Folia Neuropathologica

Abstract

1/2023 vol. 61
Original paper

Loss of lncRNA UCA1 ameliorates the injury managed by cerebral ischemia-reperfusion by sponging miR-18a-5p

Jingyi Yan 1
,
Yang Gao 2
,
Jianyuan Huang 3
,
Wei Gao 4
,
Yang Li 5
,
Baishun Lin 6
  1. Juquan New Town Community Health Service Center, Gucun Town, Baoshan District, Shanghai 201907, China
  2. Department of Neurosurgery, Binzhou Medical University Hospital, Binzhou, Shandong 256603, China
  3. General Surgery (thyroid Gland/blood Vessel), The First People’s Hospital of Neijiang, Neijiang, 641099, Sichuan, China
  4. Department of Anesthesia and Perioperative Medicine, Dongying Hospital of Traditional Chinese Medicine, Dongying, Shandong 257055, China
  5. Department of Neurology, Zibo No. 4 People’s Hospital, Zibo, Shandong 255022, China
  6. Department of Emergency, The First Affiliated Hospital of Nanhua University, Hengyang, Hunan 421001, China
Folia Neuropathol 2023; 61 (1): 77-87
DOI: https://doi.org/10.5114/fn.2022.122497
Online publish date: 2023/01/09
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Introduction:

Acute ischemic stroke (AIS) is a disease with high morbidity and mortality in the clinic. The current experiments aimed to study the effects of UCA1 interfering miR-18a-5p on cerebral ischemia-reperfusion (CI/R).

Material and methods:

For rat models undergoing middle cerebral artery infarction (MCAO) surgery, the expression of UCA1 and miR-18a-5p was evaluated by qRT-PCR, and underlying function was identified by detecting infarct size, neurological scores, and inflammation. Luciferase report was applied to verify the relationship between UCA1 and miR-18a-5p. In the cell models, the impacts of UCA1 and miR-18a-5p were validated by CCK-8 assay, flow cytometry analysis, and ELISA. In patients with AIS, Pearson correlation was carried out to unveil the association between UCA1 and miR-18a-5p.

Results:

The expression of UCA1 was at high levels and miR-18a-5p was at low levels in AIS patients. UCA1 knockdown showed a protective role in infarct size, neurofunction, and inflammation via binding miR-18a-5p. MiR-18a-5p participated in the regulation of UCA1 on cell viability, cell apoptosis, lactate dehydrogenase (LDH) levels, and inflammation. In patients with AIS, overexpression of UCA1 and underexpression of miR-18a-5p had a reverse correlation.

Conclusions:

Elimination of UCA1 was favourable to the recovery of the rat model and cells from CI/R damage by efficaciously sponging miR-18a-5p.

Keywords

UCA1, cerebral ischemia-reperfusion, inflammation, neurofunction, miR-18a-5p

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