DUSP19 mediates spinal cord injury-induced apoptosis and inflammation in mouse primary microglia cells via the NF-kB signaling pathway

Xie, Xiankuan; Xu, Zhengkuan; Xu, Kan; Xiao, Yu

doi:10.1080/01616412.2019.1685068

Cited by 25 publications

(15 citation statements)

References 28 publications

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“…As a result of the activation of the aforementioned receptors, the transcription factor NF-kB (nuclear factor kappa B) triggers the expression of genes encoding pro-inflammatory molecules, including IL-1b (interleukin-1b), IL-6, IL-8 (interleukin 8), IL-18 (interleukin 18), and TNF-a. Another activated transcription factor involved in the expression of pro-inflammatory genes is AP-1 (activator protein 1), an important activator of IL-1 and TNF-a expression and the promotion of the expression of some adhesion molecules (50)(51)(52). The path from TLR4 receptors to NF-kB and AP-1 activation is mainly through the MyD88 protein (myeloid differentiation primary response protein) (53,54).…”

Section: General Viewmentioning

confidence: 99%

Understanding the Connection Between Common Stroke Comorbidities, Their Associated Inflammation, and the Course of the Cerebral Ischemia/Reperfusion Cascade

Przykaza

2021

Front. Immunol.

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Despite the enormous progress in the understanding of the course of the ischemic stroke over the last few decades, a therapy that effectively protects neurovascular units (NVUs) and significantly improves neurological functions in stroke patients has still not been achieved. The reasons for this state are unclear, but it is obvious that the cerebral ischemia and reperfusion cascade is a highly complex phenomenon, which includes the intense neuroinflammatory processes, and comorbid stroke risk factors strongly worsen stroke outcomes and likely make a substantial contribution to the pathophysiology of the ischemia/reperfusion, enhancing difficulties in searching of successful treatment. Common concomitant stroke risk factors (arterial hypertension, diabetes mellitus and hyperlipidemia) strongly drive inflammatory processes during cerebral ischemia/reperfusion; because these factors are often present for a long time before a stroke, causing low-grade background inflammation in the brain, and already initially disrupting the proper functions of NVUs. Broad consideration of this situation in basic research may prove to be crucial for the success of future clinical trials of neuroprotection, vasculoprotection and immunomodulation in stroke. This review focuses on the mechanism by which coexisting common risk factors for stroke intertwine in cerebral ischemic/reperfusion cascade and the dysfunction and disintegration of NVUs through inflammatory processes, principally activation of pattern recognition receptors, alterations in the expression of adhesion molecules and the subsequent pathophysiological consequences.

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Section: General Viewmentioning

confidence: 99%

Understanding the Connection Between Common Stroke Comorbidities, Their Associated Inflammation, and the Course of the Cerebral Ischemia/Reperfusion Cascade

Przykaza

2021

Front. Immunol.

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“…Given the fundamental nature of NF-κB signaling pathway activation to neuroinflammation and SCI pathophysiology [ 64 , 65 , 66 ], the modulation of NF-κB signaling could ameliorate inflammation, reduce the impact of the secondary damage stage, and preserve neuronal function. A previous study reported that curcumin reduced neuroinflammation after SCI by specifically suppressing the TLR4/NF-κB signaling pathway [ 67 ].…”

Section: Discussionmentioning

confidence: 99%

Human-Induced Neural and Mesenchymal Stem Cell Therapy Combined with a Curcumin Nanoconjugate as a Spinal Cord Injury Treatment

