Danio rerio
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA384318 | ENA |
REPOSITORIES: ENA
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Project description:Fibrotic scar tissue formation is conserved throughout the central nervous system in humans and mice, and impairs tissue regeneration and functional recovery. However, the origin of scar-forming stromal fibroblasts is controversial. Here, we show that stromal fibroblasts found after spinal cord injury derive from two populations of perivascular cells that are anatomically and transcriptionally defined as pericytes and perivascular fibroblasts. We identify two distinct perivascular cell populations, which activate and transcriptionally converge on the generation of stromal myofibroblasts after injury. Our results suggest potential targets to improve tissue regeneration and functional recovery after central nervous system injuries.
2024-05-10 | GSE229916 | GEO
Project description:Fibrotic scar tissue formation is conserved throughout the central nervous system in humans and mice, and impairs tissue regeneration and functional recovery. However, the origin of scar-forming stromal fibroblasts is controversial. Here, we show that stromal fibroblasts found after spinal cord injury derive from two populations of perivascular cells that are anatomically and transcriptionally defined as pericytes and perivascular fibroblasts. We identify two distinct perivascular cell populations, which activate and transcriptionally converge on the generation of stromal myofibroblasts after injury. Our results suggest potential targets to improve tissue regeneration and functional recovery after central nervous system injuries.
2024-05-10 | GSE266251 | GEO
Project description:Fibrotic scar tissue formation is conserved throughout the central nervous system in humans and mice, and impairs tissue regeneration and functional recovery. However, the origin of scar-forming stromal fibroblasts is controversial. Here, we show that stromal fibroblasts found after spinal cord injury derive from two populations of perivascular cells that are anatomically and transcriptionally defined as pericytes and perivascular fibroblasts. We identify two distinct perivascular cell populations, which activate and transcriptionally converge on the generation of stromal myofibroblasts after injury. Our results suggest potential targets to improve tissue regeneration and functional recovery after central nervous system injuries.
2024-05-10 | GSE266250 | GEO
Project description:Scar formation is a major hindrance to central nervous system regeneration upon traumatic injury. Glial cells are key players during the wound healing process, and their reaction to injury determines the extent of tissue restoration. Here, we used the regenerative potential of the zebrafish telencephalon to identify specific molecular and cellular mechanisms regulating glial scar formation. We demonstrated that contact of the cerebrospinal fluid with the brain parenchyma after injury activates toll-like receptor 2 (Tlr2) and the chemokine receptor 3 (Cxcr3) innate immunity pathways leading to initiation of a glial scar. These pathways were critical for scarring even after ablation of microglia and infiltrating monocytes. Our data support a specific role for the injury-induced Tlr1/2 and Cxcr3 signaling pathways in controlling proliferation of the oligodendrocyte progenitors and therefore exacerbated glial reactivity, contributing to scar formation. Interference with the Tlr1/2 and Cxcr3 pathways after injury alleviated glial scar formation and improved tissue restoration.
2022-01-18 | GSE98217 | GEO
Project description:Macrophages directly contribute collagen to scar formation during zebrafish heart regeneration and mouse heart repair
| PRJNA390533 | ENA
Project description:Early depletion of primordial germ cells in zebrafish promotes testis formation
| PRJNA245318 | ENA
Project description:Deficiency in hematopoietic phosphatase Ptpn6/Shp1 hyperactivates the innate immune system and impairs control of bacterial infections in zebrafish embryos
| PRJNA150999 | ENA
Project description:Adult zebrafish have the ability to recover from spinal cord injury and exhibit re-growth of descending axons from the brainstem to the spinal cord. We performed gene expression analysis using microarray to find damage-induced genes after spinal cord injury, which shows that Sox11b mRNA is up-regulated at 11 days after injury. However, the functional relevance of Sox11b for regeneration is not known. Here, we report that the up-regulation of Sox11b mRNA after spinal cord injury is mainly localized in ependymal cells lining the central canal and in newly differentiating neuronal precursors or immature neurons. Using an in vivo morpholino-based gene knockout approach, we demonstrate that Sox11b is essential for locomotor recovery after spinal cord injury. In the injured spinal cord, expression of the neural stem cell associated gene, Nestin, and the proneural gene Ascl1a (Mash1a), which are involved in the self-renewal and cell fate specification of endogenous neural stem cells, respectively, is regulated by Sox11b. Our data indicate that Sox11b promotes neuronal determination of endogenous stem cells and regenerative neurogenesis after spinal cord injury in the adult zebrafish. Enhancing Sox11b expression to promote proliferation and neurogenic determination of endogenous neural stem cells after injury may be a promising strategy in restorative therapy after spinal cord injury in mammals. Spinal cord injury or control sham injury was performed on adult zebrafish. After 4, 12, or 264 hrs, a 5 mm segment of spinal cord was dissected and processed (as a pool from 5 animals) in three replicate groups for each time point and treatment.
2010-10-19 | E-GEOD-20460 | biostudies-arrayexpress
Project description:Promoting residential cells, particularly endogenous neural stem and progenitor cells (NSPCs), for tissue regeneration represents a potential strategy for the treatment of spinal cord injury (SCI). However, adult NSPCs differentiate mainly into glial cells and contribute to glial scar formation at the site of injury. Gsx1 is known to regulate the generation of excitatory and inhibitory interneurons during embryonic development of the spinal cord. Here we show that lentivirus-mediated expression of Gsx1 increases the number of NSPCs in a mouse model of lateral hemisection SCI during the acute stage. Subsequently, Gsx1 expression increases the generation of glutamatergic and cholinergic interneurons and decreases the generation of GABAergic interneurons in the chronic stage of SCI. Importantly, Gsx1 reduces reactive astrogliosis and glial scar formation, promotes 5-HT neuronal activity, and improves the locomotor function of the injured mice. Moreover, RNA-seq analysis reveals that Gsx1-induced transcriptome regulation correlates with NSPC signaling, NSPC activation, neuronal differentiation, and inhibition of astrogliosis and scar formation. Collectively, our study provides molecular insights for Gsx1-mediated functional recovery and identifies Gsx1 gene regulation as a potential application for injuries in the spinal cord and possibly other parts of the central nervous system.
2021-05-01 | GSE171441 | GEO