A Comprehensive Review on the Importance of MiRNA-206 in the Animal
Model and Human Diseases

Wang, Qi; Guan, Wei

doi:10.2174/1570159x21666230407124146

Cited by 2 publications

(2 citation statements)

References 122 publications

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“…1F), suggesting that LPS administration successfully established an ALI animal model. miRNA-206-3p reportedly has a pivotal role in the progression of various human ailments, including cancers, osteoarthritis, and depression 22 . Meanwhile, the essential role of miRNA-206-3p in regulating the inflammatory response has also been described [23][24][25] .…”

Section: Mirna206-3p Is Downregulated In Lps-induced Ali In Vitro And...mentioning

confidence: 99%

miRNA-206-3p alleviates LPS-induced acute lung injury via inhibiting inflammation and pyroptosis through modulating TLR4/NF-κB/NLRP3 pathway

Chen,

Zhang,

Huang

et al. 2024

Sci Rep

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Acute lung injury (ALI) is life-threatening. MicroRNAs (miRNAs) are often abnormally expressed in inflammatory diseases and are closely associated with ALI. This study investigates whether miRNA-206-3p attenuates pyroptosis in ALI and elucidates the underlying molecular mechanisms. ALI mouse and cell models were established through lipopolysaccharide (LPS) treatment for 24 h. Subsequently, the models were evaluated based on ultrasonography, the lung tissue wet/dry (W/D) ratio, pathological section assessment, electron microscopy, and western blotting. Pyroptosis in RAW264.7 cells was then assessed via electron microscopy, immunofluorescence, and western blotting. Additionally, the regulatory relationship between miRNA-206-3p and the Toll-like receptor (TLR)4/nuclear factor (NF)-κB/Nod-like receptor protein-3 (NLRP3) pathway was verified. Finally, luciferase reporter gene and RNA pull-down assays were used to verify the targeting relationship between miRNA-206-3p and TLR4. miRNA206-3p levels are significantly decreased in the LPS-induced ALI model. Overexpression of miRNA-206-3p improves ALI, manifested as improved lung ultrasound, improved pathological changes of lung tissue, reduced W/D ratio of lung tissue, release of inflammatory factors in lung tissue, and reduced pyroptosis. Furthermore, overexpression of miRNA-206-3p contributed to reversing the ALI-promoting effect of LPS by hindering TLR4, myeloid differentiation primary response 88 (MyD88), NF-κB, and NLRP3 expression. In fact, miRNA-206-3p binds directly to TLR4. In conclusion, miRNA-206-3p alleviates LPS-induced ALI by inhibiting inflammation and pyroptosis via TLR4/NF-κB/NLRP3 pathway modulation.

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Section: Mirna206-3p Is Downregulated In Lps-induced Ali In Vitro And...mentioning

confidence: 99%

miRNA-206-3p alleviates LPS-induced acute lung injury via inhibiting inflammation and pyroptosis through modulating TLR4/NF-κB/NLRP3 pathway

Chen,

Zhang,

Huang

et al. 2024

Sci Rep

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“…This inhibition of TPPP by specific oligonucleotides revealed the crucial physiological role of TPPP in the differentiation of the progenitor OLGs. miRNA-206 also plays an important role in the pathomechanism of various diseases [103,104]. It was suggested as a possible biomarker and a therapeutic target in Alzheimer's disease.…”

Section: Targeting Mrna In Parkinsonismmentioning

confidence: 99%

Perspective Strategies for Interventions in Parkinsonism: Remedying the Neglected Role of TPPP

Oláh,

Norris,

Lehotzky

et al. 2024

Cells

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Neurological disorders such as Parkinsonism cause serious socio-economic problems as there are, at present, only therapies that treat their symptoms. The well-established hallmark alpha-synuclein (SYN) is enriched in the inclusion bodies characteristic of Parkinsonism. We discovered a prominent partner of SYN, termed Tubulin Polymerization Promoting Protein (TPPP), which has important physiological and pathological activities such as the regulation of the microtubule network and the promotion of SYN aggregation. The role of TPPP in Parkinsonism is often neglected in research, which we here attempt to remedy. In the normal brain, SYN and TPPP are expressed endogenously in neurons and oligodendrocytes, respectively, whilst, at an early stage of Parkinsonism, soluble hetero-associations of these proteins are found in both cell types. The cell-to-cell transmission of these proteins, which is central to disease progression, provides a unique situation for specific drug targeting. Different strategies for intervention and for the discovery of biomarkers include (i) interface targeting of the SYN-TPPP hetero-complex; (ii) proteolytic degradation of SYN and/or TPPP using the PROTAC technology; and (iii) depletion of the proteins by miRNA technology. We also discuss the potential roles of SYN and TPPP in the phenotype stabilization of neurons and oligodendrocytes.

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A Comprehensive Review on the Importance of MiRNA-206 in the Animal Model and Human Diseases

Cited by 2 publications

References 122 publications

miRNA-206-3p alleviates LPS-induced acute lung injury via inhibiting inflammation and pyroptosis through modulating TLR4/NF-κB/NLRP3 pathway

miRNA-206-3p alleviates LPS-induced acute lung injury via inhibiting inflammation and pyroptosis through modulating TLR4/NF-κB/NLRP3 pathway

Perspective Strategies for Interventions in Parkinsonism: Remedying the Neglected Role of TPPP

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