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Transcriptional Network Analysis Reveals the Role of miR-223-5p During Diabetic Corneal Epithelial Regeneration

ABSTRACT: Transcriptional Network Analysis Reveals the Role of miR-223-5p During Diabetic Corneal Epithelial Regeneration

PROVIDER: PRJNA748997 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15202500.fastq.gz	Fastqsanger.gz
	SRR15202501.fastq.gz	Fastqsanger.gz
	SRR15202006_1.fastq.gz	Fastqsanger.gz
	SRR15202006_2.fastq.gz	Fastqsanger.gz
	SRR15202007_1.fastq.gz	Fastqsanger.gz

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Transcriptional Network Analysis Reveals the Role of miR-223-5p During Diabetic Corneal Epithelial Regeneration [RNA-seq]

Project description:Diabetes mellitus (DM) is a complex metabolic disorder. Long-term hyperglycemia may induce diabetic keratopathy (DK), which is mainly characterized by delayed corneal epithelial regeneration. MicroRNAs (miRNAs) have been reported to play regulatory roles during tissue regeneration. However, the molecular mechanism by which miRNAs influence epithelial regeneration in DK is largely unknown. In this study, we performed miRNA and mRNA sequencing of regenerative corneal epithelium tissue from streptozotocin-induced type 1 diabetic (T1DM) and wild-type mice to screen for differentially expressed miRNAs and mRNAs. Based on regulatory network analysis, miR-223-5p was selected for subsequent experiments and Hpgds was then identified as a direct target gene. MiR-223-5p downregulation significantly promoted diabetic corneal epithelial wound healing and nerve regeneration. However, the beneficial effects of miR-223-5p inhibition were abolished by an Hpgds inhibitor. Furthermore, mechanistic studies demonstrated that miR-223-5p suppression ameliorated inflammation and enhanced cell proliferation signaling in DK. Taken together, our findings revealed that the regulatory role of miR-223-5p in diabetic corneal epithelial and nerve regeneration by mediating inflammatory processes and cell proliferation signaling. And silencing miR-223-5p may contribute to the development of potential therapeutic strategies for DK.

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Transcriptional Network Analysis Reveals the Role of miR-223-5p During Diabetic Corneal Epithelial Regeneration [miRNA-seq]

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Transcriptional Network Analysis Reveals the Role of miR-223-5p During Diabetic Corneal Epithelial Regeneration [RNA-seq]

Project description:Transcriptional Network Analysis Reveals the Role of miR-223-5p During Diabetic Corneal Epithelial Regeneration [RNA-seq]

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Transcriptional Network Analysis Reveals the Role of miR-223-5p During Diabetic Corneal Epithelial Regeneration [miRNA-seq]

Project description:Transcriptional Network Analysis Reveals the Role of miR-223-5p During Diabetic Corneal Epithelial Regeneration [miRNA-seq]

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scRNAseq of diabetic corneal epithelium

Project description:We performed single cell transcriptional profiling of mouse corneal epithelium in streptozotocin-induced diabetic mice.

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Oxidative stress-regulatory role of miR-10b-5p in the diabetic human cornea revealed through integrated multi-omics analysis

Project description:The corneal epithelium is maintained by limbal epithelial stem cells (LESCs) and are largely responsible for corneal optical transparency and protection by continuous population of corneal epithelial cells. Diabetes mellitus (DM) has been shown to affect all structures of the eye including the cornea which can result in delayed wound healing and potential vision loss. MicroRNAs (miRNAs) are short non-coding oligonucleotides that regulate various cellular functions, including oxidative stress response, by repressing translation. miR-10b-5p was previously identified to be upregulated in diabetic vs. non-diabetic limbal cells and our purpose was to understand the role of miR-10b-5p in human limbal epithelial cells in normal and pathological conditions such as diabetes mellitus. It was hypothesized that miR-10b-5p influences corneal epithelial homeostasis by modulating antioxidant defenses and wound healing processes. Through integrated transcriptomic and proteomic analyses, we identified GCLM and LANCL1 as key miR-10b-5p targets, revealing its profound impact on glutathione metabolism, sulfur compound biosynthesis processes, and antioxidant defenses. Our finding suggests that miR-10b suppression disrupts redox balance which potentially leads to heightened oxidative stress, impaired wound healing and increased cellular vulnerability in diabetic corneas. Further research into miR-10b inhibitors or gene modulation strategies may pave the way for novel treatments aimed at mitigating oxidative stress-related corneal dysfunction, particularly in diabetes-induced ocular diseases.

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Integrated genomics and proteomics analysis uncovers the oxidative stress role of miR-10b targets in healthy and diabetic human limbal epithelial cells

Project description:The corneal epithelium is maintained by limbal epithelial stem cells (LESCs) and is largely responsible for corneal optical transparency and protection by continuously renewing population of corneal epithelial cells. Diabetes mellitus (DM) affects all structures of the eye including the cornea, which can result in delayed wound healing and potential vision loss. MicroRNAs (miRNAs) are short non-coding oligonucleotides that regulate various cellular functions, including oxidative stress response, by repressing protein translation. MiR-10b-5p was previously identified to be upregulated in diabetic vs. non-diabetic limbal cells, and our purpose was to understand the role of miR-10b-5p in human limbal epithelial cells in healthy and diabetic conditions. Through integrated transcriptomic and proteomic analyses, we identified GCLM and LANCL1 as key miR-10b-5p targets, revealing its profound impact on glutathione metabolism, sulfur compound biosynthesis processes, and antioxidant defenses. Our findings suggest that overexpression of miR-10b disrupts redox balance, which potentially leads to heightened oxidative stress and increased cellular vulnerability in diabetic corneas. Understanding miR-10b function in corneal epithelial cells may pave the way for novel therapeutic strategies to mitigate oxidative stress and normalize corneal health in diabetic patients.

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