Molecular basis of mitomycin C enhanced corneal sensory nerve repair
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA474682 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7264030.fastq.gz | Fastqsanger.gz | |||
| SRR7264040.fastq.gz | Fastqsanger.gz | |||
| SRR7264050.fastq.gz | Fastqsanger.gz | |||
| SRR7264031.fastq.gz | Fastqsanger.gz | |||
| SRR7264041.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 32 |
Similar Datasets
Project description:We performed RNASeq and confocal imaging analysis to characterize the gene expression changes in the cornea after wounding that modulate sensory axon integrity. We show that by preserving the ability of axons to attach to one another and to corneal epithelial cells, mitomycin C enhances sensory nerve recovery after mechanical injury.
2018-12-01 | GSE115355 | GEO
Project description: Not available
| S-EPMC6240058 | biostudies-literature
Project description:Corneal nerve, originated from trigeminal ganglia, play an important role in conreal sensation and homeotasis. Under disease conditions when corneal nerves are damaged, such as diabetes, corneal injury, or eye surgury, patients suffer from dry eye, pain, delayed wound healing, or urceration. Current treatments are limited, underscoring the need for a regenerative therapy. Here we show that a non-invasive neural modulation therapy, transcutaneous electrical stimulation (ES), significantly restore the nerve density and sensory function in both streptozotocin-induced diabetes mice and keratectomy model. This transcriptomics analysis of TGs from in vivo ES in keratectomy models aims to find mechanistic insights into the ES-induced corneal reinnervation. The results point to ion transport and Ca2+ signaling alteration, alongside activation of neural regeneration pathways. Consistently, membrane potential recording in TGs shows a rapid hyperpolarization upon ES accompanied by increased [Ca2+]i level. Inhibition of potassium intermediate/small conductance calcium-activated channel (KCNN) abolishes the hyperpolarization and neural regeneration effect, whereas activation of KCNN channel significantly enhances nerve regeneration in the STZ model compared with sham treatment. Overall, ES restores corneal nerve density and function via KCNN activation in a diabetic mouse model, offering a novel, non-invasive, and clinically translatable therapeutic strategy for diabetic neuropathy.
2026-07-15 | GSE330561 | GEO
Project description:Purpose: Pitx2-associated developmental glaucoma is characterized by anterior segment dysgenesis, ocular hypertension, and optic neuropathy. Its consequences for corneal sensory innervation remain poorly understood. We investigated whether this disease alters corneal nerve structure and sensory function in a sex-dependent manner. Methods: Male and female Pitx2egl1/egl1 and Pitx2+/+ mice were examined at 1 and 3 months. Ocular phenotyping included intraocular pressure, fundus imaging, visual evoked potentials, and optic nerve ultrastructure. RNA sequencing of corneas and trigeminal ganglia was performed at 3 months. Corneal innervation was assessed by βIII-tubulin immunofluorescence and volumetric quantification of nerve fibers. Corneal sensitivity was measured using Von Frey filaments. Results: Pitx2egl1/egl1 mice developed progressive ocular hypertension, fundus abnormalities, reduced visual evoked potential amplitudes, and optic nerve degeneration, supporting the model as early-onset glaucoma. Baseline sex-related transcriptional differences were limited in both cornea and trigeminal ganglia. In contrast, Pitx2 mutation induced sex-dependent molecular responses. Female corneas showed broader transcriptional changes enriched in inflammatory, stress-response, and tissue-remodeling pathways, whereas male corneas showed a more restricted response involving metabolic and homeostatic processes. Similar sex divergence was observed in trigeminal ganglia. Corneal nerve fiber volume was reduced in both sexes at 3 months but not at 1 month, whereas reduced sensitivity was detected only in mutant males. Conclusions: This study identifies corneal denervation as a component of Pitx2-associated developmental glaucoma. These findings suggest that glaucoma may affect the corneal sensory system beyond optic nerve pathology, highlighting a potentially overlooked dimension of disease relevant to ocular surface monitoring and patient management.
2026-07-12 | GSE336875 | GEO
Project description:Purpose: Pitx2-associated developmental glaucoma is characterized by anterior segment dysgenesis, ocular hypertension, and optic neuropathy. Its consequences for corneal sensory innervation remain poorly understood. We investigated whether this disease alters corneal nerve structure and sensory function in a sex-dependent manner. Methods: Male and female Pitx2egl1/egl1 and Pitx2+/+ mice were examined at 1 and 3 months. Ocular phenotyping included intraocular pressure, fundus imaging, visual evoked potentials, and optic nerve ultrastructure. RNA sequencing of corneas and trigeminal ganglia was performed at 3 months. Corneal innervation was assessed by βIII-tubulin immunofluorescence and volumetric quantification of nerve fibers. Corneal sensitivity was measured using Von Frey filaments. Results: Pitx2egl1/egl1 mice developed progressive ocular hypertension, fundus abnormalities, reduced visual evoked potential amplitudes, and optic nerve degeneration, supporting the model as early-onset glaucoma. Baseline sex-related transcriptional differences were limited in both cornea and trigeminal ganglia. In contrast, Pitx2 mutation induced sex-dependent molecular responses. Female corneas showed broader transcriptional changes enriched in inflammatory, stress-response, and tissue-remodeling pathways, whereas male corneas showed a more restricted response involving metabolic and homeostatic processes. Similar sex divergence was observed in trigeminal ganglia. Corneal nerve fiber volume was reduced in both sexes at 3 months but not at 1 month, whereas reduced sensitivity was detected only in mutant males. Conclusions: This study identifies corneal denervation as a component of Pitx2-associated developmental glaucoma. These findings suggest that glaucoma may affect the corneal sensory system beyond optic nerve pathology, highlighting a potentially overlooked dimension of disease relevant to ocular surface monitoring and patient management.
