miRNA-146a and miRNA-202-3p Attenuate Inflammatory Response by Inhibiting TLR4, IRAK1, and TRAF6 Expressions in Rats following Spinal Cord Injury

Feng, Sun; Zhang, Haiwei; Shi, Jianhui; Huang, Tianwen; Wang, Yansong

doi:10.1155/2021/5452239

Cited by 6 publications

(8 citation statements)

References 30 publications

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“…Different studies report that l-carnosine favors cell survival by inducing the antiapoptotic marker Bcl-2 and suppressing the apoptotic marker Bax, which is associated with a decreased ratio of Bcl-2/Bax (Cheng et al 2011;Abdel Baky et al 2016;Wang et al 2013). Apoptosis plays an important role in cell death in spinal cord tissue after SCI (Ding et al 2020;Sun et al 2020), and dipeptide findings indicate that it significantly contributes to the positive balance between the antiapoptotic marker Bcl2 and the apoptotic marker Bax shown by Tre-car in survival signaling pathway activation against SCI. The increased Nrf2 and the inhibited NF-κB (Yehia et al 2019) may partly be related to an antiapoptotic effect, further supporting our suggestion regarding the complex signaling pathway of protection activated by l-carnosine.…”

Section: Discussionmentioning

confidence: 99%

Trehalose–Carnosine Prevents the Effects of Spinal Cord Injury Through Regulating Acute Inflammation and Zinc(II) Ion Homeostasis

et al. 2022

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Spinal cord injury (SCI) leads to long-term and permanent motor dysfunctions, and nervous system abnormalities. Injury to the spinal cord triggers a signaling cascade that results in activation of the inflammatory cascade, apoptosis, and Zn(II) ion homeostasis. Trehalose (Tre), a nonreducing disaccharide, and l-carnosine (Car), (β-alanyl-l-histidine), one of the endogenous histidine dipeptides have been recognized to suppress early inflammatory effects, oxidative stress and to possess neuroprotective effects. We report on the effects of the conjugation of Tre with Car (Tre–car) in reducing inflammation in in vitro and in vivo models. The in vitro study was performed using rat pheochromocytoma cells (PC12 cell line). After 24 h, Tre–car, Car, Tre, and Tre + Car mixture treatments, cells were collected and used to investigate Zn2+ homeostasis. The in vivo model of SCI was induced by extradural compression of the spinal cord at the T6–T8 levels. After treatments with Tre, Car and Tre–Car conjugate 1 and 6 h after SCI, spinal cord tissue was collected for analysis. In vitro results demonstrated the ionophore effect and chelating features of l-carnosine and its conjugate. In vivo, the Tre–car conjugate treatment counteracted the activation of the early inflammatory cascade, oxidative stress and apoptosis after SCI. The Tre–car conjugate stimulated neurotrophic factors release, and influenced Zn2+ homeostasis. We demonstrated that Tre–car, Tre and Car treatments improved tissue recovery after SCI. Tre–car decreased proinflammatory, oxidative stress mediators release, upregulated neurotrophic factors and restored Zn2+ homeostasis, suggesting that Tre–car may represent a promising therapeutic agent for counteracting the consequences of SCI.

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Section: Discussionmentioning

confidence: 99%

Trehalose–Carnosine Prevents the Effects of Spinal Cord Injury Through Regulating Acute Inflammation and Zinc(II) Ion Homeostasis

et al. 2022

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“…miRNA-940, miRNA-182, miRNA-488, and miRNA-543-5p are involved in the NF-KB pathway to inhibit the release of pro-inflammatory factors such as tumour necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) and subsequently regulate the inflammatory response after SCI in rats [34][35][36][37]. miRNA-411, miRNA-129-5p, miRNA-9-5p, and miRNA-7a inhibit apoptosis of neuronal cells after SCI in rats [38][39][40][41]. miRNA-466c-3p and miRNA-155 are involved in the regulation of mitochondrial function after SCI in rats [42,43].…”

