Research articles
ScienceAsia 50 (2024):ID 2024095 1-11 |doi:
10.2306/scienceasia1513-1874.2024.095
miR-218-5p regulates the phenotypic transformation of
vascular smooth muscle cells in rat intracranial aneurysms by
targeting HMGB1
Jie Penga, JieQiong Lib,*
ABSTRACT: To explore the potential biological effects of miR-218-5p targeting high-mobility group protein B1
(HMGB1) mediating the phenotypic transformation of vascular smooth muscle cells (VSMCs) in intracranial aneurysm
(IA) rats, an IA rat model was established, and the lentivirus vector miR-218-5p agomir or shRNA-HMBG1 was given to
IA rats. The elastic fibers of the aneurysm were analyzed by Victoria Blue staining. Real-time PCR analyzed miR-218-
5p, HMGB1, and phenotypic markers (?-SMA, SM-22?, MMP2, OPN). Western blot analysis of HMGB1, SM-22?, and
OPN was also performed. miR-218-5p mimics and/or HMBG1 overexpression vectors were transfected into VSMCs.
The effects of miR-218-5p on cell proliferation and migration were detected by EdU method and scratch method.
Dual luciferase reporter gene assay verified the targeting relationship between miR-218-5p and HMGB1. The fibers of
IA rats were broken, the elastic fibers were reduced, miR-218-5p was down-regulated, and HMGB1 was up-regulated.
Treatment with miR-218-5p agomir and sh-HMGB1 protected tissue elastic fiber breakage induced by IA, upregulated ?SMA and SM-22?, and down-regulated HMGB1, OPN, and MMP2. Elevating miR-218-5p inhibited VSMC proliferation
and migration, increased SM-22?, and decreased OPN expression. Upregulating HMGB1 had the opposite effect. The
upregulation of HMGB1 expression counteracts the inhibitory impact of miR-218-5p overexpression on the proliferative,
migratory, and phenotypic transformation capacities of VSMCs. By downregulating HMGB1, miR-218-5p mediates
the phenotypic transformation of VSMCs in IA rats, providing a certain research basis for further research on clinical
prevention and treatment of IA.
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| a |
Department of Neurosurgery, The First Hospital of Changsha (The Affiliated Changsha Hospital of Xiangya School
of Medicine, Central South University), Changsha, Hunan 410005 China |
| b |
Department of Pediatrics, The First Hospital of Changsha (The Affiliated Changsha Hospital of Xiangya School of
Medicine, Central South University), Changsha, Hunan 410005 China |
* Corresponding author, E-mail: lijieqiong0812@hotmail.com
Received 21 Sep 2023, Accepted 27 May 2024
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