microRNA pathological mechanisms between Parkinson's disease, Alzheimer's disease, glaucoma and macular degeneration

Wang, Hsiuying

doi:10.1017/erm.2023.19

Cited by 6 publications

(1 citation statement)

References 157 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As a kind of small non-coding RNA with a length of 20–22 nucleotides, microRNAs (miRNAs) participate in mRNA cleavage or post-transcriptional silencing via targeting messenger RNA (mRNA) 3′-untranslated region (3′UTR), thus regulating the expression of related genes [ 5 , 6 ]. MiRNAs are dysregulated in many diseases including PD [ 7 ].…”

Section: Introductionmentioning

confidence: 99%

miR-101a-3p/ROCK2 axis regulates neuronal injury in Parkinson’s disease models

Tao,

Zhang,

Chen

et al. 2024

Aging

View full text Add to dashboard Cite

Background: Parkinson’s disease (PD) is a neurodegenerative disease characterized by the loss of dopaminergic neurons in substantia nigra pars compacta (SNpc). This study focuses on deciphering the role of microRNA (miR)-101a-3p in the neuronal injury of PD and its regulatory mechanism. Methods: We constructed a mouse model of PD by intraperitoneal injection of 1-methyl 4-phenyl 1, 2, 3, 6-tetrahydropyridine hydrochloride (MPTP), and used 1-methyl-4-phenylpyridinium (MPP+) to treat Neuro-2a cells to construct an in-vitro PD model. Neurological dysfunction in mice was evaluated by swimming test and traction test. qRT-PCR was utilized to examine miR-101a-3p expression and ROCK2 expression in mouse brain tissues and Neuro-2a cells. Western blot was conducted to detect the expression of α-synuclein protein and ROCK2 in mouse brain tissues and Neuro-2a cells. The targeting relationship between miR-101a-3p and ROCK2 was determined by dual-luciferase reporter gene assay. The apoptosis of neuro-2a cells was assessed by flow cytometry. Results: Low miR-101a-3p expression and high ROCK2 expression were found in the brain tissues of PD mice and MPP+-treated Neuro-2a cells; PD mice showed decreased neurological disorders, and apoptosis of Neuro-2a cells was increased after MPP+ treatment, both of which were accompanied by increased accumulation of α-synuclein protein. After miR-101a-3p was overexpressed, the neurological function of PD mice was improved, and the apoptosis of Neuro-2a cells induced by MPP+ was alleviated, and the accumulation of α-synuclein protein was reduced; ROCK2 overexpression counteracted the protective effect of miR-101a-3p. Additionally, ROCK2 was identified as the direct target of miR-101a-3p. Conclusion: MiR-101a-3p can reduce neuronal apoptosis and neurological deficit in PD mice by inhibiting ROCK2 expression, suggesting that miR-101a-3p is a promising therapeutic target for PD.

show abstract

Section: Introductionmentioning

confidence: 99%

miR-101a-3p/ROCK2 axis regulates neuronal injury in Parkinson’s disease models

Tao,

Zhang,

Chen

et al. 2024

Aging

View full text Add to dashboard Cite

show abstract

Small RNAs in plasma extracellular vesicles define biomarkers of premanifest changes in Huntington's disease

Herrero‐Lorenzo,

Pérez‐Pérez,

Escaramís

et al. 2024

J of Extracellular Vesicle

View full text Add to dashboard Cite

Despite the advances in the understanding of Huntington's disease (HD), there is a need for molecular biomarkers to categorize mutation carriers during the preclinical stage of the disease preceding functional decline. Small RNAs (sRNAs) are a promising source of biomarkers since their expression levels are highly sensitive to pathobiological processes. Here, using an optimized method for plasma extracellular vesicles (EVs) purification and an exhaustive analysis pipeline of sRNA sequencing data, we show that EV‐sRNAs are downregulated early in mutation carriers and that this deregulation is associated with premanifest cognitive performance. Seven candidate sRNAs (tRF‐Glu‐CTC, tRF‐Gly‐GCC, miR‐451a, miR‐21‐5p, miR‐26a‐5p, miR‐27a‐3p and let7a‐5p) were validated in additional subjects, showing a significant diagnostic accuracy at premanifest stages. Of these, miR‐21‐5p was significantly decreased over time in a longitudinal study; and miR‐21‐5p and miR‐26a‐5p levels correlated with cognitive changes in the premanifest cohort. In summary, the present results suggest that deregulated plasma EV‐sRNAs define an early biosignature in mutation carriers with specific species highlighting the progression and cognitive changes occurring at the premanifest stage.

show abstract