Evidence map›Paper›PMID 36411684›Full record

ArticleZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences2022

UBIAD1 protects against oxygen-glucose deprivation/reoxygenation injury via nNOS/NO pathway.

Haiping Zheng, Ranran Tu, Chunli Chen, Zhiping Hu

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Article in Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
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0citing papers in PubMed
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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

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0 citing papers in PubMed, 0 citations in OpenAlex.

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4 · The record

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5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Haiping ZhengDepartment of Neurology, Second Xiangya Hospital, Central South University, Changsha 410011, China. 507410@csu.edu.cn.
Ranran TuDepartment of Neurology, Second Xiangya Hospital, Central South University, Changsha 410011, China.
Chunli ChenDepartment of Neurology, Second Xiangya Hospital, Central South University, Changsha 410011, China.
Zhiping HuDepartment of Neurology, Second Xiangya Hospital, Central South University, Changsha 410011, China. zhipinghu@csu.edu.cn.
Central South University · CN

Funding

the National Natural Science Foundation 8197052473
6 · The paper itself

Abstract

objectivesCerebral infarction is a subtype of stroke with high incidence and disability rate. Ischemia reperfusion injury (IRI) is the key point of cerebral infarction treatment. UbiA prenyltransferase domain containing 1 (UBIAD1) is a kind of enzyme with various biological functions including electron transport in mitochondrial respiratory chain, lipid metabolism, and oxidative stress which are related to IRI. The purpose of this study aims to determine the neuroprotective effects and the underlying mechanisms of UBIAD1 in cerebral IRI.

methodsWe employed oxygen-glucose deprivation/reoxygenation (OGD/R) model in mouse neuroblastoma Neuro2a (N2a) cells to mimic cerebral IRI. Lentivirus vector over-expressed UBIAD1 was transfacted into N2a cells to maintain high and stable expression of UBIAD1. In the first part of the experiment, N2a cells were divided into 5 groups: A non-OGD (N2a cells without exposure to OGD) group, groups of reoxygenation 0, 4, 12 and 24 h after 4 h of OGD, respectively. In the second part of the experiment, N2a cells were divided into 6 groups: A Con (normal cell)+non-OGD group, an EV (cell transfected with empty vector)+non-OGD group, an OE (over-expressed UBIAD1)+non-OGD group, a Con+OGD/R group, an EV+OGD/R group, and an OE+OGD/R group. In the third part, the N2a cells were divided into 8 groups: A Con+non-OGD group, an OE+non-OGD group, a Con+non-OGD+nNOS inhibitior 7-nitroindazole (7-NI) group, an OE+non-OGD+7-NI group, a Con+OGD/R group, an OE+OGD/R group, a Con+OGD/R+7-NI group, and an OE+OGD/R+7-NI group. The morphological changes of Golgi apparatus were observed under the confocal laser scanning microscope. The mRNA and protein levels of

resultsCompared with the non-OGD group, the expression levels of

conclusionsUBIAD1 may exerts protective effects on OGD/R induced N2a cells by ameliorating Golgi apparatus dysfunction via the nNOS/NO pathway.

Indexed as

DimethylallyltranstransferaseOxygenAnimalsCell SurvivalCerebral InfarctionGlucoseLipid MetabolismMiceNitric OxideNitric Oxide Synthase Type IDimethylallyltranstransferaseGlucoseNitric OxideNitric Oxide Synthase Type INos1 protein, mouseOxygenUbiad1 protein, mouseGolgi apparatusischemia reperfusion injuryneuronal NOS/NO pathwayoxygen-glucose deprivation/reoxygenationsecretory pathway Ca 2+-ATPase isoform 1UbiA prenyltransferase domain containing 1

Identifiers

PMID36411684
PMCPMC10930366
OpenAlexW4309659304

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