Section: Characterization Of Mirna Expression After Spinal Cord Injur...mentioning

confidence: 99%

Research Progress of MicroRNAs in Spinal Cord Injury

Deng¹,

Chen²

2023

J. Integr. Neurosci.

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Spinal cord injury is a serious and devastating condition. Recently, research into microRNAs (miRNAs) has become increasingly exhaustive and it has been determined that they are closely related to the pathophysiological processes of spinal cord injury. They participate in the regulation of the inflammatory response of spinal cord injury, the death of neuronal cells, and the repair of neural functions, which are related to the recovery of spinal cord injury. This review focuses on the relationship between miRNA and spinal cord injury, lists miRNA-324-5p, miRNA-221 and miRNA-124, which are helpful for the repair of spinal cord injury, and finally summarizes the current research progress of miRNA-based therapies, so as to provide a foundational reference for clinical and scientific researchers.

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“…In particular, microglia are important for removing damaged cells during membrane PS externalization and apoptosis [106,131,145,277,278,298,308,[324][325][326][327]]. Yet, microglia can lead to the generation of oxidative stress through the production of ROS [8,165,167,246,250,[328][329][330][331], which can require modulation by non-coding RNAs [251,[332][333][334][335][336], Wnt signaling [27,28,106,115,276,[337][338][339], and trophic factor pathways with erythropoietin (EPO) [27,[340][341][342][343][344][345][346]. In other scenarios, microglial cells can be helpful for protection during amyotrophic lateral sclerosis [347], remove brain amyloid [348,349], and preserve cholesterol homeostasis with autophagy …”

Section: Cellular Mechanisms Of Oxidative Stress Energy Metabolism An...mentioning

confidence: 99%

“…Through pathways that are dependent upon TREM2, new therapies using microglia are being considered to improve cognition, reduce memory loss, block inflammation, and be important tools for identifying metabolic disease progression. The therapeutic pathways that oversee microglia function are intimately tied to non-coding RNAs that oversee inflammatory pathways [251,[332][333][334][335][336], Wnt signaling, and growth factors, such as EPO. Growth factors, such as EPO, are also being seen as necessary to control AMPK and non-coding RNA pathways.…”

Section: Conclusion and Future Perspectivesmentioning

confidence: 99%

Cornerstone Cellular Pathways for Metabolic Disorders and Diabetes Mellitus: Non-Coding RNAs, Wnt Signaling, and AMPK

Maiese

2023

Cells

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Metabolic disorders and diabetes (DM) impact more than five hundred million individuals throughout the world and are insidious in onset, chronic in nature, and yield significant disability and death. Current therapies that address nutritional status, weight management, and pharmacological options may delay disability but cannot alter disease course or functional organ loss, such as dementia and degeneration of systemic bodily functions. Underlying these challenges are the onset of aging disorders associated with increased lifespan, telomere dysfunction, and oxidative stress generation that lead to multi-system dysfunction. These significant hurdles point to the urgent need to address underlying disease mechanisms with innovative applications. New treatment strategies involve non-coding RNA pathways with microRNAs (miRNAs) and circular ribonucleic acids (circRNAs), Wnt signaling, and Wnt1 inducible signaling pathway protein 1 (WISP1) that are dependent upon programmed cell death pathways, cellular metabolic pathways with AMP-activated protein kinase (AMPK) and nicotinamide, and growth factor applications. Non-coding RNAs, Wnt signaling, and AMPK are cornerstone mechanisms for overseeing complex metabolic pathways that offer innovative treatment avenues for metabolic disease and DM but will necessitate continued appreciation of the ability of each of these cellular mechanisms to independently and in unison influence clinical outcome.

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miRNA-146a and miRNA-202-3p Attenuate Inflammatory Response by Inhibiting TLR4, IRAK1, and TRAF6 Expressions in Rats following Spinal Cord Injury

Cited by 6 publications

References 30 publications

Trehalose–Carnosine Prevents the Effects of Spinal Cord Injury Through Regulating Acute Inflammation and Zinc(II) Ion Homeostasis

Trehalose–Carnosine Prevents the Effects of Spinal Cord Injury Through Regulating Acute Inflammation and Zinc(II) Ion Homeostasis

Research Progress of MicroRNAs in Spinal Cord Injury

Cornerstone Cellular Pathways for Metabolic Disorders and Diabetes Mellitus: Non-Coding RNAs, Wnt Signaling, and AMPK

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