Effect of acupuncture treatments on retinal transcriptome after optic nerve injury
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ABSTRACT:
PROVIDER: PRJNA543831 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9090980_1.fastq.gz | Fastqsanger.gz | |||
| SRR9090980_2.fastq.gz | Fastqsanger.gz | |||
| SRR9090981_1.fastq.gz | Fastqsanger.gz | |||
| SRR9090981_2.fastq.gz | Fastqsanger.gz | |||
| SRR9090982_1.fastq.gz | Fastqsanger.gz |
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Project description:Purpose: We used RNA sequencing to investigate the effect of acupuncture treatment on retinal transcritome after optic nerve injury Methods: Retinal mRNA profiles of 5-week-old wild-type (WT), optic nerve crush injury (ONC), ONC injury with acupuncture treatment at acupoint GB20 (ONC-F) and ONC injury with acupuncture treatment at acupoint BL1 (ONC-J) mice were generated by deep sequencing, in triplicate, using Illumina Hiseq platform. The sequence reads that passed quality filters were analyzed with DESeq2 R package to identify differently expressed genes with padj<0.05. qRT–PCR validation was performed using TaqMan and SYBR Green assays Results: RNA-seq revealed that 436 genes including 31 transcription factors (TFs) were changed after injury, which include many well-known neural degeneration related TFs such as Jun, Ddit3, Atf3 and Atf4. Interestingly, acupuncture treatment at acupoint GB20 (Fengchi) or BL1(Jingming) after ONC injury both resulted in change of retinal gene expression, compared with ONC injury without treatment; furthermore, acupuncture treatment also reversed several gene expression status induced by axon injury. Conclusions: Our research first reported that acupuncture treatment after injury can regulated retinal transcriptome and reversed the gene expression level induced after injury, which will provide novel therapeutic targets for treatment of retinopathy diseases.
2019-11-12 | GSE131486 | GEO
Project description:To investigate the role of aldose reductase (AR) inhibition using Sorbinil on retinal microglia (RMG) activation, retinal ganglion cell (RGC) survival, and axon regeneration after optic nerve trauma. We observed that AR inhibition using Sorbinil attenuates RMG activation and subsequently promotes RGC survival and delays axon degeneration one week after optic nerve crush.
2023-04-05 | GSE200233 | GEO
Project description:Objective: To identify genes that are differentially expressed in retinal ganglion cells undergoing axon regeneration after optic nerve injury. Adult mice that express cyan-fluorescent protein (CFP) in RGCs were treated with pro-regenerative treatment after optic nerve injury. The treated RGCs were selected by FACS (CFP+mcherry) and their RNA profiles were analyzed.
2020-12-29 | GSE142881 | GEO
Project description:Various retinal disorder such as glaucomatous, retinal ischemia reperfusion, and traumatic optic neuropathy, are involved in the pathogenesis of neurodegeneration via glutamate exicitotoxicity. However, the proteomic characteristics and modulation of the neural-microenvironment with NMDA-induced neurodegeneration in retina and optic nerve remain partly understood. We established a protein sketch of NMDA-induced injury by comparing the proteomes of the PBS-operated, NMDA-operated and control groups. We carried out mass spectrometry-based label-free quantitative proteomics to investigate the exicitotoxic neurodegeneration mechanisms and identify key proteins that regulated neural cell death related signaling pathway in retina and optic nerve spatially. Using LC-MS/MS proteomics analysis, in total, we identified 3532 proteins in retina, 2593 proteins in optic nerve. According to Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), the protein changes and energy metabolism in retina and optic nerve tissue were comprehensively evaluated.
2021-12-30 | PXD022466 | Pride
Project description:Various retinal disorder such as glaucomatous, retinal ischemia reperfusion, and traumatic optic neuropathy, are involved in the pathogenesis of neurodegeneration via glutamate exicitotoxicity. However, the proteomic characteristics and modulation of the neural-microenvironment with NMDA-induced neurodegeneration in retina and optic nerve remain partly understood. We established a protein sketch of NMDA-induced injury by comparing the proteomes of the PBS-operated, NMDA-operated and control groups. We carried out mass spectrometry-based label-free quantitative proteomics to investigate the exicitotoxic neurodegeneration mechanisms and identify key proteins that regulated neural cell death related signaling pathway in retina and optic nerve spatially. Using LC-MS/MS proteomics analysis, in total, we identified 3532 proteins in retina, 2593 proteins in optic nerve. According to Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), the protein changes and energy metabolism in retina and optic nerve tissue were comprehensively evaluated.
