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RNA sequencing of L4-L6 mouse Dorsal Root Ganglia 3 days post sciatic nerve crush and naive following 10 days of Indole-3-propionic acid treatment

ABSTRACT: Purpose: compare the response of DRG neurons to indole-3-propionic acid treatment before and after sciatic nerve injury Results: we found that IPA induced transcription changes before and after injury inside the DRG tissue. In particular expression of immune system related genes

ORGANISM(S): Mus musculus

PROVIDER: GSE161342 | GEO | 2022/01/01

REPOSITORIES: GEO

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RNA sequencing of L4-L6 mouse Dorsal Root Ganglia 3 days post sciatic nerve crush and naive following 10 days of Indole-3-propionic acid treatment

Project description:RNA sequencing of L4-L6 mouse Dorsal Root Ganglia 3 days post sciatic nerve crush and naive following 10 days of Indole-3-propionic acid treatment

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H3K9ac, H3K27ac, H3K27me3 ChIP sequencing and ATAC sequencing of L4-L6 Dorsal Root Ganglia upon spinal or sciatic axonal injury

Project description:Purpose: compare the epigenetic response of DRG neurons to an axonal injury in the peripheral vs central nervous system by measuring accessible chromatin and several histone marks Results: we found that after peripheral axonal injury there is a much greater number of epigenetic changes than after central spinal injury, and that these epigenetic changes after peripheral axotomy tended toward increased chromatin accessibility.

2019-06-19 | GSE108806 | GEO

Gut-derived indole propionic acid alleviates liver fibrosis by modulating pro-fibrogenic macrophage phenotype and biological function

Project description:Recently, gut metabolites have been recognized to play significant roles in liver diseases via the gut-liver axis. In this study, we investigate the regulatory effects of the tryptophan metabolite, indole-3-propionic acid (IPA), on immune cells during liver fibrogenesis using single-cell RNA sequencing (scRNA-seq).

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scRNAseq analysis of mouse L4 whole dorsal root ganglions following sciatic nerve cush, dorsal root crush and spinal cord injury

Project description:After an injury in the adult mammalian central nervous system, lesioned axons fail to regenerate. This failure to regenerate contrasts with the remarkable potential of axons to grow following an injury in the peripheral nervous system. Peripheral sensory neurons with cell soma in dorsal root ganglia (DRG) switch to a regenerative state after nerve injury to enable axon regeneration and functional recovery. Decades of research have focused on the signaling pathways elicited by injury in sensory neurons and in Schwann cells that insulate axons as central mechanisms regulating nerve repair. However, neuronal microenvironment is far more complex and is composed of multiple cell types including endothelial, immune and glial cells. Whether the microenvironment surrounding neuronal soma contribute to the poor regenerative outcomes following central injuries remains largely unexplored. To answer this question, we performed a single cell transcriptional profiling of the DRG neuronal microenvironment response to peripheral and central injuries. In dissecting the roles of the microenvironment contribution, we have focused on a poorly studied glia population of Satellite Glial Cells (SGC) surrounding the neuronal cell soma. Upon a peripheral injury, SGC contribute to axon regeneration via Fatty acid synthase (Fasn)-PPARα signaling pathway. Our analysis reveals that in response to central injuries, SGC do not activate the PPAR signaling pathway. However, induction of this pathway with fenofibrate, an FDA- approved PPARα agonist used for dyslipidemia treatment, rescued axon regeneration following an injury to the central nerves. Collectively, our results uncovered a previously unappreciated role of the neuronal microenvironment differential response in central and peripheral injuries.

