LncRNA RMST contributes to neuroinflammation after traumatic brain injury by targeting miR-139-5p

Yangwei Zhang; Yinhua Chen; Yanli Zhang; Ye Su; Juan Wang; Kang Zhang; Ningning Zhang

doi:10.5114/fn.2024.144259

eISSN: 1509-572x
ISSN: 1641-4640

Folia Neuropathologica

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abstract:

Original paper

LncRNA RMST contributes to neuroinflammation after traumatic brain injury by targeting miR-139-5p

Yangwei Zhang

¹

,

Yinhua Chen

²

,

Yanli Zhang

³

,

Ye Su

⁴

,

Juan Wang

⁴

,

Kang Zhang

⁵

,

Ningning Zhang

⁶

Department of Neurology, The Second Clinical College of North Sichuan Medical College, Nanchong Hospital of Beijing Anzhen Hospital & Sichuan Clinical Research Center for Neurological Diseases, Nanchong 637000, China
Department of Neurology, Nanjing BenQ Medical Center, The Affiliated BenQ Hospital of Nanjing Medical University, Nanjing, Jiangsu Province 210019, China
Department of Neuromonitoring, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China
Department of Critical Care Medicine, Hebei Yanda Hospital, Hebei 065201, China
Department of Neurosurgery, The Second Affiliated Hospital of Nanjing University of Chinese Medicine, Jiangsu 210000, China
Department of Orthopedics, Affiliated Hospital of Hebei Engineering University, Handan, Hebei Province 056000, China

Folia Neuropathol 2025; 63

DOI: https://doi.org/10.5114/fn.2024.144259

Online publish date: 2025/05/20

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Introduction:
Neuroinflammation plays a significant role in the pathological progression of traumatic brain injury (TBI) and represents a promising therapeutic target. The present study focused on exploring the mechanism of long noncoding RNA rhabdomyosarcoma 2 associated transcripts (RMST) in TBI-induced neuroinflammation.

Material and methods:
Controlled cortex injury was constructed as an in vivo TBI rat model and lipopolysaccharide (LPS)-induced microglia BV2 was constructed as an in vitro cellular model. Reverse transcription-quantity polymerase chain reaction (RT-qPCR) was employed to detect RMST levels in cerebral cortical tissues and BV2 cells. The modified neurological severity score (mNSS) and Morris water maze test were used to analyze neurological deficits and cognitive dysfunction. Enzyme-linked immunosorbent assay (ELISA) assay and flow cytometry were conducted to examine inflammatory factor levels and apoptosis. Dual luciferase reporter and RNA immunoprecipitation (RIP) assays were used to validate the target relationship between microRNA (miR)-139-5p and RMST.

Results:
RMST was present at high levels in TBI cerebral cortex tissues and LPS-induced BV2 cells, while miR-139-5p was reduced compared with the sham. Silencing RMST alleviated neurological deficits and cognitive dysfunction in TBI rats, but this alleviation was partially eliminated by the reduction of miR-139-5p. Additionally, overactivated neuroinflammatory factors in the TBI cerebral cortex were also suppressed by the knockdown of RMST, but partially restored by reduced miR-139-5p. Finally, the promotion of apoptosis and inflammatory mediator secretion of BV2 by LPS was diminished by silencing of RMST. These effects were all partially attenuated by silencing of miR-139-5p.

Conclusions:
RMST can aggravate neuroinflammation and apoptosis in microglia after TBI and thereby affect neurological dysfunction by regulating miR-139-5p.

keywords:

TBI, RMST, miR-139-5p, neuroinflammation, apoptosis

EVENTS

LncRNA RMST contributes to neuroinflammation after traumatic brain injury by targeting miR-139-5p

Yangwei Zhang 1 , Yinhua Chen 2 , Yanli Zhang 3 , Ye Su 4 , Juan Wang 4 , Kang Zhang 5 , Ningning Zhang 6

TBI, RMST, miR-139-5p, neuroinflammation, apoptosis

Yangwei Zhang

¹

,

Yinhua Chen

²

,

Yanli Zhang

³

,

Ye Su

⁴

,

Juan Wang

⁴

,

Kang Zhang

⁵

,

Ningning Zhang

⁶