Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1303812 | ENA |
REPOSITORIES: ENA
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Project description:This study presents the first application of comprehensive single-nuclei RNA sequencing (snRNA-seq) of dorsal root ganglion (DRG) neurons in a rat model using Parse technology. Our dataset includes two experimental models: (1) control rats representing both sexes and (2) rats with disc-associated chronic lower back pain, alongside sham-treated animals. By leveraging high-resolution transcriptomic profiling, this study provides novel insights into the molecular landscape of DRG neurons, offering a valuable resource for understanding the cellular mechanisms underlying chronic pain.
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Project description:Preconditioning nerve injury drives pro-regenerative perineuronal macrophage activation in dorsal root ganglia (DRG). The present study reports that oncomodulin (ONCM) is produced from the regeneration-associated macrophages (RAMs) and strongly influences regeneration of DRG sensory axons. ONCM in macrophages was necessary to produce RAMs in the in vitro model of neuron-macrophage interaction and played an essential role in for preconditioning-induced neurite outgrowth. In order to gain insight on potential mechanisms downstream of ONCM for potent neurite outgrowth activity, we performed RNA-seq using cultured DRG neurons treated with ONCM.
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Project description:To explore the changes of local microenvironment in the feto-maternal interface during early pregnancy in RSA, we next examined the transcriptional profiles of the decidua tissue by RNA sequencing using samples from 3 RSA patients and 3 healthy controls
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Project description:Botulinum Neurotoxin A1 (BoNT/A1) is an effective treatment for chronic migraines, but its direct mechanism of action on human sensory neurons has not been tested. While rodent studies on dorsal root ganglion (DRG) and trigeminal ganglion (TG) show that BoNT/A1 inhibits neurotransmission, including calcitonin gene-related peptide (CGRP) release, by cleaving SNAP-25, only one previous study has assessed its effect on human DRG neurons . The objective of this study was to understand the mechanism of action of BoNT/A1 in human sensory neurons and assess, using RNA sequencing, the transcriptomic consequences of BoNT/A1 treatment. Using DRGs obtained from organ donors the expression of key targets, including SNAP25, SV2C, & CALCA, was validated by mining existing transcriptomic datasets as well as immunohistochemistry. Cultured dissociated human DRG neurons treated with BoNT/A1 were used to examine cleavage of SNAP25, release of CGRP and transcriptomic changes after BoNT/A1 treatment. SV2C was found to be widely expressed in human DRG neurons in a pattern that completely overlapped with CGRP expression. Consistent with this finding, BoNT/A1 disrupted SNARE protein complexes in human DRG neurons as demonstrated by SNAP-25 cleavage in most somatosensory neurons and a reduction in capsaicin-evoked CGRP release, indicating impaired vesicle fusion. Moreover, Bulk RNA sequencing experiments revealed downregulated expression of a large subset of genes responsible for neurotransmitter and neuropeptide release from neurons suggesting a novel mechanism through which BoNT/A regulates neurotransmission. These results provide new insight into the molecular mechanisms by which BoNT/A may exert its pain-relieving effects in humans.
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Project description:We employed LC-MS/MS to determine downstream targets of the stem cell factor (SCF)/c-Kit axis in the dorsal root ganglion (DRG). Briefly, we dissected lumbar DRG from male C57BL/6 mice and treated ex vivo with vehicle or SCF for 10 min or 1 hour. DRG were then subjected to LC-MS/MS.
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