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Updated: Aug 23, 2026

A Low Mortality Rat Model to Assess Delayed Cerebral Vasospasm After Experimental Subarachnoid Hemorrhage
Published on: January 17, 2013
microRNA-130b May Induce Cerebral Vasospasm after Subarachnoid Hemorrhage via Modulating Kruppel-like Factor 4
Zewei Huang1, Jiliang Hu2,3, Jiongfu Xu2
1Department of Critical Care Medicine, Shenzhen People's Hospital (The Second Clinical Medical College, Jinan University; The First Affiliated Hospital, Southern University of Science and Technology), Shenzhen, P. R. China.
Abstract:
Recently, the diverse functions of microRNAs (miRNAs) in brain diseases have been demonstrated. We intended to uncover the functional role of microRNA-130b (miR-130b) in cerebral vasospasm (CVS) following subarachnoid hemorrhage (SAH). SAH was induced by injecting the autologous blood into the cisterna magna of Sprague Dawley rats. The cerebral vascular smooth muscle cells (cVSMCs) were extracted for in vitro experimentation. In vitro and in vivo assays were implemented with transfection of miR-130b mimic/inhibitor, sh-Kruppel-like factor 4 (KLF4), oe-KLF4 plasmids or p38/MAPK signaling pathway agonist (anisomycin), respectively, to elaborate the role of miR-130b in CVS following SAH. Elevated miR-130b and reduced KLF4 were found in SAH patients and rat models of SAH. KLF4 was the target gene of miR-130b. miR-130b promoted the proliferation and migration of cVSMCs through the Inhibition of KLF4. Besides, KLF4 inhibited the proliferation and migration of cVSMCs through blockage of the p38/MAPK pathway. Furthermore, in vivo assay confirmed the inhibitory effect of decreased miR-130b in CVS following SAH. In conclusion, miR-130b may activate the p38/MAPK signaling pathway through targeted inhibition of KLF4, thereby contributing to some extent to the development of cerebral vasospasm after SAH.
Insights
MicroRNA-130b (miR-130b) promotes cerebral vasospasm after subarachnoid hemorrhage by inhibiting KLF4 and activating the p38/MAPK pathway. Decreasing miR-130b shows potential therapeutic benefits for this condition.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- MicroRNAs (miRNAs) play diverse roles in brain diseases.
- Cerebral vasospasm (CVS) is a serious complication following subarachnoid hemorrhage (SAH).
- The specific role of microRNA-130b (miR-130b) in CVS post-SAH requires elucidation.
Purpose of the Study:
- To investigate the functional role of miR-130b in the development of cerebral vasospasm following subarachnoid hemorrhage.
- To explore the underlying molecular mechanisms involving KLF4 and the p38/MAPK signaling pathway.
Main Methods:
- SAH models were established in Sprague Dawley rats.
- Cerebral vascular smooth muscle cells (cVSMCs) were utilized for in vitro studies.
- Transfection with miR-130b mimic/inhibitor, KLF4-targeting vectors, and p38/MAPK pathway modulators were employed.
Main Results:
- Elevated miR-130b and reduced KLF4 expression were observed in SAH patients and rat models.
- miR-130b directly targets and inhibits KLF4, promoting cVSMC proliferation and migration.
- KLF4 suppresses cVSMC proliferation and migration by blocking the p38/MAPK pathway.
- In vivo studies confirmed that reduced miR-130b inhibits CVS post-SAH.
Conclusions:
- miR-130b contributes to cerebral vasospasm post-SAH by targeting KLF4 and activating the p38/MAPK pathway.
- Targeting miR-130b may represent a potential therapeutic strategy for managing CVS after SAH.
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