Adapted Murine Sepsis Score: Improving the Research in Experimental Sepsis Mouse Model

Sulzbacher, Maicon Machado; Sulzbacher, Lucas Machado; Passos, Felipe Rafael; Bilibio, Bruna Letícia Endl; Oliveira, Kauana de; Althaus, Wellington Felipe; Frizzo, Matias Nunes; Ludwig, Mirna Stela; Cruz, Ivana Beatrice Mânica da; Heck, Thiago Gomes

doi:10.1155/2022/5700853

Cited by 6 publications

(2 citation statements)

References 39 publications

(47 reference statements)

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“…A similar result was observed when using a fluorescent virus to track the spinal tract’s downward projection: axons were present closer to the scar boundary in the loose group than in the vehicle group ( Figures 3C–E ). The weight of the mice was recorded as an index to evaluate the overall health status ( Sulzbacher et al, 2022 ). We found that the body weight of the PLX3397 group was slightly higher than that of the wild type after surgery ( Figure 3F and Supplementary Figure S1D ).…”

Section: Resultsmentioning

confidence: 99%

Continual Deletion of Spinal Microglia Reforms Astrocyte Scar Favoring Axonal Regeneration

Xia

Tang

et al. 2022

Front. Pharmacol.

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Astrocyte scar formation after spinal cord injury (SCI) efficiently limits the accurate damage but physically restricts the following axon regeneration. Lately, fine tuning scar formation is becoming a novel strategy to develop SCI treatment, yet how to leverage these opposite effects remains challenging. Here, utilizing an improved drug administration approach, we show that in a mouse model of spinal cord injury, continual deletion of microglia, especially upon scar formation, by pexidartinib decreases the amount of microglia-derived collagen I and reforms the astrocyte scar. The astrocytes become less compacted in the scar, which permits axon regeneration and extension. Although continual microglia deletion did not significantly improve the locomotive performance of the SCI mice, it did ameliorate their weight loss, possibly by improving their relevant health conditions. We thus identified a novel approach to regulate astrocyte scars for improved axon regeneration, which is indicative of the clinical treatment of SCI patients.

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Section: Resultsmentioning

confidence: 99%

Continual Deletion of Spinal Microglia Reforms Astrocyte Scar Favoring Axonal Regeneration

Xia

Tang

et al. 2022

Front. Pharmacol.

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“…4B). The murine sepsis score (MSS) is used to assess the severity of sepsis in mice based on observational characteristics 20 . The results showed that murine sepsis symptoms alleviated in the RIPK3 −/− mice (Fig.…”

Section: Ripk3 Regulated Htnv Replication Through Jak-stat Pathwaysmentioning

confidence: 99%

RIPK3 Promotes Hantaviral Replication by Restricting JAK-STAT Signaling but not Triggering Necroptosis.

Zhang

et al. 2022

Preprint

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Hantaan virus (HTNV) is a rodent-borne virus that can cause hemorrhagic fever with renal syndrome (HFRS) with a case fatality rate of 15% and is listed as a re-emerging infectious disease (REID) in China. At present, no specific therapeutic strategies against HTNV are available. Interferon (IFN) is a crucial antiviral molecular which can trigger interferon-stimulated genes (ISGs) expression through the Janus kinase-signal transducer and activator of transcription 1 (JAK-STAT) pathway. Large quantities of IFN produced at the late stage of HTNV infection could not effectively restrain viral replication, the mechanism of which is still unclear. Here, we identified the receptor-interacting protein kinase 3 (RIPK3), a critical molecular to mediate necroptosis, could facilitate HTNV infection by blocking JAK/STAT signaling. HTNV infection promoted the total expression level of RIPK3, but not the phosphorylation of RIPK3, thus not leading to cell death. RIPK3 ablation could restrain HTNV replication by enhancing the expression of multiple ISGs, during which the type I IFN generation did not strengthened. Exogenously expressing RIPK3 might hinder the host anti-hantaviral responses. RIPK3−/− mice also maintained a robust ability to clear HTNV promptly with enhanced innate immune responses. Mechanistically, RIPK3 restricted STAT1 activation by bonding to STAT1 and blocking its phosphorylation sites, hence interfering with host IFN responses. Overall, these observations demonstrated a noncanonical function of RIPK3 during viral infection, and shed light on the novel evasion strategy of host innate immunity by HTNV.

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Electroacupuncture pre-treatment exerts a protective effect on LPS-induced cardiomyopathy in mice through the delivery of miR-381 via exosomes

Chen,

Zhang

et al. 2024

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Adapted Murine Sepsis Score: Improving the Research in Experimental Sepsis Mouse Model

Cited by 6 publications

References 39 publications

Continual Deletion of Spinal Microglia Reforms Astrocyte Scar Favoring Axonal Regeneration

Continual Deletion of Spinal Microglia Reforms Astrocyte Scar Favoring Axonal Regeneration

RIPK3 Promotes Hantaviral Replication by Restricting JAK-STAT Signaling but not Triggering Necroptosis.

Electroacupuncture pre-treatment exerts a protective effect on LPS-induced cardiomyopathy in mice through the delivery of miR-381 via exosomes

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