2026-07-12 | GSE336872 | GEO
Project description:Peripheral nerve repair and functional recovery depend on the rate of nerve regeneration and the quality of target reinnervation. It is important to fully understand the cellular and molecular basis underlying the specificity of peripheral nerve regeneration, which means the achieving of respective correct pathfinding and accurate target reinnervation for regrowing motor and sensory axons. In this study, a quantitative proteomic technique, based on isobaric tags for relative and absolute quantitation (iTRAQ) was used to profile the protein expression pattern between single motor and sensory nerves at 14 days after peripheral nerve transection. Among a total of 1259 proteins identified, 176 proteins showed the differential expressions between injured motor and sensory nerves. Quantitative real-time RT-PCR and Western blot analysis were applied to validate the proteomic data on representative differentially expressed proteins. Functional categorization indicated that differentially expressed proteins were linked to a diverse array of molecular functions, including axonogenesis, response to axon injury, tissue remodeling, axon ensheathment, cell proliferation and adhesion, vesicle-mediated transport, response to oxidative stress, internal signal cascade, and macromolecular complex assembly, which might play an essential role in peripheral motor and sensory nerve regeneration. Overall, we hope that the proteomic database obtained in this study could serve as a solid foundation for the comprehensive investigation of differentially expressed proteins between injured motor and sensory nerves and for the mechanism elucidation of the specificity of peripheral nerve regeneration.
2020-12-10 | PXD022097 | Pride
Project description:In this study, a quantitative proteomic technique based on isobaric tags for relative and absolute quantitation (iTRAQ) was used to compare the proteome of cultured sensory and motor nerve fibroblasts (Fbs). Among a total of 2597 overlapping proteins identified, we obtained 148 differentially expressed proteins, of which 116 proteins were significantly higher expressed in sensory Fbs, and 32 proteins were significantly higher expressed in motor Fbs. Western blot and qPCR analysis were applied to validate differentially expressed proteins. Functional categorization indicated that differentially expressed proteins were linked to a diverse array of biological processes , including regeneration, axon guidance, cytoskeleton organization, cell proliferation, cell migration, cell adhesion, and tissue remodeling, which might play a critical role in the specificity of peripheral nerve regeneration. Furthermore, following co-culture of motor neurons with motor or sensory Fbs , motor Fbs significantly enhanced neurite growth than sensory Fbs. These findings indicated that nerve Fbs expressed the distinct motor and sensory phenotypes involved in different patterns of protein expression, biological processes, and effects on neurons.
2023-03-11 | PXD034827 | Pride
Project description:Sensory cells of the gut epithelium and vagus nerve are key regulators of various physiological processes including satiety and metabolism. In this study, we profile sensory cells of the gut (enteroendocrine cells, EECs) and vagus nerve (neurons) using 10X Genomics single cell sequencing.
2025-10-27 | GSE295033 | GEO
Project description:We performed the RNA-seq analysis to unravel the underlying mechanism of corneal nerve regeneration after treatment with our identified RvD6 isomer and RvD6 standard.
2020-03-18 | GSE138685 | GEO
Project description:Any person that has broken a bone can attest to the existence of sensory innervation of the skeleton. Beyond afferent functions, sensory neurons have been implicated in the orchestration of bone repair via the release of neuroregulatory signals. Yet, these neurosecretory effects have principally been deciphered through loss-of-function studies. Indeed, the potential therapeutic benefit of boosting nerve-to-bone interactions remains cursorily studied. Here, using a mouse calvarial bone defect model, pharmacologic activation of TrkA with a small molecule partial agonist induced bone-associated nerve ingrowth and significantly improved calvarial bone healing. Single-cell RNA sequencing analysis of cells from the defect site revealed shifts in cluster proportions, with enrichment of immune cell populations in TrkA agonist-treated mice. Within the skeletal cell lineage, TrkA agonism enhanced osteoblast differentiation while suppressing fibroblastic differentiation. Pathway analysis showed increased Hedgehog signaling activity, and interactome analyses between trigeminal ganglia sensory neurons and skeletal cells implicated Hedgehog signaling. The pro-regenerative effects of TrkA agonism were abolished in conditional knockout mice lacking Smoothened (Smo) in PDGFRα+ skeletal progenitor cells. In summary, boosting sensory nerve signaling enhances membranous bone repair after injury, at least in part via Hedgehog pathway activation in osteoprogenitor cells.
2026-02-05 | GSE266598 | GEO