Cited by 3MicroRNA in disease regulationIntracranial Aneurysms: Treatment and ComplicationsIntracerebral and Subarachnoid Hemorrhage Research

Downregulation of miR-23a-3p improves cognitive function in rats after subarachnoid hemorrhage by targeting VCAN

Xue, Cheng, Wang, Rong, Jia, Yu·2022·Medical Molecular Morphology

Abstract

Subarachnoid hemorrhage (SAH) is a complicated and deadly disorder. Dysregulation of miRNAs in SAH has been widely reported. This investigation elucidated the function of miR-23a-3p in the in vivo and in vitro models of SAH. The miR-23a-3p and VCAN levels in SAH rats and sham controls were detected by RT-qPCR. The SAH rats were intracerebrally administrated with miR-23a-3p antagomir. Morphological changes and brain function were assessed. The isolated brain microvascular endothelial cells (BMECs), identified by immunofluorescence staining, were used as the model of SAH in vitro. The viability and apoptosis of BMECs were evaluated using MTT, flow cytometry, and western blotting analyses. Targeted relationship between miR-23a-3p and VCAN was predicted in miRDB and validated by a luciferase reporter assay. We found that the miR-23a-3p level was upregulated in rats after SAH, while VCAN was downregulated. Silencing miR-23a-3p attenuated neurological deficits and neuronal apoptosis in rats after SAH. VCAN was verified to be targeted by miR-23a-3p. Functionally, miR-23a-3p downregulation or VCAN overexpression inhibited BMEC apoptosis and promoted cell activity. Moreover, knockdown of VCAN eliminated the influence of miR-23a-3p inhibition in BMECs. Overall, suppression of miR-23a-3p improves cognitive function after SAH by targeting VCAN.

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Crossref · 10.1007/s00795-022-00315-y

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  • Up-regulated expression of miR-23a-3p has been identified in blood samples of acute cerebral hemorrhage patients and in a rat model of subarachnoid hemorrhage, leading to augmented apoptosis of cerebral vascular endothelial cells by suppressing ZO-1, and formation of cerebral hematoma.

    “Up-regulated expression of miR-23a-3p has been identified both in the blood samples of acute cerebral hemorrhage patients and in a rat model of subarachnoid hemorrhage, leading to augmented apoptosis of cerebral vascular endothelial cells by suppressing the expression of the target gene ZO-1, as well as the formation of cerebral hematoma.”
  • Suppression of miR-23a-3p can inhibit apoptosis of cerebral microvascular endothelial cells by targeting VCAN, and promote cell activity and improve cognitive function after subarachnoid hemorrhage in rats.

    “Meanwhile, the suppression of miR-23a-3p can inhibit the apoptosis of cerebral microvascular endothelial cells by targeting VCAN, and thereafter promote cell activity and improve cognitive function after subarachnoid hemorrhage in rats [64,65].”

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Authors
Xue, C., Wang, R., & Jia, Y.
Corresponding author
Xue, Cheng
Venue
Medical Molecular Morphology
Published
2022-02-08
Volume
55
Issue
2
Pages
146-157
ISSN
  • 0918-4287 (ISSN-L)
  • 1860-1480
  • 1860-1499
OpenAlex
W4210947668
Cited by
3
References
1
Citations by year
2024: 3
FWCI
0.32
Type
journal article
Language
en
Open access
closed
Locations
  • Medical Molecular Morphology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
  • Health Sciences › Medicine › Neurology › Intracranial Aneurysms: Treatment and Complications
  • Health Sciences › Medicine › Neurology › Intracerebral and Subarachnoid Hemorrhage Research
Keywords
subarachnoid hemorrhage, miR-23a-3p, versican, microRNA, cognitive function, neuronal apoptosis, brain microvascular endothelial cells, antagomir, neuroprotection, microRNA target regulation
MeSH terms
Animals, Cognition, Subarachnoid Hemorrhage, Down-Regulation, MicroRNAs, Endothelial Cells, Rats

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