Evidence map›Paper›PMID 32580515›Full record

ArticleMolecules (Basel, Switzerland)2020

Methylpiperidinopyrazole Attenuates Estrogen-Induced Mitochondrial Energy Production and Subsequent Osteoblast Maturation via an Estrogen Receptor Alpha-Dependent Mechanism.

Poh-Shiow Yeh, Jui-Tai Chen, Yih-Giun Cherng, Shun-Tai Yang, Yu-Ting Tai, Ruei-Ming Chen

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.8field-weighted citation impact, top 31% 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

11 citing papers in PubMed, 17 citations in OpenAlex.

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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 4 institutions in 1 country.

Poh-Shiow YehDepartment of Neurology, Chi Mei Medical Center, Tainan 710, Taiwan.
Jui-Tai ChenDepartment of Anesthesiology, School of Medicine, College of Medicine, Taipei Medical University, Taipei 110, Taiwan.ORCID 0000-0002-4018-7303
Yih-Giun CherngDepartment of Anesthesiology, School of Medicine, College of Medicine, Taipei Medical University, Taipei 110, Taiwan.
Shun-Tai YangDepartment of Neurosurgery, School of Medicine, College of Medicine, Taipei Medical University, Taipei 110, Taiwan.ORCID 0000-0002-7094-9452
Yu-Ting TaiDepartment of Anesthesiology, School of Medicine, College of Medicine, Taipei Medical University, Taipei 110, Taiwan.
Ruei-Ming ChenGraduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei 110, Taiwan.ORCID 0000-0002-5728-0571
Taipei Medical University-Shuang Ho Hospital · TWWan Fang Hospital · TWChi Mei Medical Center · TWTaipei Medical University · TW

Funding

Chi Mei Medical Center 106CM-TMU-16-2
6 · The paper itself

Abstract

An estrogen deficiency is the main cause of osteoporosis in postmenopausal women. In bone remodeling, estrogen receptors (ERs) can mediate estrogen-transducing signals. Methylpiperidinopyrazole (MPP) is a highly specific antagonist of ER-alpha (ERα). This study was designed to evaluate the effects of MPP on estrogen-induced energy production, subsequent osteoblast maturation, and the possible mechanisms. Exposure of primary osteoblasts isolated from neonatal rat calvarias to MPP did not affect cell morphology or survival. Estradiol can induce translocation of ERα into mitochondria from the cytoplasm. Interestingly, pretreatment of rat calvarial osteoblasts with MPP lowered estrogen-induced ERα translocation. Sequentially, estrogen-triggered expressions of mitochondrial energy production-linked cytochrome c oxidase (COX) I and COX II messenger (m)RNAs were inhibited following pretreatment with MPP. Consequently, MPP caused decreases in estrogen-triggered augmentation of the activities of mitochondrial respiratory complex enzymes and levels of cellular adenosine phosphate (ATP). During progression of osteoblast maturation, estrogen induced bone morphogenetic protein (BMP)-6 and type I collagen mRNA expressions, but MPP treatment inhibited such induction. Consequently, estrogen-induced osteoblast activation and mineralization were attenuated after exposure to MPP. Taken together, MPP suppressed estrogen-induced osteoblast maturation through decreasing chromosomal osteogenesis-related BMP-6 and type I collagen mRNA expressions and mitochondrial ATP synthesis due to inhibiting energy production-linked COX I and II mRNA expressions. MPP can appropriately be applied to evaluate estrogen-involved bioenergetics and osteoblast maturation.

Indexed as

AnimalsBone Morphogenetic Protein 6Cell DifferentiationElectron Transport Complex IVEstrogen Receptor alphaEstrogen Receptor betaEstrogensFemaleGene Expression RegulationMitochondriaOsteoblastsOsteocalcinOsteogenesisOsteoporosisPyrazolesRatsBone Morphogenetic Protein 6Electron Transport Complex IVEstrogen Receptor alphaEstrogen Receptor betaEstrogensOsteocalcinpyrazolePyrazolesenergy productionestrogenmethylpiperidinopyrazoleosteoblast maturationosteogenesis

Identifiers

PMID32580515
PMCPMC7356510
OpenAlexW3036441457

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.