Evidence map›Paper›PMID 29663377›Full record

ArticleJournal of cellular physiology2018

UBIAD1 protects against oxygen-glucose deprivation/reperfusion-induced multiple subcellular organelles injury through PI3K/AKT pathway in N2A cells.

Yan Huang, Zhiping Hu

Abstract read
In one paragraph

Article in Journal of cellular physiology, 2018. 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
1.7field-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

11 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. UBIAD1 protects against oxygen-glucose deprivation/reoxygenation injury via nNOS/NO pathway.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2022
    Article
  3. Article
  4. Functional study of SCCD pathogenic geneMolecular medicine reports · 2021
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
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

2 authors at 1 institution in 1 country.

Yan HuangDepartment of Neurology, Second Xiangya Hospital, Central South University, Changsha, China.
Zhiping HuDepartment of Neurology, Second Xiangya Hospital, Central South University, Changsha, China.ORCID http://orcid.org/0000-0001-5194-2653
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cerebral ischemia/reperfusion-induced injury plays a significant role in the development of multi-subcellular organelles injury after ischemic stroke. UBIAD1 was discovered originally as a potential tumor suppressor protein. Recently, analysis of UBIAD1 has indicated it is a prenyltransferase enzyme for both non-mitochondrial CoQ10 and vitamin K2 production. Further, UBIAD1 has been localized to multiple subcellular organelles. Particularly, UBIAD1 plays an important role in the regulation of oxidative stress, apoptosis and cell proliferation, cholesterol and lipid metabolism, which was closely associated with the cerebral ischemic/reperfusion mechanism. However, the mechanism underlying effects of UBIAD1 on cerebral ischemia/reperfusion-induced injury remains largely unknown. We aimed to investigate the effects of UBIAD1 on ischemia/reperfusion-induced multiple subcellular organelles injury in vitro, mouse N2A cells were subjected to a classical oxygen-glucose deprivation and reperfusion (OGD/R) insult. The expression of UBIAD1 was reduced in mouse N2A cells after OGD/R. UBIAD1 exhibits multi-subcellular organelles co-localization in N2a cells, including in the mitochondria, endoplasmic reticulum, and Golgi apparatus. The over-expression of UBIAD1 significantly protects against OGD/R-induced cell death. UBIAD1 over-expression also attenuated OGD/R-induced mitochondrial fragmentation and dysfunction and mediated the level of apoptosis-associated protein. Moreover, we observed that the over-expression of UBIAD1 ameliorated OGD/R-induced fragmentation and reduced the level of oxidative stress-related protein expression in both the endoplasmic reticulum and Golgi apparatus. Besides, the neuroprotective effect of UBIAD1 was correlated with the PI3K/AKT pathway, which was demonstrated using the PI3K inhibitor LY294002 and perifosion. Collectively, these findings identified that UBIAD1 protects against OGD/R-induced multiple subcellular organelles injury through PI3K/AKT Pathway.

Indexed as

Adenosine TriphosphateAnimalsAntioxidantsApoptosisCell Line, TumorDimethylallyltranstransferaseEndoplasmic ReticulumEndoplasmic Reticulum StressGlucoseGolgi ApparatusMembrane Potential, MitochondrialMiceMitochondriaOrganellesOxidative StressOxygenAdenosine TriphosphateAntioxidantsDimethylallyltranstransferaseGlucoseOxygenPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReactive Oxygen SpeciesRNA, MessengerUbiad1 protein, mouseneuroprotectionOGD/RPI3K/AKTsubcellular organelleUBIAD1

Identifiers

PMID29663377
PMCPMC13482144
OpenAlexW2800774142

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.