Evidence map›Paper›PMID 33733597›Full record

ArticleJournal of cellular and molecular medicine2021

Post-menopausal oestrogen deficiency induces osteoblast apoptosis via regulating HOTAIR/miRNA-138 signalling and suppressing TIMP1 expression.

Shao-Yong Xu, Peng Shi, Rui-Ming Zhou

Open access · goldAbstract read
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. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

18 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. The effects of extracorporeal shockwave therapy on the lumbar spine of osteoporotic rat models.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2026
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  10. Noncoding RNAs: the crucial role of programmed cell death in osteoporosis.Frontiers in cell and developmental biology · 2024
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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

3 authors at 3 institutions in 1 country.

Shao-Yong XuDivision of Orthopedics and Traumatology, Department of Orthopedics, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Peng ShiDepartment of Spine Orthopedics, Liuzhou Traditional Chinese Medical Hospital, Liuzhou, China.
Rui-Ming ZhouDepartment of Orthopedics, The Second People Hospital of NanSha, Guangzhou, China.ORCID 0000-0001-9504-4855
Liuzhou Maternal and Child Health Hospital · CNNanfang Hospital · CNSecond Affiliated Hospital of Guangzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In this study, we aimed to explore the molecular mechanisms underlying the development of osteoporosis in post-menopausal females. Real-time PCR was conducted to measure the expression of potential lncRNAs involved in the osteoporosis of post-menopausal females. In addition, Western blot and IHC assays were used to study the possible correlation among HOTAIR, miR-138 and TIMP1, while a computational analysis was carried out to predict the 'seed sequence' responsible for the binding between miR-138 and HOTAIR/TIMP1. Furthermore, luciferase reporter assays were conducted to validate the negative regulatory relationship between miR-138 and TIMP1/HOTAIR. To evaluate the effect of oestrogen on the function of HOATIR and its downstream effectors, luciferase activity was measured in cells cotransfected with different vectors or treated with different doses of oestrogen. The results of the luciferase assay were further validated by real-time PCR, Western blot, MTT assay and flow cytometry. Among the candidate lncRNAs, HOTAIR was the only lncRNA down-regulated in post-menopausal females. HOTAIR bound to miR-138 and negatively regulated its expression. Meanwhile, miR-138 could also bind to TIMP1 mRNA and reduce its expression. Furthermore, a dose-dependent up-regulation of HOTAIR was observed in cells treated with oestrogen, and the elevated HOTAIR increased the level of TIMP1 by targeting miR-138. In addition, oestrogen promoted cell viability and suppressed cell apoptosis, and effects of oestrogen were blocked by the silencing of HOTAIR. Therefore, it can be concluded that oestrogen deficiency could induce the apoptosis of osteoblasts and lead to osteoporosis in post-menopausal females via modulation of the HOTAIR/miR-138/TIMP1 signalling axis.

Indexed as

PostmenopauseAdultApoptosisBiomarkersCell ProliferationCells, CulturedEstrogensFemaleGene Expression RegulationHumansMicroRNAsMiddle AgedOsteoblastsPremenopauseRNA, Long NoncodingTissue Inhibitor of Metalloproteinase-1BiomarkersEstrogensHOTAIR long untranslated RNA, humanMicroRNAsMIRN138 microRNA, humanRNA, Long NoncodingTIMP1 protein, humanTissue Inhibitor of Metalloproteinase-1HOTAIRmenopausemiR-138oestrogenosteoporosisTIMP1

Identifiers

PMID33733597
PMCPMC8107111
OpenAlexW3136686835

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.