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Effect of Endogenous Stimuli-Responsive Separating Microneedles to Inhibit Hypertrophic Scar on Rabbit Ear

ABSTRACT: Effect of Endogenous Stimuli-Responsive Separating Microneedles to Inhibit Hypertrophic Scar on Rabbit Ear

PROVIDER: PRJNA1069096 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27784820_1.fastq.gz	Fastqsanger.gz
	SRR27784820_2.fastq.gz	Fastqsanger.gz
	SRR27784821_1.fastq.gz	Fastqsanger.gz
	SRR27784821_2.fastq.gz	Fastqsanger.gz
	SRR27784822_1.fastq.gz	Fastqsanger.gz

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Effect of Endogenous Stimuli-Responsive Separating Microneedles to Inhibit Hypertrophic Scar on Rabbit Ear

Project description:Effect of Endogenous Stimuli-Responsive Separating Microneedles to Inhibit Hypertrophic Scar on Rabbit Ear

| PRJNA1071002 | ENA

Effect of Endogenous Stimuli-Responsive Separating Microneedles to Inhibit Hypertrophic Scar on Rabbit Ear

Project description:Hypertrophic scar (HS) considerably affects the appearance and causes tissue dysfunction in patients. Here we show a separating microneedle (MN) consisting of photo-crosslinked GelMA and 5-FuA-Pep-MA prodrug in response to high reactive oxygen species (ROS) levels and overexpression of matrix metalloproteinases (MMPs) in the HS pathological microenvironment. RNA sequencing analyses confirm that drug-loaded MNs could reverse skin fibrosis through down-regulation of BCL-2-associated death promoter (BAD), insulin-like growth factor 1 receptor (IGF1R) pathways, simultaneously regulate inflammatory response and keratinocyte differentiation via up-regulation of toll-like receptors (TOLL), interleukin-1 receptor (IL1R) and keratinocyte pathways.

2024-01-30 | GSE254263 | GEO

Effect of Endogenous Stimuli-Responsive Separating Microneedles to Inhibit Hypertrophic Scar on Rabbit Ear

Project description:Hypertrophic scar (HS) considerably affects the appearance and causes tissue dysfunction in patients. Here we show a separating microneedle (MN) consisting of photo-crosslinked GelMA and 5-FuA-Pep-MA prodrug in response to high reactive oxygen species (ROS) levels and overexpression of matrix metalloproteinases (MMPs) in the HS pathological microenvironment. Bulk and single cell RNA sequencing analyses confirm that drug-loaded MNs could reverse skin fibrosis through down-regulation of BCL-2-associated death promoter (BAD), insulin-like growth factor 1 receptor (IGF1R) pathways, simultaneously regulate inflammatory response and keratinocyte differentiation via up-regulation of toll-like receptors (TOLL), interleukin-1 receptor (IL1R) and keratinocyte pathways, and promote the interactions between fibroblasts and keratinocytes via ligand-receptor pair of proteoglycans 2 (HSPG2)-dystroglycan 1(DAG1). This study reveals the potential therapeutic mechanism of drug-loaded MNs in HS treatment and presents a broad prospect for clinical application.

2024-02-04 | GSE254543 | GEO