Inflammasome: Its role in traumatic brain and spinal cord injury

Mortezaee, Keywan; Khanlarkhani, Neda; Beyer, Cordian; Zendedel, Adib

doi:10.1002/jcp.26287

Cited by 206 publications

(179 citation statements)

References 72 publications

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“…Melatonin is a secretory product of the pineal gland and gastrointestinal tract during night and daytime, respectively (Margheri et al, ). Melatonin is responsible for a variety of physiological functions (Mortezaee, Khanlarkhani, Sabbaghziarani et al, ; Mortezaee, Sabbaghziarani et al, ), including antioxidant (Mortezaee & Khanlarkhani, ; Mortezaee et al, ; Mortezaee, Khanlarkhani, Beyer, & Zendedel, ), anti‐apoptotic (Mortezaee, Majidpoor, Daneshi, Abouzaripour, & Abdi, ), and pro‐apoptotic (Lin et al, ) activities. Melatonin is the only known chronobotic hormone for regulation of neoplastic cell growth (Blask, Sauer, & Dauchy, ).…”

Section: Introductionmentioning

confidence: 99%

Human hepatocellular carcinoma: Protection by melatonin

Mortezaee

2018

Journal Cellular Physiology

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Despite great scientific breakthroughs toward understanding the identity of human hepatocellular carcinoma (HCC) mechanistically, there are still no clinically efficient therapeutic methods for this cancer. Melatonin (N-acetyl-5-methoxytryptamine) is a multi-tasking hormone that has long been known for its anti-cancer activity against various human cancers including HCC, which is a focus of this review. PubMed database was searched for relevant articles with the keywords: hepatocellular carcinoma (HCC), melatonin, apoptosis, proliferation, invasion, angiogenesis, autophagy, oxidative stress, tumor immunity, and mitogen-activated protein kinase (MAPK) focusing on just human cell lines and English language articles. Melatonin inhibits apoptosis resistance and activates both extrinsic and intrinsic pathways of apoptosis in HCC. Melatonin induces ensoplasmic reticulum (ER)- and autophagy-mediated apoptosis in cancer cells. Melatonin works against cancer cell proliferation, motility, and invasiveness by modulating actions of a variety of transcription factors and related pathways. Melatonin also relieves an immunosuppressive state in HCC cancer cells through making a control over tumor-derived exosomes. Both pro-and anti-oxidative functions of melatonin are necessary for combating HCC. Combination of melatonin with chemotherapy could also provide cumulative effects on cancer cells. Melatonin exerts most of these roles by acting on the members of MAPK family.

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Section: Introductionmentioning

confidence: 99%

Human hepatocellular carcinoma: Protection by melatonin

Mortezaee

2018

Journal Cellular Physiology

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“…This tissue damage and cellular stress promote immune responses that are intended to aid in the disposal of neurotoxic material and coordinate tissue repair [8,9]. While immune responses initially play beneficial roles in TBI, unchecked and/or chronic immune activation following brain trauma can lead to secondary tissue damage, brain atrophy, and eventual neurological dysfunction [8][9][10][11][12][13]. Notably, the inability to properly dispose of danger/damage-associated molecular patterns (DAMPs) such as protein aggregates, necrotic cells, and cellular debris has been shown to be a pivotal driver of both persistent and maladaptive immune activation in numerous neurological disorders [14,15].…”

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confidence: 99%

Meningeal lymphatic dysfunction exacerbates traumatic brain injury pathogenesis

Bolte

Hurt

Smirnov

et al. 2019

Preprint

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Traumatic brain injury (TBI) has emerged as a leading cause of death and disability. Despite being a growing medical issue, the biological factors that promote central nervous system (CNS) pathology and neurological dysfunction following TBI remain poorly characterized. Recently, the meningeal lymphatic system was identified as a critical mediator of drainage from the CNS. In comparison to other peripheral organs, our understanding of how defects in lymphatic drainage from the CNS contribute to disease is limited. It is still unknown how TBI impacts meningeal lymphatic function and whether disruptions in this drainage pathway are involved in driving TBI pathogenesis. Here we demonstrate that even mild forms of brain trauma cause severe deficits in meningeal lymphatic drainage that can last out to at least two weeks post-injury. To investigate a mechanism behind impaired lymphatic function in TBI, we examined how increased intracranial pressure (ICP) influences the meningeal lymphatics, as increased ICP commonly occurs in TBI. We demonstrate that increased ICP is capable of provoking meningeal lymphatic dysfunction. Moreover, we show that pre-existing lymphatic dysfunction mediated by targeted photoablation before TBI leads to increased neuroinflammation and cognitive deficits. These findings provide new insights into both the causes and consequences of meningeal lymphatic dysfunction in TBI and suggest that therapeutics targeting the meningeal lymphatic system may offer strategies to treat TBI.

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“…The term neuroinflammation is currently used to describe the inflammatory response originated in the CNS after suffering an injury (Morales, Guzmán‐Martínez, Cerda‐Troncoso, Farías, & Maccioni, ; Mortezaee, Khanlarkhani, Beyer, & Zendedel, ). Neuroinflammation is characterized by an increase in microglial activation, oxidative stress, and by the upregulation of inflammatory cytokines such as IL‐1β and IL‐18 (Deleidi, Jäggle, & Rubino, ; Figure ).…”

Section: Discussionmentioning

confidence: 99%

Autophagy and NLRP3 inflammasome crosstalk in neuroinflammation in aged bovine brains

Biase

Piegari

Prisco

et al. 2020

Journal Cellular Physiology

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NLRP3 inflammasome is a multiprotein complex that can sense several stimuli such as autophagy dysregulation and increased reactive oxygen species production stimulating inflammation by priming the maturation of proinflammatory cytokines interleukin‐1β and interleukin‐18 in their active form. In the aging brain, these cytokines can mediate the innate immunity response priming microglial activation. Here, we describe the results of immunohistochemical and molecular analysis carried out on bovine brains. Our results support the hypothesis that the age‐related impairment in cellular housekeeping mechanisms and the increased oxidative stress can trigger the inflammatory danger sensor NLRP3. Moreover, according to the recent scientific literature, we demonstrate the presence of an age‐related proinflammatory environment in aged brains consisting in an upregulation of interleukin‐1β, an increased microglial activation and increased NLRP3 expression. Finally, we suggest that bovine may potentially be a pivotal animal model for brain aging studies.

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Inflammasome: Its role in traumatic brain and spinal cord injury

Cited by 206 publications

References 72 publications

Human hepatocellular carcinoma: Protection by melatonin

Human hepatocellular carcinoma: Protection by melatonin

Meningeal lymphatic dysfunction exacerbates traumatic brain injury pathogenesis

Autophagy and NLRP3 inflammasome crosstalk in neuroinflammation in aged bovine brains

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