Evidence map›Paper›PMID 28415790›Full record

ArticleOncotarget2017

Hyperglycemia via activation of thromboxane A2 receptor impairs the integrity and function of blood-brain barrier in microvascular endothelial cells.

Zhihong Zhao, Jue Hu, Xiaoping Gao, Hui Liang, Haiya Yu, Suosi Liu, Zhan Liu

RetractedOpen access · diamondAbstract readRetracted Publication
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.9field-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

14 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
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  4. Effects of fasudil on blood-brain barrier integrity.Fluids and barriers of the CNS · 2022
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  11. Observational
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Zhihong ZhaoDepartment of Neurology, The First Affiliated Hospital (People's Hospital of Hunan Province), Hunan Normal University, Changsha, Hunan, China.
Jue HuDepartment of Neurology, Changsha Central Hospital, Changsha, Hunan, China.
Xiaoping GaoDepartment of Neurology, The First Affiliated Hospital (People's Hospital of Hunan Province), Hunan Normal University, Changsha, Hunan, China.
Hui LiangDepartment of Neurology, The First Affiliated Hospital (People's Hospital of Hunan Province), Hunan Normal University, Changsha, Hunan, China.
Haiya YuDepartment of Neurology, The People's Hospital of Xishui, Huangang, Hubei, China.
Suosi LiuDepartment of Neurology, The First Affiliated Hospital (People's Hospital of Hunan Province), Hunan Normal University, Changsha, Hunan, China.
Zhan LiuDepartment of Clinical Nutrition and Gastroenterology, The First Affiliated Hospital (People's Hospital of Hunan Province), Hunan Normal University, Changsha, Hunan, China.
Hunan Normal University · CNChangsha Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes is one of high risk factors for cardio- and cerebra-vascular diseases, including stroke, atherosclerosis and hypertension. This study was conducted to elucidate whether and how thromboxane receptor (TPr) activation contributes to blood-brain barrier (BBB) dysfunction in diabetes. Human brain microvascular endothelial cells (HBMECs) were cultured. The levels of phosphorylated endothelial nitric oxide synthase (eNOS) at Ser1177 (p-eNOS) and Akt at Ser473 (p-Akt) were assayed by western blot. Exposure of HBMECs to either high glucose (HG) or thromboxane A2 (TxA2) mimetic U46619, significantly reduced p-eNOS and p-Akt. These effects were abolished by pharmacological or genetic inhibitors of TPr. HG/U46619-induced suppressions of eNOS and Akt phosphorylation were accompanied by upregulation of PTEN and Ser380/Thr382/383 PTEN phosphorylation. PTEN-specific siRNA restored Akt-eNOS signaling in the face of TPr activation or HG. The small GTPase, Rho, was also activated by HG stimulation, and pretreatment of HBMECs with Y27632, a Rho-associated kinase (ROCK) inhibitor, rescued HG-impaired Akt-eNOS signaling. In STZ-injected rats, we found that hyperglycemia dramatically increased the levels of PTEN and PTEN-Ser380/Thr382/383 phosphorylation, reduced both levels of p-eNOS and p-Akt, and disrupted BBB function assayed by Evans blue staining, which were abolished by SQ29548 treatment. We conclude that hyperglycemia activates thromboxane A2 receptor to impair the integrity and function of blood-brain barrier via the ROCK-PTEN-Akt-eNOS pathway.

Indexed as

AnimalsBlood-Brain BarrierBlood GlucoseCapillary PermeabilityEndothelial CellsHumansHyperglycemiaMaleNitric Oxide Synthase Type IIIPhosphorylationProto-Oncogene Proteins c-aktRatsReceptors, Thromboxane A2, Prostaglandin H2rhoA GTP-Binding Proteinrho-Associated KinasesSignal TransductionBlood GlucoseNitric Oxide Synthase Type IIIProto-Oncogene Proteins c-aktReceptors, Thromboxane A2, Prostaglandin H2rhoA GTP-Binding Proteinrho-Associated Kinasesblood-brain barrierdiabetesthromboxane A2 receptor

Identifiers

PMID28415790
PMCPMC5444723
OpenAlexW2595170317

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.