CRID3, a blocker of apoptosis associated speck like protein containing a card, ameliorates murine spinal cord injury by improving local immune microenvironment

Chen, Yuqing; Wang, Sainan; Shi, Yujiao; Chen, Jing; Ding, Songtao; Tang, Jie; Shen, Lin; Wang, Rui; Ding, Hengfei; Hu, Jianguo; Lü, He‐Zuo

doi:10.1186/s12974-020-01937-8

Cited by 21 publications

(9 citation statements)

References 73 publications

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“…SCI-induced inflammation and oxidative stress are highly disordered metabolic processes, mainly manifested as an imbalance of the microenvironment, ultimately leading to injury recovery and progressive tissue degradation [ 15 , 38 , 39 ]. Macrophages play a vital role in tissue repair in the inflammatory microenvironment of SCI, but this process often results in a state where the damaged tissue cannot be repaired due to the change of macrophage polarization direction.…”

Section: Discussionmentioning

confidence: 99%

“…Macrophages are one of the first activated inflammatory cells and play an important role in the inflammatory process [ 12 ]. As the predominant effector cells, macrophages enter the injured site and polarize into M1 and M2 type in inflammatory responses [ 15 , 16 ]. Activated M1-type macrophages are characterized by the production of ROS that indicates a rapid and powerful response to trigger inflammation [ 17–19 ].…”

Section: Introductionmentioning

confidence: 99%

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Selenium nanoparticles derived from Proteus mirabilis YC801 alleviate oxidative stress and inflammatory response to promote nerve repair in rats with spinal cord injury

Liu

Mao

Huang

et al. 2022

Regenerative Biomaterials

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Microbial biotransformation and detoxification of biotoxic selenite into selenium nanoparticles (SeNPs) has emerged as an efficient technique for the utilization of selenium. SeNPs are characterized by high bioavailability and have several therapeutic effects owing to their antioxidant, anti-inflammatory, and neuroprotective activities. However, their influence on microenvironment disturbances and neuroprotection after spinal cord injury (SCI) is yet to be elucidated. This study aimed to assess the influence of SeNPs on SCI and explore the underlying protective mechanisms. Overall, the proliferation and differentiation of neural stem cells (NSCs) were facilitated by SeNPs derived from Proteus mirabilis YC801 via the Wnt/β-catenin signaling pathway. The SeNPs increased the number of neurons to a greater extent than astrocytes after differentiation and improved nerve regeneration. A therapeutic dose of SeNPs remarkably protected the integrity of the spinal cord to improve the motor function of the hind limbs after SCI, and decreased the expression of several inflammatory factors such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in vivo and enhanced the production of M2-type macrophages by regulating their polarization, indicating the suppressed inflammatory response. Besides, SeNPs reversed the SCI-mediated production of reactive oxygen species. In conclusion, SeNPs treatment holds the potential to improve the disturbed microenvironment and promote nerve regeneration, representing a promising therapeutic approach for SCI.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Selenium nanoparticles derived from Proteus mirabilis YC801 alleviate oxidative stress and inflammatory response to promote nerve repair in rats with spinal cord injury

Liu

Mao

Huang

et al. 2022

Regenerative Biomaterials

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“…Surviving motor neurons were quantified by counting all such cells in the ventral horn. The three staining methods were described previously ( Chen et al, 2020 ).…”

Section: Methodsmentioning

confidence: 99%

Neuroprotective Effects of the Pannexin-1 Channel Inhibitor: Probenecid on Spinal Cord Injury in Rats

Wang

et al. 2022

Front. Mol. Neurosci.

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Proinflammatory immune cell subsets constitute the majority in the local microenvironment after spinal cord injury (SCI), leading to secondary pathological injury. Previous studies have demonstrated that inflammasomes act as an important part of the inflammatory process after SCI. Probenecid, an inhibitor of the Pannexin-1 channel, can inhibit the activation of inflammasomes. This article focuses on the effects of probenecid on the local immune microenvironment, histopathology, and behavior of SCI. Our data show that probenecid inhibited the expression and activation of nucleotide-binding oligomerization domain receptor pyrindomain-containing 1 (NLRP1), apoptosis-associated speck-like protein containing a CARD (ASC) and caspase-1, interleukin-1β (IL-1β), and caspase-3 proteins associated with inflammasomes, thereby suppressing the proportion of M1 cells. And consequently, probenecid reduced the lesion area and demyelination in SCI. Moreover, the drug increased the survival of motor neurons, which resulted in tissue repair and improved locomotor function in the injured SC. Altogether, existing studies indicated that probenecid can alleviate inflammation by blocking Pannexin-1 channels to inhibit the expression of caspase-1 and IL-1β, which in turn restores the balance of immune cell subsets and exerts neuroprotective effects in rats with SCI.

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“…Chen et al. demonstrated that a stronger local immune microenvironment inhibited apoptosis, thus aiding recovery in murine SCI ( 24 ). Mohrman et al.…”

Section: The Role Of the Immune Response In Pathophysiological Proces...mentioning

confidence: 99%

The role of immune cells and associated immunological factors in the immune response to spinal cord injury

Tang¹,

Gu²,

Jiang³

et al. 2023

Front. Immunol.

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Spinal cord injury (SCI) is a devastating neurological condition prevalent worldwide. Where the pathological mechanisms underlying SCI are concerned, we can distinguish between primary injury caused by initial mechanical damage and secondary injury characterized by a series of biological responses, such as vascular dysfunction, oxidative stress, neurotransmitter toxicity, lipid peroxidation, and immune-inflammatory response. Secondary injury causes further tissue loss and dysfunction, and the immune response appears to be the key molecular mechanism affecting injured tissue regeneration and functional recovery from SCI. Immune response after SCI involves the activation of different immune cells and the production of immunity-associated chemicals. With the development of new biological technologies, such as transcriptomics, the heterogeneity of immune cells and chemicals can be classified with greater precision. In this review, we focus on the current understanding of the heterogeneity of these immune components and the roles they play in SCI, including reactive astrogliosis and glial scar formation, neutrophil migration, macrophage transformation, resident microglia activation and proliferation, and the humoral immunity mediated by T and B cells. We also summarize findings from clinical trials of immunomodulatory therapies for SCI and briefly review promising therapeutic drugs currently being researched.

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CRID3, a blocker of apoptosis associated speck like protein containing a card, ameliorates murine spinal cord injury by improving local immune microenvironment

Cited by 21 publications

References 73 publications

Selenium nanoparticles derived from Proteus mirabilis YC801 alleviate oxidative stress and inflammatory response to promote nerve repair in rats with spinal cord injury

Selenium nanoparticles derived from Proteus mirabilis YC801 alleviate oxidative stress and inflammatory response to promote nerve repair in rats with spinal cord injury

Neuroprotective Effects of the Pannexin-1 Channel Inhibitor: Probenecid on Spinal Cord Injury in Rats

The role of immune cells and associated immunological factors in the immune response to spinal cord injury

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