Evidence map›Paper›PMID 30930751›Full record

ArticleFrontiers in cellular neuroscience2019

Homer1a Attenuates Endoplasmic Reticulum Stress-Induced Mitochondrial Stress After Ischemic Reperfusion Injury by Inhibiting the PERK Pathway.

Jialiang Wei, Xiuquan Wu, Peng Luo, Kangyi Yue, Yang Yu, Jingnan Pu, Lei Zhang, Shuhui Dai, Donghui Han, Zhou Fei

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in cellular neuroscience, 2019. 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
2.0field-weighted citation impact, top 15% 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, 42 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

10 authors at 2 institutions in 1 country.

Jialiang WeiDepartment of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Xiuquan WuDepartment of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Peng LuoDepartment of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Kangyi YueDepartment of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Yang YuDepartment of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Jingnan PuDepartment of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Lei ZhangDepartment of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Shuhui DaiDepartment of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Donghui HanDepartment of Urology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Zhou FeiDepartment of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Xijing Hospital · CNAir Force Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Homer1a is the short form of a scaffold protein that plays a protective role in many forms of stress. However, the role of Homer1a in cerebral ischemia/reperfusion (I/R) injury and its potential mechanism is still unknown. In this study, we found that Homer1a was upregulated by oxygen and glucose deprivation (OGD) and that overexpression of Homer1a alleviated OGD-induced lactate dehydrogenase (LDH) release and cell death in cultured cortical neurons. After OGD treatment, the overexpression of Homer1a preserved mitochondrial function, as evidenced by less cytochrome c release, less reactive oxygen species (ROS) production, less ATP and mitochondrial membrane potential (MMP) loss, less caspase-9 activation, and inhibition of endoplasmic reticulum (ER) stress confirmed by the decreased expression of phosphate-PKR-like ER Kinase (p-PERK)/PERK and phosphate- inositol-requiring enzyme 1 (p-IRE1)/IRE1 and immunofluorescence (IF) staining. In addition, mitochondrial protection of Homer1a was blocked by the ER stress activator Tunicamycin (TM) with a re-escalated ROS level, increasing ATP and MMP loss. Furthermore, Homer1a overexpression-induced mitochondrial stress attenuation was significantly reversed by activating the PERK pathway with TM and p-IRE1 inhibitor 3,5-dibromosalicylaldehyde (DBSA), as evidenced by increased cytochrome c release, increased ATP loss and a higher ROS level. However, activating the IRE1 pathway with TM and p-PERK inhibitor GSK2656157 showed little change in cytochrome c release and exhibited a moderate upgrade of ATP loss and ROS production in neurons. In summary, these findings demonstrated that Homer1a protects against OGD-induced injury by preserving mitochondrial function through inhibiting the PERK pathway. Our finding may reveal a promising target of protecting neurons from cerebral I/R injury.

Indexed as

endoplasmic reticulum stresshomer1aischemic strokemitochondrial dysfunctionPERK kinase

Identifiers

PMID30930751
PMCPMC6428733
OpenAlexW2921005501

What OpenQuestion holds

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LicenceCC BY
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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.