Evidence map›Paper›PMID 36335301›Full record

ArticleBMC neuroscience2022

Cholesterol efflux regulator ABCA1 exerts protective role against high shear stress-induced injury of HBMECs via regulating PI3K/Akt/eNOS signaling.

Zhe Li, Jia-Nan Li, Qiang Li, Chun Liu, Lin-Hua Zhou, Qi Zhang, Yi Xu

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

Article in BMC neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.7field-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

3 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
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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

7 authors at 3 institutions in 1 country.

Zhe Li *Neurovascular Center, Changhai Hospital, Naval Medical University, No. 168 Changhai Rd, Shanghai, 200433, China.
Jia-Nan Li *Department of Neurosurgery, General Hospital of Northern Theater Command, 83 Wenhua Road, Shenyang, Liaoning Province, China.
Qiang LiNeurovascular Center, Changhai Hospital, Naval Medical University, No. 168 Changhai Rd, Shanghai, 200433, China.
Chun LiuDepartment of Cerebrovascular Diseases, Blue Cross Brain Hospital Affiliated to Tongji University, No. 2880 Qixin Road, Shanghai, 201101, China.
Lin-Hua ZhouDepartment of Cerebrovascular Diseases, Blue Cross Brain Hospital Affiliated to Tongji University, No. 2880 Qixin Road, Shanghai, 201101, China.
Qi ZhangDepartment of Cerebrovascular Diseases, Blue Cross Brain Hospital Affiliated to Tongji University, No. 2880 Qixin Road, Shanghai, 201101, China. zhqiciao@126.com.
Yi XuNeurovascular Center, Changhai Hospital, Naval Medical University, No. 168 Changhai Rd, Shanghai, 200433, China. xuyichyy@163.com.
Second Military Medical University · CNTongji University · CNGeneral Hospital of Shenyang Military Region · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn brain, microvascular endothelial cells are exposed to various forces, including shear stress (SS). However, little is known about the effects of high shear stress (HSS) on human brain microvascular endothelial cells (HBMECs) and the underlying mechanism. The cholesterol efflux regulator ATP-binding cassette subfamily A member 1 (ABCA1) has been demonstrated to exert protective effect on HBMECs. However, whether ABCA1 is involved in the mechanism underneath the effect of HSS on HBMECs remains obscure. In the present study, a series of experiments were performed to better understand the effect of HSS on cellular processes of HBMECs and the possible involvement of ABCA1 and PI3K/Akt/eNOS in the underlying mechanisms.

resultsHBMECs were subjected to physiological SS (PSS) or high SS (HSS). Cell migration was evaluated using Transwell assay. Apoptotic HBMECs were detected by flow cytometry or caspase3/7 activity. IL-1β, IL-6, MCP-1 and TNF-α levels were measured by ELISA. RT-qPCR and western blotting were used for mRNA and protein expression detection, respectively. ROS and NO levels were detected using specific detection kits. Compared to PSS, HBMECs exhibited decreased cell viability and migration and increased cell apoptosis, increased levels of inflammatory cytokines, and improved ROS and NO productions after HSS treatment. Moreover, HSS downregulated ABCA1 but upregulated the cholesterol efflux-related proteins MMP9, AQP4, and CYP46 and activated PI3K/Akt/eNOS pathway. Overexpression of ABCA1 in HBMECS inhibited PI3K/Akt/eNOS pathway and counteracted the deleterious effects of HSS. Contrary effects were observed by ABCA1 silencing. Inhibiting PI3K/Akt/eNOS pathway mimicked ABCA1 effects, suggesting that ABCA1 protects HBMECs from HSS via PI3K/Akt/eNOS signaling.

conclusionThese results advanced our understanding on the mechanisms of HSS on HBMECs and potentiated ABCA1/PI3K/Akt/eNOS pathway as therapeutic target for cerebrovascular diseases.

Indexed as

Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktATP Binding Cassette Transporter 1BrainCholesterolEndothelial CellsHumansNitric Oxide Synthase Type IIIReactive Oxygen SpeciesABCA1 protein, humanATP Binding Cassette Transporter 1CholesterolNitric Oxide Synthase Type IIIPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReactive Oxygen SpeciesABCA1AtherosclerosisCholesterol effluxHigh shear stressHuman brain microvascular endothelial cellsPI3K/Akt/eNOS pathway

Identifiers

PMID36335301
PMCPMC9636808
OpenAlexW4308302470

What OpenQuestion holds

Textmetadata
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.