2021-09-12 | GSE158892 | GEO

ATAC sequencing and RNA sequencing of L4-L6 mouse Dorsal Root Ganglia upon dorsal column axotomy plus injection of the histone deacetylase inhibitor MS275

Project description:Purpose: compare the response of DRG neurons to a central axonal injury in presence of histone deacetylase inhibitor by measuring accessible chromatin and transcription Results: we found that MS-275 was able to induce changes in chromatin accessibility and gene expression. In particular, an increased accessibility correlated with changes in gene expression, and a decreased accessibility correlated with gene downregulation

2019-06-19 | GSE132382 | GEO

scRNAseq analysis of mouse L4 whole dorsal root ganglions with and without sciatic nerve crush injury

Project description:Peripheral sensory neurons with cell body in dorsal root ganglia (DRG) switch to a regenerative state after nerve injury to enable axon regeneration and functional recovery. Studies of nerve injury responses in sensory neurons have revealed signaling and transcriptional mechanisms that increase their intrinsic regenerative capacity. However, the extent to which satellite glial cells (SGC), which completely surround the neuronal soma contribute to these responses remains unexplored. Using single cell RNA-seq, we defined the transcriptional profile of SGC in naïve and injured conditions and identified Fabp7, also known as BLBP, as a novel marker of SGC. We report that nerve injury elicits gene expression changes in SGC, which are mostly related to lipid metabolism, specifically fatty acid synthesis and the peroxisome proliferator-activated receptor (PPAR) signaling. Conditional deletion of Fatty acid synthase (Fasn), the key enzyme in de novo fatty acid synthesis, specifically in SGC, impairs axon regeneration. Treatment with fenofibrate, a PPARa agonist, rescues the impaired regeneration, suggesting that PPRAa, which belongs to a family of lipid regulated transcription factors, functions downstream of fatty acid synthesis in SGC to promote axon regeneration. These results unravel fatty acid synthesis in SGC as a fundamental novel mechanism mediating axon regeneration in mature peripheral nerves.

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HDAC3 ChIP sequencing of L4-L6 Dorsal Root Ganglia upon spinal or sciatic axonal injury

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Gut-derived indole propionic acid alleviates liver fibrosis by modulating pro-fibrogenic macrophage phenotype and biological function

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New Indole-3-Propionic Acid and 5-Methoxy-Indole Carboxylic Acid Derived Hydrazone Hybrids as Multifunctional Neuroprotectors.

Project description:In light of the known neuroprotective properties of indole compounds and the promising potential of hydrazone derivatives, two series of aldehyde-heterocyclic hybrids combining those pharmacophores were synthesized as new multifunctional neuroprotectors. The obtained derivatives of indole-3-propionic acid (IPA) and 5-methoxy-indole carboxylic acid (5MICA) had good safety profiles: Hemolytic effects < 5% (200 μM) and IC50 > 150 µM were found in the majority of the SH-SY5Y and bEnd3 cell lines. The 2,3-dihydroxy, 2-hydroxy-4-methoxy, and syringaldehyde derivatives of 5MICA exhibited the strongest neuroprotection against H2O2-induced oxidative stress in SH-SY5Y cells and 6-OHDA-induced neurotoxicity in rat-brain synaptosomes. All the compounds suppressed the iron-induced lipid peroxidation. The hydroxyl derivatives were also the most active in terms of deoxyribose-degradation inhibition, whereas the 3,4-dihydroxy derivatives were able to decrease the superoxide-anion generation. Both series of compounds showed an increased inhibition of hMAO-B, with greater expression detected in the 5MICA hybrids. The in vitro BBB model with the bEnd3 cell line showed that some compounds increased the permeability of the endothelial monolayer while maintaining the tight junctions. The combined results demonstrated that the derivatives of IPA and 5MICA showed strong neuroprotective, antioxidant, MAO-B inhibitory activity and could be considered as prospective multifunctional compounds for the treatment of neurodegenerative disorders.

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Mouse DRG RNA-Seq

Project description:Multiple myeloma (MM) is a neoplasia of B plasma cells that often induces bone pain. However, the mechanisms underlying myeloma-induced bone (MIBP) pain are mostly unknown. Using a localized MM mouse model, we investigated MM induced gene expression changes in the dorsal root ganglia (DRG) innervating the MM-bearing bone and found alterations in pathways associated with cell cycle, immune response and neuronal signalling. The MM transcriptional signature was consistent with metastatic MM infiltration to the DRG, a never-before described feature of the disease that we further demonstrated histologically. In the DRG, MM cells caused loss of vascularization and neuronal injury, which may contribute to late-stage MIBP.

2023-06-26 | GSE216802 | GEO

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