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Transcriptional profiling of microglia in the injured brain reveals distinct molecular features underlying neurodegeneration

ABSTRACT: We applied whole transcriptome analysis of microglia acutely isolated at different timepoints after a cortical stab wound injury to gain insight into genes that might be dysregulated and transcriptionally different between males and females after cortical injury.

ORGANISM(S): Mus musculus

PROVIDER: GSE163691 | GEO | 2021/02/22

REPOSITORIES: GEO

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Smartseq3 Single-cell RNA-seq analysis of acutely FACS-purified tdTomato+ astrocyte derived cells from aged injured mice in vivo

Project description:To investigate the mechanisms that underlie astrocyte dedifferentiation, we performed single cell RNA sequencing analysis of tdTomato+ astrocyte derived cells approx 1 year after stab-wound injury. 2-3 month old GFAP-CreERT2;p53flox/flox;LSL-tdTomato (p53Gfap-icKO) mice were subjected to intracortical endoxifen injection to enable deletion of p53 gene and simultaneous expression of tdTomato for fate-mapping specifically in astrocytes (GFAP+) in the context of a stab-wound injury. GFAP-CreERT2;p53wt/wt;LSL-tdTomato (p53Gfapwt/wt) mice were used as control whereby p53 remains fate-mapped tdTomato+ astrocytes remain p53 wildtype after endoxifen injection. Approx 10-12 months after injury, mice were sacrificed and the peri-wound region was dissected. Mice of the same genotypes were pooled (3 p53Gfap-icKO and 2 p53Gfapwt/wt) and digested using the Miltenyi Adult brain dissociation kit. Single cell suspension was FACS sorted for tdTomato+ cells into 384 well plates and then Smartseq3 libraries were generated.

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Transcription profiling of mouse rat cortical axons from un-injured and injured animals isolated after 13 days in culture

Project description:Efficient growth cone regeneration requires protein synthesis in the adult mammalian brain and spinal cord. Recent evidence suggests that the local availability of protein synthesis machinery in adult mammalian axons may be an indicator of their regenerative capacity. Here we investigated the local protein synthesis capacity in matured cortical axons, which have poor regenerative capacity, yet are critical for recovery following injury due to traumatic brain injury and stroke. This work is the first to biochemically isolate and identify mRNA from mammalian cortical axons, making use of a unique microfluidic platform to isolate axons free of other cellular debris. We first sought to identify mRNA in naÃ¯ve axons that makes up the pool of mRNA available for translation initiated following axotomy. Next, we investigated changes in the mRNA population localized to axons 2 days following axotomy and growth cone regeneration. Experiment Overall Design: Cortical axons were harvested using the compartmentalized microfluidic platform after 13 days in culture at a time when they express mature synaptic proteins. A total of 7 Genechips were used for the uninjured cortical axons from 3 different culture batches. 3 Genechips were used for neurons isolated from the neuronal compartment of the microfluidic platfrom. The neuronal Genechip were used to compare mRNA populations with axonal Genechips and for quality control purposes. 3 Genechips were used for regenerating axons; for these, axons were axotomized at 11 days in culture, then allowed to regrow for 2 days before harvesting.

2009-01-14 | E-GEOD-11730 | biostudies-arrayexpress

mRNAs in un-injured and injured rat cortical axons isolated after 13 days in culture

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RNA-seq of Injured Nerve in Schwann cell conditional knockout of Eed

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analysis of the immune and astrocytic cell fraction 12h after cortical injury in Sema4B knockout mice

Project description:After central nervous system injury, a rapid neuroinflammatory response is induced. This response can be both beneficial and detrimental to neuronal survival in the first few days and increase the risk for neurodegeneration if it persists. Semaphorin4B (Sema4B), a transmembrane protein primarily expressed by cortical astrocytes, has been shown to play a role in neuronal cell death following injury. Our study shows that neuroinflammation is attenuated in Sema4B knockout mice and microglia/macrophage activation is reduced after cortical stab wound injury. In vitro, recombinant Sema4B enhances the activation of microglia following injury, suggesting astrocytic Sema4B functions as a ligand. Moreover, injury-induced activation of microglia is attenuated in the presence of Sema4B knockout astrocytes compared to heterozygous astrocytes. In vitro, experiments indicate Plexin-B2 is the Sema4B receptor on microglia. Consistent with this, microglia-specific Plexin-B2 knockout mice, similar to Sema4B knockout mice, also show a reduction in microglial activation after cortical injury. Finally, in Sema4B/Plexin-B2 double heterozygous mice, microglial activation is also reduced after injury, thus supporting the idea that both Sema4B and Plexin-B2 are part of the same signaling pathway. Taken together, we propose a model in which following injury, astrocytic Sema4B enhances the pro-inflammatory response of microglia/macrophages via Plexin-B2, leading to increased neuroinflammation.

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Project description:Decreasing the activation of pathology-activated microglia is crucial to prevent chronic inflammation and tissue scarring. In this study, we used a stab wound injury model in zebrafish and identified an injury-induced microglial state characterized by the accumulation of lipid droplets and TAR DNA-binding protein of 43 kDa (TDP-43)+ condensates. Granulin-mediated clearance of both lipid droplets and TDP-43+ condensates was necessary and sufficient to promote the return of microglia back to the basal state and achieve scarless regeneration. Moreover, in postmortem cortical brain tissues from patients with traumatic brain injury, the extent of microglial activation correlated with the accumulation of lipid droplets and TDP-43+ condensates. Together, our results reveal a mechanism required for restoring microglia to a nonactivated state after injury, which has potential for new therapeutic applications in humans.

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Transcriptional profiling of microglia in the injured brain reveals distinct molecular features underlying neurodegeneration

Project description:Transcriptional profiling of microglia in the injured brain reveals distinct molecular features underlying neurodegeneration

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Expression data from injured murine kidney

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2013-03-01 | E-GEOD-42247 | biostudies-arrayexpress

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