The Expression and Regulatory Role of lncRNA CRNDE in Ischemic Stroke

Abstract Background Ischemic stroke (IS) is a disease caused by the occlusion of cerebral arteries with lack of oxygen and blood supply and is characterized by high morbidity and mortality. The role of lncRNA CRNDE in IS remains unclear. Objective This study focused on investigating the function of...

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Main Authors: Yuan Cheng, Qiujun Lu, Yuanyuan Su, Runxi Xu, Shuqi Huang, Chong Yang, Yunhua Hao, Jun Yang
Format: Article
Language:English
Published: BMC 2025-04-01
Series:Artery Research
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Online Access:https://doi.org/10.1007/s44200-025-00079-7
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author Yuan Cheng
Qiujun Lu
Yuanyuan Su
Runxi Xu
Shuqi Huang
Chong Yang
Yunhua Hao
Jun Yang
author_facet Yuan Cheng
Qiujun Lu
Yuanyuan Su
Runxi Xu
Shuqi Huang
Chong Yang
Yunhua Hao
Jun Yang
author_sort Yuan Cheng
collection DOAJ
description Abstract Background Ischemic stroke (IS) is a disease caused by the occlusion of cerebral arteries with lack of oxygen and blood supply and is characterized by high morbidity and mortality. The role of lncRNA CRNDE in IS remains unclear. Objective This study focused on investigating the function of lncRNA CRNDE in IS. Materials and Methods 237 participants were enrolled in this study, including 135 patients with ischemic stroke (Ischemic stroke group) and 102 healthy individuals (Control group). The human brain microvascular endothelial cells (BMECs) treated with oxygen–glucose deprivation (OGD) were used to establish an IS cell model in vitro. The qRT-PCR was used to analyze the expression level of lncRNA CRNDE, miR-451, and MIF. The cell proliferation ability and migration were detected by CCK-8 and Transwell assay, respectively, while cell apoptosis was determined by apoptosis assay kit and flow cytometry. Additionally, the target relationship of CRNDE/miR-451 and miR-451/MIF was verified by dual-luciferase system. Results LncRNA CRNDE exhibited an up-regulated expression in IS patients and the IS cell model. Down-regulated lncRNA CRNDE not only contributed to cell proliferation ability and migration but also inhibited cell apoptosis. The miR-451 was a potential target of lncRNA CRNDE. The increased MIF was covalently bound to miR-451 and MIF reduction caused by CRNDE silence was significantly rescued by the inhibition of miR-451. Conclusion Up-regulated lncRNA CRNDE exacerbated IS by regulating proliferation, migration, and apoptosis in IS cell model. MiR-451/MIF was a potential downstream target of lncRNA CRNDE.
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spelling doaj-art-7f9335a3b3b248c6a168ddb313f20b6f2025-08-20T01:47:33ZengBMCArtery Research1876-44012025-04-013111910.1007/s44200-025-00079-7The Expression and Regulatory Role of lncRNA CRNDE in Ischemic StrokeYuan Cheng0Qiujun Lu1Yuanyuan Su2Runxi Xu3Shuqi Huang4Chong Yang5Yunhua Hao6Jun Yang7Geriatric Department 2, Chengdu Dekang HospitalDepartment of Rehabilitation, Xuzhou Central HospitalDepartment of Neurology, Tianyou Hospital, Tongji UniversityDepartment of Neurology, Tianyou Hospital, Tongji UniversityDepartment of Neurology, Tianyou Hospital, Tongji UniversityDepartment of Neurology, Tianyou Hospital, Tongji UniversityDepartment of Neurology, Tianyou Hospital, Tongji UniversityDepartment of Neurosurgery, The No.2 People’s Hospital of LanzhouAbstract Background Ischemic stroke (IS) is a disease caused by the occlusion of cerebral arteries with lack of oxygen and blood supply and is characterized by high morbidity and mortality. The role of lncRNA CRNDE in IS remains unclear. Objective This study focused on investigating the function of lncRNA CRNDE in IS. Materials and Methods 237 participants were enrolled in this study, including 135 patients with ischemic stroke (Ischemic stroke group) and 102 healthy individuals (Control group). The human brain microvascular endothelial cells (BMECs) treated with oxygen–glucose deprivation (OGD) were used to establish an IS cell model in vitro. The qRT-PCR was used to analyze the expression level of lncRNA CRNDE, miR-451, and MIF. The cell proliferation ability and migration were detected by CCK-8 and Transwell assay, respectively, while cell apoptosis was determined by apoptosis assay kit and flow cytometry. Additionally, the target relationship of CRNDE/miR-451 and miR-451/MIF was verified by dual-luciferase system. Results LncRNA CRNDE exhibited an up-regulated expression in IS patients and the IS cell model. Down-regulated lncRNA CRNDE not only contributed to cell proliferation ability and migration but also inhibited cell apoptosis. The miR-451 was a potential target of lncRNA CRNDE. The increased MIF was covalently bound to miR-451 and MIF reduction caused by CRNDE silence was significantly rescued by the inhibition of miR-451. Conclusion Up-regulated lncRNA CRNDE exacerbated IS by regulating proliferation, migration, and apoptosis in IS cell model. MiR-451/MIF was a potential downstream target of lncRNA CRNDE.https://doi.org/10.1007/s44200-025-00079-7CRNDEIschemic strokemiR-451
spellingShingle Yuan Cheng
Qiujun Lu
Yuanyuan Su
Runxi Xu
Shuqi Huang
Chong Yang
Yunhua Hao
Jun Yang
The Expression and Regulatory Role of lncRNA CRNDE in Ischemic Stroke
Artery Research
CRNDE
Ischemic stroke
miR-451
title The Expression and Regulatory Role of lncRNA CRNDE in Ischemic Stroke
title_full The Expression and Regulatory Role of lncRNA CRNDE in Ischemic Stroke
title_fullStr The Expression and Regulatory Role of lncRNA CRNDE in Ischemic Stroke
title_full_unstemmed The Expression and Regulatory Role of lncRNA CRNDE in Ischemic Stroke
title_short The Expression and Regulatory Role of lncRNA CRNDE in Ischemic Stroke
title_sort expression and regulatory role of lncrna crnde in ischemic stroke
topic CRNDE
Ischemic stroke
miR-451
url https://doi.org/10.1007/s44200-025-00079-7
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