Journal
MOLECULAR NEUROBIOLOGY
Volume 59, Issue 5, Pages 2808-2821Publisher
SPRINGER
DOI: 10.1007/s12035-021-02632-2
Keywords
Ischemic stroke; Long non-coding RNA rhabdomyosarcoma 2 related transcript; MicroRNA-221-3p; Phosphoinositide-3-kinase regulatory subunit 1; Transforming growth factor signaling; Neurological function
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Funding
- Scientific Research Fund of the Second Affiliated Hospital of Harbin Medical University [Kybs2015-02]
- Funds for postdoctoral research in Heilongjiang Province [2017-078]
- Heilongjiang Health and Family Planning Commission Research Project [2017-078]
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This study investigated the role of long non-coding RNA RMST in ischemic stroke through the miR-221-3p/PIK3R1/TGF-beta axis in MCAO mice. The results showed that elevated RMST and PIK3R1, downregulated miR-221-3p, and activated TGF-beta pathway were associated with MCAO, and restoring miR-221-3p or depleting RMST improved neurological functions and pathological damage. Additionally, depleting PIK3R1 or restoring miR-221-3p could counteract the negative effects of RMST overexpression in MCAO mice.
Much efforts have been made to probe the mechanism underlying ischemic stroke (IS). This study was proposed to uncover the role of long non-coding RNA rhabdomyosarcoma 2 related transcript (RMST) in IS through microRNA-221-3p (miR-221-3p)/phosphoinositide-3-kinase regulatory subunit 1 (PIK3R1)/transforming growth factor-beta (TGF-beta) axis. Neurological behavioral function, pathological changes in brain tissue, oxidative stress, and inflammation responses in middle cerebral artery occlusion (MCAO) mice were tested. RMST, miR-221-3p, PIK3R1, and TGF-beta signaling-related protein expression in brain tissues of MCAO mice were detected. RMST and PIK3R1 were elevated, miR-221-3p was downregulated, and TGF-beta pathway was activated in mice after MCAO. Restored miR-221-3p or depleted RMST improved neurological behavioral functions, relieved pathological injury in brain tissue, and repressed oxidative stress and inflammation in mice after MCAO. Depleted PIK3R1 or restored miR-221-3p offsets the negative effects of overexpressed RMST on mice with MCAO. The present work highlights that RMST augments IS through reducing miR-221-3p-mediated regulation of PIK3R1 and activating TGF-beta pathway.
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