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

ABSTRACT: 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.

ORGANISM(S): Oryctolagus cuniculus

PROVIDER: GSE254263 | GEO | 2024/01/30

REPOSITORIES: GEO

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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

Single cell analysis of iPSC-derived cortical organoids in biofunctionalized gelatin hydrogels

Project description:Human neural organoid models have become an important tool for studying neurobiology. In this work, we compared Matrigel to an N-cadherin peptide-functionalized gelatin methacryloyl hydrogel (termed GelMA-Cad) for culturing cortical neural organoids. Specifically, we compare five materials: (1) Matrigel, (2) GelMA-Cad with high crosslinker (HC), (3) GelMA-Cad with low crosslinker (LC), (4) GelMA HC and (5) GelMA LC. We determined that both mechanical properties and peptide presentation can tune cell fate and diversity in gelatin-based matrices during differentiation. Of particular note, cortical organoids cultured in GelMA-Cad produce higher numbers of neurogenic and ciliated radial glia and upper-layer excitatory neurons—an important population for modeling neurodegenerative disease—compared to GelMA and Matrigel controls.

2024-02-28 | E-MTAB-13828 | biostudies-arrayexpress

The m6A RNA modification modulates gene expression and fibrosis-related pathways in hypertrophic scar

Project description:Purpose: To systematically analyze the overall m6A modification pattern in hyperplastic scars (HS). Methods: The m6A modification patterns in HS and normal skin (NS) tissues were described by m6A sequencing and RNA sequencing, and subsequently bioinformatics analysis was performed. The m6A-related RNA was immunoprecipitated and verified by real-time quantitative PCR. Results: The appearance of 14,791 new m6A peaks in the HS sample was accompanied by the disappearance of 7,835 peaks. The unique m6A-related genes in HS were thus associated with fibrosis-related pathways. We identified the differentially expressed mRNA transcripts in HS samples with hyper-methylated or hypo-methylated m6A peaks. Conclusion: This study is the first to map the m6A transcriptome of human HS, which may help clarify the possible mechanism of m6A-mediated gene expression regulation.

2021-08-08 | GSE181540 | GEO

Microarray profiling analysis of microRNAs expression in Hypertrophic scar

Project description:Excessive repair after burn or trauma will lead to the formation of pathological scar. TGF-β1 is a powerful growth factor after wound healing. It is considered to be a key regulator of HS and various fibrotic diseases. MicroRNAs (miRNAs) can widely participate in the pathophysiological processes of various diseases by participating in post transcriptional gene regulation. At present, there is no research report on miR-361 and hypertrophic scar. This study found that miR-361 in HS is down-regulated. MiR-361 can inhibit the proliferation of HS fibroblasts and promote their apoptosis by inhibiting TGF-β1. Moreover, miR-361 can inhibit the formation of rabbit ear scar by inhibiting the expression of TGF-β1.

2021-11-22 | GSE189134 | GEO

Glucocorticoid promotes fatty acids metabolism in hypertrophic scar tissues and fibroblasts via the microRNA

Project description:Hypertrophic scar (HS) is a skin lesion due to abnormal wound healing after skin injury; histologically, HS is characterized by deposition of excessive amounts of the extracellular matrix and collagen produced by wound healing-induced proliferative fibroblasts. Clinically, HS management includes surgical resection of HS, topical glucocorticoid therapy or drug injections, pressure therapy, fractional carbon dioxide laser therapy, and cryotherapy. In terms of non-surgical therapy, glucocorticoids (like Triamcinolone acetonide, a synthetic corticosteroid medication used topically to treat various skin conditions) was able to effectively inhibit HS formation safely for decades. The effects of glucocorticoids may either be due to its anti-inflammatory, anti-allergenic and immunomodulatory effects or activate fatty acids metabolism by promotion of lipid accumulation in fibroblasts. However, it is no clear why and how glucocorticoids-upregulated fatty acid metabolisms benefit in HS treatment and prevention.And it remains to be defined how altered microRNAs regulated-fatty acid metabolism involved in pathological scars.

