Transcriptional landscape of human neuroblastoma cells in response to SARS-CoV-2

Yang, Ruicheng; Huang, Kun; Zhang, Hui-Peng; Li, Liang; Tan, Chen; Chen, Huanchun; Jin, Meilin

doi:10.1186/s12868-022-00728-6

Cited by 3 publications

(2 citation statements)

References 55 publications

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“…Even though we tried to explain such a cytopathic effect via cytoskeletal alterations, no changes in the expression of microtubule subunits or microtubule-associated proteins (e.g., tau protein) were objectivated. Conversely, a transcriptomic study on neuroblastoma SK-N-SH cells revealed that SARS-CoV-2 infection induced a downregulation of several members of building blocks of the cytoskeleton, as well as some of their regulators (i.e., TUBA1A, TUBA4A, TUBB4A, STMN4, TMSB15A, SYNPO2) [60]. In brain organoids, the infection with SARS-CoV-2 induced a relocation of tau protein from neurite to neuronal cell soma and was associated with tau hyperphosphorylation at Thr231 [46].…”

Section: Discussionmentioning

confidence: 99%

Viral Entry Inhibitors Protect against SARS-CoV-2-Induced Neurite Shortening in Differentiated SH-SY5Y Cells

Mignolet,

Gilloteaux,

Halloin

et al. 2023

Viruses

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The utility of human neuroblastoma cell lines as in vitro model to study neuro-invasiveness and neuro-virulence of SARS-CoV-2 has been demonstrated by our laboratory and others. The aim of this report is to further characterize the associated cellular responses caused by a pre-alpha SARS-CoV-2 strain on differentiated SH-SY5Y and to prevent its cytopathic effect by using a set of entry inhibitors. The susceptibility of SH-SY5Y to SARS-CoV-2 was confirmed at high multiplicity-of-infection, without viral replication or release. Infection caused a reduction in the length of neuritic processes, occurrence of plasma membrane blebs, cell clustering, and changes in lipid droplets electron density. No changes in the expression of cytoskeletal proteins, such as tubulins or tau, could explain neurite shortening. To counteract the toxic effect on neurites, entry inhibitors targeting TMPRSS2, ACE2, NRP1 receptors, and Spike RBD were co-incubated with the viral inoculum. The neurite shortening could be prevented by the highest concentration of camostat mesylate, anti-RBD antibody, and NRP1 inhibitor, but not by soluble ACE2. According to the degree of entry inhibition, the average amount of intracellular viral RNA was negatively correlated to neurite length. This study demonstrated that targeting specific SARS-CoV-2 host receptors could reverse its neurocytopathic effect on SH-SY5Y.

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Section: Discussionmentioning

confidence: 99%

Viral Entry Inhibitors Protect against SARS-CoV-2-Induced Neurite Shortening in Differentiated SH-SY5Y Cells

Mignolet,

Gilloteaux,

Halloin

et al. 2023

Viruses

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show abstract

“…Although the CNS is not a common viral target, many viruses can infect the brain and induce neuroinflammation, which is characterized by severe neuronal injury and microgliosis/astrogliosis. Microglia and astrocytes actively respond to both RNA and DNA viruses by releasing various inflammatory mediators to activate the immune system and combat infection [ 170 – 172 ].…”

Section: Introductionmentioning

confidence: 99%

Emerging role of non-coding RNAs in neuroinflammation mediated by microglia and astrocytes

Yang

Liu

et al. 2023

J Neuroinflammation

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Neuroinflammation has been implicated in the initiation and progression of several central nervous system (CNS) disorders, including Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, multiple sclerosis, ischemic stroke, traumatic brain injury, spinal cord injury, viral encephalitis, and bacterial encephalitis. Microglia and astrocytes are essential in neural development, maintenance of synaptic connections, and homeostasis in a healthy brain. The activation of astrocytes and microglia is a defense mechanism of the brain against damaged tissues and harmful pathogens. However, their activation triggers neuroinflammation, which can exacerbate or induce CNS injury. Non-coding RNAs (ncRNAs) are functional RNA molecules that lack coding capabilities but can actively regulate mRNA expression and function through various mechanisms. ncRNAs are highly expressed in astrocytes and microglia and are potential mediators of neuroinflammation. We reviewed the recent research progress on the role of miRNAs, lncRNAs, and circRNAs in regulating neuroinflammation in various CNS diseases. Understanding how these ncRNAs affect neuroinflammation will provide important therapeutic insights for preventing and managing CNS dysfunction.

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Blood–Brain Barrier Integrity Damage in Bacterial Meningitis: The Underlying Link, Mechanisms, and Therapeutic Targets

Yang

Wang

et al. 2023

IJMS

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Despite advances in supportive care and antimicrobial treatment, bacterial meningitis remains the most serious infection of the central nervous system (CNS) that poses a serious risk to life. This clinical dilemma is largely due to our insufficient knowledge of the pathology behind this disease. By controlling the entry of molecules into the CNS microenvironment, the blood–brain barrier (BBB), a highly selective cellular monolayer that is specific to the CNS’s microvasculature, regulates communication between the CNS and the rest of the body. A defining feature of the pathogenesis of bacterial meningitis is the increase in BBB permeability. So far, several contributing factors for BBB disruption have been reported, including direct cellular damage brought on by bacterial virulence factors, as well as host-specific proteins or inflammatory pathways being activated. Recent studies have demonstrated that targeting pathological factors contributing to enhanced BBB permeability is an effective therapeutic complement to antimicrobial therapy for treating bacterial meningitis. Hence, understanding how these meningitis-causing pathogens affect the BBB permeability will provide novel perspectives for investigating bacterial meningitis’s pathogenesis, prevention, and therapies. Here, we summarized the recent research progress on meningitis-causing pathogens disrupting the barrier function of BBB. This review provides handy information on BBB disruption by meningitis-causing pathogens, and helps design future research as well as develop potential combination therapies.

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Transcriptional landscape of human neuroblastoma cells in response to SARS-CoV-2

Cited by 3 publications

References 55 publications

Viral Entry Inhibitors Protect against SARS-CoV-2-Induced Neurite Shortening in Differentiated SH-SY5Y Cells

Viral Entry Inhibitors Protect against SARS-CoV-2-Induced Neurite Shortening in Differentiated SH-SY5Y Cells

Emerging role of non-coding RNAs in neuroinflammation mediated by microglia and astrocytes

Blood–Brain Barrier Integrity Damage in Bacterial Meningitis: The Underlying Link, Mechanisms, and Therapeutic Targets

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