Evidence map›Paper›PMID 24933421›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2014

17β-Estradiol inhibits ER stress-induced apoptosis through promotion of TFII-I-dependent Grp78 induction in osteoblasts.

Yun-Shan Guo, Zhen Sun, Jie Ma, Wei Cui, Bo Gao, Hong-Yang Zhang, Yue-Hu Han, Hui-Min Hu, Long Wang, Jing Fan and 3 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

23 citing papers in PubMed, 34 citations in OpenAlex.

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  18. RasGRF Couples Nox4-Dependent Endoplasmic Reticulum Signaling to Ras.Arteriosclerosis, thrombosis, and vascular biology · 2017
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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

13 authors at 2 institutions in 1 country.

Yun-Shan Guo1] Department of Orthopedics, Xijing Hospital, Fourth Military Medical University, Xi'an, China [2] Cell Engineering Research Centre, Fourth Military Medical University, Xi'an, China.
Zhen SunDepartment of Orthopedics, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Jie MaDepartment of Neurosurgery, Tangdu Hospital, Fourth Military Medical University, Xi'an, China.
Wei CuiDepartment of Endocrinology and Metabolism, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Bo GaoDepartment of Orthopedics, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Hong-Yang ZhangDepartment of Orthopedics, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Yue-Hu HanDepartment of Orthopedics, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Hui-Min HuDepartment of Orthopedics, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Long WangDepartment of Orthopedics, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Jing FanDepartment of Orthopedics, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Liu YangDepartment of Orthopedics, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Juan TangCell Engineering Research Centre, Fourth Military Medical University, Xi'an, China.
Zhuo-Jing LuoDepartment of Orthopedics, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Air Force Medical University · CNXijing Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although many studies have suggested that estrogen prevents postmenopausal bone loss partially due to its anti-apoptosis effects in osteoblasts, the underlying mechanism has not been fully elucidated. In the present study, we found that 17β-estradiol (17β-E₂), one of the primary estrogens, inhibited endoplasmic reticulum (ER) stress-induced apoptosis in MC3T3-E1 cells and primary osteoblasts. Interestingly, 17β-E₂-promoted Grp78 induction, but not CHOP induction in response to ER stress. We further confirmed that Grp78-specific siRNA reversed the inhibition of 17β-E₂ on ER stress-induced apoptosis by activating caspase-12 and caspase-3. Moreover, we found that 17β-E₂ markedly increased the phosphorylated TFII-I levels and nuclear localization of TFII-I in ER stress conditions. 17β-E₂ stimulated Grp78 promoter activity in a dose-dependent manner in the presence of TFII-I and enhanced the binding of TFII-I to the Grp78 promoter. In addition, 17β-E₂ notably increased phosphorylated ERK1/2 levels and Ras kinase activity in MC3T3-E1 cells. The ERK1/2 activity-specific inhibitor U0126 remarkably blocked 17β-E₂-induced TFII-I phosphorylation and Grp78 expression in response to ER stress. Together, 17β-E₂ protected MC3T3-E1 cells against ER stress-induced apoptosis by promoting Ras-ERK1/2-TFII-I signaling pathway-dependent Grp78 induction.

Indexed as

AnimalsAnimals, NewbornApoptosisBone Density Conservation AgentsCell LineCells, CulturedEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressEstradiolEstrogensHeat-Shock ProteinsHumansMiceMice, Inbred C57BLOsteoblastsOsteoporosisBone Density Conservation AgentsEndoplasmic Reticulum Chaperone BiPEstradiolEstrogensHeat-Shock ProteinsHSPA5 protein, humanHspa5 protein, mouseRecombinant ProteinsTranscription Factor TFIIA

Identifiers

PMID24933421
OpenAlexW2082904092

What OpenQuestion holds

Textmetadata
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.