Bonilla

Hernández

Giraldo

et al. 2021

IJMS

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We currently lack effective treatments for the devastating loss of neural function associated with spinal cord injury (SCI). In this study, we evaluated a combination therapy comprising human neural stem cells derived from induced pluripotent stem cells (iPSC-NSC), human mesenchymal stem cells (MSC), and a pH-responsive polyacetal–curcumin nanoconjugate (PA-C) that allows the sustained release of curcumin. In vitro analysis demonstrated that PA-C treatment protected iPSC-NSC from oxidative damage in vitro, while MSC co-culture prevented lipopolysaccharide-induced activation of nuclear factor-κB (NF-κB) in iPSC-NSC. Then, we evaluated the combination of PA-C delivery into the intrathecal space in a rat model of contusive SCI with stem cell transplantation. While we failed to observe significant improvements in locomotor function (BBB scale) in treated animals, histological analysis revealed that PA-C-treated or PA-C and iPSC-NSC + MSC-treated animals displayed significantly smaller scars, while PA-C and iPSC-NSC + MSC treatment induced the preservation of β-III Tubulin-positive axons. iPSC-NSC + MSC transplantation fostered the preservation of motoneurons and myelinated tracts, while PA-C treatment polarized microglia into an anti-inflammatory phenotype. Overall, the combination of stem cell transplantation and PA-C treatment confers higher neuroprotective effects compared to individual treatments.

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“…Compared with the levels in the model group, the PI3K, p-AKT/AKT and p-mTOR/mTOR levels were decreased in the 50 mg/kg TMP group, indicating that autophagy was activated in the 50 mg/kg TMP group, possibly through the PI3K/AKT/mTOR signaling pathway. Studies have shown that various external factors can activate the NF-κB signaling pathway, including cellular stress, ionizing radiation, LPS, cellular membrane proteins and virus-related membrane proteins (25,26). The NF-κB signaling pathway is an important pathway that regulates inflammatory responses.…”

Section: Discussionmentioning

confidence: 99%

Ligustrazine ameliorates lipopolysaccharide‑induced neurocognitive impairment by activating autophagy via the PI3K/AKT/mTOR pathway

Liu

Wang

et al. 2020

Int J Mol Med

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Autophagy is a lysosome-mediated cell contentdependent degradation pathway that leads to enhanced inflammation in an uncontrolled state. This study examined the role of autophagy in lipopolysaccharide (LPS)-induced brain inflammation and the effects of the traditional chinese medicine ligustrazine on LPS-induced neurocognitive impairment in rats. Furthermore, the molecular mechanisms by which ligustrazine influences neurocognitive impairments were explored. The production of the inflammatory mediators interleukin (IL)-1β and tumor necrosis factor (TNF)-α was analyzed using ELISAs, and the expression levels of the autophagy marker microtubule-associated protein light chain 3 (Lc3) II/I were analyzed using western blotting. LPS exposure upregulated the expression of IL-1β and TNF-α and downregulated the expression of Lc3 II/I. Ligustrazine activated autophagy by preventing the expression of phosphoinositide 3-kinase (PI3K), phosphorylated protein kinase B (p-AKT), and phosphorylated mammalian target of rapamycin (p-mTOR). The present results suggest that ligustrazine improved LPS-induced neurocognitive impairments by activating autophagy and ameliorated neuronal injury by regulating the PI3K/AKT/mTOR signaling pathway. These findings provide an important reference for the prevention and treatment of neuroinflammation.

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DUSP19 mediates spinal cord injury-induced apoptosis and inflammation in mouse primary microglia cells via the NF-kB signaling pathway

Cited by 25 publications

References 28 publications

Understanding the Connection Between Common Stroke Comorbidities, Their Associated Inflammation, and the Course of the Cerebral Ischemia/Reperfusion Cascade

Understanding the Connection Between Common Stroke Comorbidities, Their Associated Inflammation, and the Course of the Cerebral Ischemia/Reperfusion Cascade

Human-Induced Neural and Mesenchymal Stem Cell Therapy Combined with a Curcumin Nanoconjugate as a Spinal Cord Injury Treatment

Ligustrazine ameliorates lipopolysaccharide‑induced neurocognitive impairment by activating autophagy via the PI3K/AKT/mTOR pathway

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