Shock waves induce an evolutionary conserved mechanism of spinal cord regeneration via Toll-like receptor 3
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ABSTRACT:
PROVIDER: PRJNA628694 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11616276.fastq.gz | Fastqsanger.gz | |||
| SRR11616277.fastq.gz | Fastqsanger.gz | |||
| SRR11616278.fastq.gz | Fastqsanger.gz | |||
| SRR11616279.fastq.gz | Fastqsanger.gz |
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Project description:Shock wave therapy (SWT) is improving motor function and decreasing lesion size in wild-type but not Tlr3-/- mice via IL6 dependent differentiation of neuronal progenitor cells. Both SWT and TLR3 stimulation enhance neuronal sprouting and survival, even in human spinal cord cultures. We could also identify tlr3 as a crucial enhancer of spinal cord generation in zebrafish. In order to substantiate underlying mechanisms of the SWT for spinal cords, cultured human neurons (neuroblastoma cell line) were treated with SWT and gene expression profiling were performed by RNAseq.
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Project description:Spinal cord injury (SCI) remains a devastating condition with poor prognosis and very limited treatment options. Affected patients are severely restricted in their daily activities. Shock wave therapy (SWT) has shown potent regenerative properties in bone fractures, wounds, and ischemic myocardium via activation of the innate immune receptor TLR3. Here, we report on the efficacy of SWT for regeneration of SCI. SWT improved motor function and decreased lesion size in WT but not Tlr3-/- mice via inhibition of neuronal degeneration and IL6-dependent recruitment and differentiation of neuronal progenitor cells. Both SWT and TLR3 stimulation enhanced neuronal sprouting and improved neuronal survival, even in human spinal cord cultures. We identified tlr3 as crucial enhancer of spinal cord regeneration in zebrafish. Our findings indicate that TLR3 signaling is involved in neuroprotection and spinal cord repair and suggest that TLR3 stimulation via SWT could become a potent regenerative treatment option.
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Project description:Shock waves are widely used to treat various diseases and have numerous medical applications. In particular, extracorporeal shock waves (ESV) can substantially inhibit tumour growth. However, the therapeutic efficacy of ESV in colorectal cancer and its underlying mechanisms are not well understood. To address this gap in our knowledge, colorectal cancer cell lines HT29 and SW620 were used to generate xenograft mouse models and examined the therapeutic effects of a stepwise increase in ESV energy on tumour growth. In vivo, 60 mJ ESV significantly delayed xenograft growth compared with 120 and 240 mJ ESV, with no impact on body weight or hepatic and renal function. Transcriptome analysis revealed that 60 mJ ESV suppressed colorectal cancer cell proliferation and induced apoptosis and ferroptosis; these findings were further confirmed by immunohistochemical staining and western blotting. The in vitro study showed that ESV mechanistically suppressed cell proliferation and induced apoptosis and ferroptosis by activating the p53 signaling pathway. In conclusion, 60 mJ ESV substantially inhibited colorectal cancer growth by activating p53 pathway-related proliferation inhibition and cell death. These findings indicate that ESV therapy is a promising therapeutic strategy for colorectal cancer.
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Project description:BackgroundReduced pelvic limb reflexes in dogs with spinal cord injury typically suggests a lesion of the L4-S3 spinal cord segments. However, pelvic limb reflexes might also be reduced in dogs with a T3-L3 myelopathy and concurrent spinal shock.Hypothesis/objectivesWe hypothesized that statistical models could be used to identify clinical variables associated with spinal shock in dogs with spinal cord injuries.AnimalsCohort of 59 dogs with T3-L3 myelopathies and spinal shock and 13 dogs with L4-S3 myelopathies.MethodsData used for this study were prospectively entered by partner institutions into the International Canine Spinal Cord Injury observational registry between October 2016 and July 2019. Univariable logistic regression analyses were performed to assess the association between independent variables and the presence of spinal shock. Independent variables were selected for inclusion in a multivariable logistic regression model if they had a significant effect (P ≤ .1) on the odds of spinal shock in univariable logistic regression.ResultsThe final multivariable model included the natural log of weight (kg), the natural log of duration of clinical signs (hours), severity (paresis vs paraplegia), and pelvic limb tone (normal vs decreased/absent). The odds of spinal shock decreased with increasing weight (odds ratio [OR] = 0.28, P = .09; confidence interval [CI] 0.07-1.2), increasing duration (OR = 0.44, P = .02; CI 0.21-0.9), decreased pelvic limb tone (OR = 0.04, P = .003; CI 0.01-0.36), and increased in the presence of paraplegia (OR = 7.87, P = .04; CI 1.1-56.62).Conclusions and clinical importanceA formula, as developed by the present study and after external validation, could be useful for assisting clinicians in determining the likelihood of spinal shock in various clinical scenarios and aid in diagnostic planning.
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Project description:Tissue morphogenesis requires the spatial control over actomyosin contractility to drive cell shape changes. How developmental patterning information controls cell mechanics is poorly understood. In the Drosophila embryo ectoderm, Myosin-II is enriched at the interface between antero-posterior neighboring cells, leading to planar polarized cell intercalation. G protein-coupled receptors (GPCRs) are required for planar polarized Myosin-II activation at junctions and Toll receptors provide a positional code underlying this process. How Toll receptors polarize actomyosin contractility remains unknown. Here we report that cells expressing different levels of a single Toll receptor Toll-8 activate Myosin-II at their interface. Surprisingly, the Toll-8 intracellular domain is not required for signaling at cell interfaces suggesting signaling by proxy. We found that Toll-8 forms a molecular complex with the adhesion GPCR Cirl/Latrophilin that is required for Toll-8 dependent junctional Myosin-II activation. Strikingly, the interfaces between Cirl expressing and cirl mutant cells also activate Myosin-II suggesting that Toll-8 induces Cirl asymmetric signaling at cell interfaces. We further showed that Toll-8 recruits Cirl both in trans and in cis, inducing asymmetric Cirl localization at the boundary of the Toll-8 expression domain. Finally, we found that Toll-8 and Cirl exhibit dynamic interdependent planar polarization when neighboring cells express different levels of Toll-8. Through this feedback, Toll-8 and Cirl self-organize planar polarized signaling.
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