2021-12-30 | PXD022729 | Pride
Project description:The removal of the Structure Specific Recognition Protein 1 (Ssrp1) gene from retinal ganglion cells has been shown to improve their survival after acute optic nerve injury in mice. To investigate the transcriptional mechanisms underlying the negative regulation of neuronal survival by Ssrp1, we obtained the bulk transcriptome of pooled RGCs at several time points (1, 2, 3, and 4 days) after optic nerve injury.
2025-05-16 | GSE233822 | GEO
Project description:Retinal ganglion cells (RGCs) convey the major output of information collected from the eye to the brain. RGCs are irreversibly lost when injured in degenerative diseases such as glaucoma; this failure can be partially reversed by eliminating the retinal mobile zinc (Zn2+) and leads to substantial axon regeneration. ZnT3 conditional knockout in retinal amacrine cells blocks the synaptic transport of Zn2+, which promotes RGC survival and axonal regeneration in optic nerve jinjury (ONC). Here, we conducted an mRNA sequencing of flow cytometry-isolated RGCs 3 days after optic nerve injury with or without ZnT3 expression in retinal amacrine cells.
2023-07-01 | GSE213937 | GEO
Project description:A major risk factor for glaucomatous optic neuropathy is the level of intraocular pressure (IOP), which can lead to retinal ganglion cell axon injury and cell death. The optic nerve has a rostral unmyelinated portion at the optic nerve head followed by a caudal myelinated region. The unmyelinated region is differentially susceptible to IOP-induced damage in rodent models and in human glaucoma. While several studies have analyzed gene expression changes in the mouse optic nerve following optic nerve injury, few were designed to consider the regional gene expression differences that exist between these distinct areas. We performed bulk RNA-sequencing on the retina and on separately micro-dissected unmyelinated and myelinated optic nerve regions from naïve C57BL/6 mice, mice after optic nerve crush, and mice with microbead-induced experimental glaucoma (total = 36). Gene expression patterns in the naïve unmyelinated optic nerve showed significant enrichment of the Wnt, Hippo, PI3K-Akt, and transforming growth factor β pathways, as well as extracellular matrix–receptor and cell membrane signaling pathways, compared to the myelinated optic nerve and retina. Gene expression changes induced by both injuries were more extensive in the myelinated optic nerve than the unmyelinated region, and greater after nerve crush than glaucoma. Changes present three and fourteen days after injury largely subsided by six weeks. Gene markers of reactive astrocytes did not consistently differ between injury states. Overall, the transcriptomic phenotype of the mouse unmyelinated optic nerve was significantly different from immediately adjacent tissues, likely dominated by expression in astrocytes, whose junctional complexes are inherently important in responding to IOP elevation.
2023-09-06 | GSE241782 | GEO
Project description:Reactive gliosis is a complex process that involves profound changes in gene expression. We used microarray to indentify differentially expressed genes and to investigate the molecular mechanisms of reactive gliosis in optic nerve head in response to optic nerve crush injury. C57Bl/6 female mice were 6-8 weeks old at the time of optic nerve crush surgery. The optic nerve in the left eye was crush 1 mm behind the globe for 10 seconds and the right eye served as contralateral control. The animals were allowed to recover for 1 day, 3 day, 1 week, 3 weeks and 3 months before the optic nerve heads were collected. The naive control mice did not receive any surgery in either eye. Due to the small tissue size of the mouse optic nerve head, two optic nerve heads were pooled together for each microarray chip. The left eyes and the right eyes of two mice were combined respectively to form one pair of experiment and control samples. There were five biological replicates (10 mice) for each condition.
2013-07-15 | E-GEOD-40857 | biostudies-arrayexpress
Project description:We used two groups of C57BL/6J mice, one with optic nerve crush on one eye, and another with no crush as control. Three mice were subjected to optic nerve crush, with sample names 121, 113, 114 and two were used as control with sample names 118 and 119. For the optic nerve crush, a surgical peritomy was made behind and above the eyeball and the eye muscles were gently retracted to expose the optic nerve. Dumont #5 forceps (FST) were used to crush the optic nerve approximately 0.5-1 mm behind the globe without damaging retinal vessels or affecting the blood supply.
2020-05-26 | PXD016197 | Pride