication
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

9 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Review
  3. Retraction.Journal of cellular and molecular medicine · 2023
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4 · The record

Corrections and comments

  • Retraction · 2022-11-02Investigation by Third Party · Paper Mill · Unreliable Results and/or Conclusions · · see also: https://pubpeer.com/publications/C44A9E642C3C6AB6F15AD8C46FD7DE
  • Retracted
5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

ChangSheng YangDivision of Spine Surgery, Section II, Department of Orthopedics, The Third Affiliated Hospital of Southern Medical University, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Southern Medical University, Academy of Orthopedics of Guangdong Province, Guangzhou, China.
ZhengTao GuDepartment of Treatment Center For Traumatic Injuries, The Third Affifiliated Hospital of Southern Medical University, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Southern Medical University, Academy of Orthopedics of Guangdong Province, Guangzhou, China.
Rui DingDivision of Spine Surgery, Section II, Department of Orthopedics, The Third Affiliated Hospital of Southern Medical University, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Southern Medical University, Academy of Orthopedics of Guangdong Province, Guangzhou, China.
CaiQiang HuangDivision of Spine Surgery, Section II, Department of Orthopedics, The Third Affiliated Hospital of Southern Medical University, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Southern Medical University, Academy of Orthopedics of Guangdong Province, Guangzhou, China.
QingChu LiDivision of Joint Surgery, Department of Orthopedics, The Third Affiliated Hospital of Southern Medical University, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Southern Medical University, Academy of Orthopedics of Guangdong Province, Guangzhou, China.
DengHui XieDivision of Spine Surgery, Section II, Department of Orthopedics, The Third Affiliated Hospital of Southern Medical University, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Southern Medical University, Academy of Orthopedics of Guangdong Province, Guangzhou, China.
RongKai ZhangDivision of Spine Surgery, Section II, Department of Orthopedics, The Third Affiliated Hospital of Southern Medical University, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Southern Medical University, Academy of Orthopedics of Guangdong Province, Guangzhou, China.
YiYan QiuDivision of Spine Surgery, Section II, Department of Orthopedics, The Third Affiliated Hospital of Southern Medical University, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Southern Medical University, Academy of Orthopedics of Guangdong Province, Guangzhou, China.ORCID 0000-0002-4697-1932
Third Affiliated Hospital of Southern Medical University · CN

Funding

National Science Foundation for young Scientists of China 8180090642
6 · The paper itself

Abstract

Studies have shown that long non-coding RNA (lncRNA) MEG3 plays a key role in osteoporosis (OP), but its regulatory mechanism is somewhat incompletely clear. Here, we intend to probe into the mechanism of MEG3 on OP development by modulating microRNA-214 (miR-214) and thioredoxin-interacting protein (TXNIP). Rat models of OP were established. MEG3, miR-214 and TXNIP mRNA expression in rat femoral tissues were detected, along with TXNIP, OPG and RANKL protein expression. BMD, BV/TV, Tb.N and Tb.Th in tissue samples were measured. Ca, P and ALP contents in rat serum were also determined. Primary osteoblasts were isolated and cultured. Viability, COL-I, COL-II and COL-Χ mRNA expression, PCNA, cyclin D1, OCN, RUNX2 and osteolix protein expresion, ALP content and activity, and mineralized nodule area of rat osteoblasts were further detected. Dual-luciferase reporter gene and RNA-pull down assays verified the targeting relationship between MEG3, miR-214 and TXNIP. MEG3 and TXNIP were up-regulated while miR-214 was down-regulated in femoral tissues of OP rats. MEG3 silencing and miR-214 overexpression increased BMD, BV/TV, Tb.N, Tb.Th, trabecular bone area, collagen area and OPG expression, and down-regulated RANKL of femoral tissues in OP rats. MEG3 silencing and miR-214 overexpression elevated Ca and P and reduced ALP in OP rat serum, elevated osteoblast viability, differentiation ability, COL-I and COL-Χ expression and ALP activity, and reduced COL-II expression of osteoblasts. MEG3 specifically bound to miR-214 to regulate TXNIP. MEG3 silencing and miR-214 overexpression promote proliferation and differentiation of osteoblasts in OP by down-regulating TXNIP, which further improves OP.

Indexed as

Gene Silencing3' Untranslated RegionsAnimalsBiomarkersCell Cycle ProteinsCell DifferentiationDisease SusceptibilityFemaleGene Expression RegulationMicroRNAsModels, BiologicalOsteoblastsOsteoporosisOsteoprotegerinRatsRNA Interference3' Untranslated RegionsBiomarkersCell Cycle ProteinsMEG3 non-coding RNA, ratMicroRNAsMirn214 microRNA, ratOsteoprotegerinRNA, Long NoncodingTXNIP protein, ratdifferentiationlong non-coding RNA maternally expressed gene 3microRNA-214osteoblastsosteoporosisosteoprotegerinproliferationthioredoxin-interacting protein

Identifiers

PMID33393160
PMCPMC7882928
OpenAlexW3117387860

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.