2023-02-25 | GSE225646 | GEO

The m6A RNA modification modulates gene expression and fibrosis-related pathways in hypertrophic scar [m6A-seq]

2022-01-24 | GSE194121 | GEO

Inhibition of PIK3CA by miR-203a-3p reduces hypertrophic scar formation via PI3K/AKT/mTOR signaling pathway

Project description:Hypertrophic scar (HS) is a skin fibroproliferative disease currently having no truly effective therapy. PIK3CA is a catalytic subunit of PI3K able to promote collagen synthesis in benign fibrotic diseases and to regulate cell survival, proliferation, and adhesion in malignancies. To explore PIK3CA’s functions in HS formation, we performed transcriptome sequencing and experimental validation. PIK3CA were overexpressed in HS tissues, and positively correlated with fibrosis. We then screened out miR-203a-3p as the most suitable endogenous inhibitor of PIK3CA through bioinformatics. Intriguingly, miR-203a-3p suppressed the proliferation, migration, collagen synthesis, and contractility, as well as trans-differentiation of fibroblasts into myofibroblasts in vitro, improved the morphology and histology of HS in vivo. Mechanistically, miR-203a-3p attenuated fibrosis by inactivating PI3K/AKT/mTOR pathway via directly targeting PIK3CA. In conclusion, Our findings identified that PIK3CA and PI3K/AKT/mTOR pathway were actively involved in HS formation and demonstrated that miR-203a-3p might serve as a potential strategy for HS therapy through targeting PIK3CA and inactivating PI3K/AKT/mTOR pathway.

2023-07-15 | GSE236983 | GEO

Epigenome analysis of normal skin and hypertrophic scar samples

Project description:Hypertrophic scarring (HS) is characterized by excessive extracellular matrix deposition, matrix metalloprotein gene activation, and fibroblast invasive growth. However, the methylation level of hypertrophic scarring is poorly understood. Genome wide DNA methylation profiling of normal skin and hypertrophic scar. The Illumina Infinium Methylation EPIC BeadChip (850K) was used to obtain DNA methylation profiles across approximately 853,307 CpGs in liquid based scar samples. Samples included 6 normal skin, and 6 hypertrophic scar.

2023-04-20 | GSE229848 | GEO

Investigation of the keratinocytic gene expression pattern in Hidradenitis suppurativa

Project description:The underlying pathogenetic factors generating the innate immune signal necessary for T cell activation, initiation and chronification of Hidradenitis suppurativa (HS, also known as Acne inversa) are still poorly understood. Emerging evidence suggests that defective keratinocyte function critically contributes to HS disease development and progression. To elucidate the role of keratinocytes in HS lesion formation, we compared the transcriptomes of isolated lesional and perilesional HS epidermis by RNA sequencing.

| EGAS00001005544 | EGA

pTAC3 and pTAC14 are required for binding of Plastid Encoded RNA Polymerase to DNA

Project description:Plastid Encoded RNA Polymerase (PEP) is a bacterial type multisubunit RNA polymerase responsible for the bulk of transcription in chloroplasts. It contains four core subunits, which are orthologs of their cyanobacterial counterparts. In Arabidopsis thaliana PEP associates with 12 PEP-associated proteins (PAPs), which serve as peripheral subunits of the RNA polymerase. The exact contributions of PAPs to PEP function remain poorly understood. We show that a peripheral subunit of PEP, PAP1 (pTAC3), binds the same genomic loci as RpoB, a core subunit of PEP. PAP1 (pTAC3) and another peripheral PEP subunit, PAP7 (pTAC14), are required for RpoB binding to DNA. RpoB and another core PEP subunit, RpoC1, are expressed in pap1 (ptac3) and pap7 (ptac14) mutants. We propose that the peripheral subunits of PEP are required for the recruitment of core PEP subunits to DNA. pTAC3, binds the same genomic loci as RpoB, a core subunit of PEP. PAP1 pTAC3 and another peripheral PEP subunit, PAP7

2024-03-05 | GSE259283 | GEO

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