Inhibition of PIK3CA by miR-203a-3p reduces hypertrophic scar formation via PI3K/AKT/mTOR signaling pathway
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA993252 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25223264_1.fastq.gz | Fastqsanger.gz | |||
| SRR25223264_2.fastq.gz | Fastqsanger.gz | |||
| SRR25223265_1.fastq.gz | Fastqsanger.gz | |||
| SRR25223265_2.fastq.gz | Fastqsanger.gz | |||
| SRR25223266_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
Similar Datasets
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
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
Project description:The goal was to obtain expression data from the deep cones in early human hypertrophic scars to be used to confirm expression data obtained in a porcine model. Three samples of early human hypertrophic scar were obtained and processed with the Affymetrix Human GeneChip® Human Genome U133 plus 2.0. Sample demographics were Black 2, White 1; upper extremity 2, neck 1; times since injury 6.7 months and 10.8 months; and patient ages were 19 and 54.
2011-12-31 | E-GEOD-26213 | biostudies-arrayexpress
Project description:human hypertrophic scar fibroblast cell treated with fkbp10 siRNA and control siRNA for 48 hours
2020-08-26 | E-MTAB-9471 | biostudies-arrayexpress
Project description:human hypertrophic scar fibroblast cell treated with pcolce siRNA and control siRNA for 48 hours
2020-08-26 | E-MTAB-9472 | biostudies-arrayexpress
Project description:Here, using a label-free quantification approach, global lactylome and proteome analyses were performed based on 4 hypertrophic scar and 4 adjacent normal skin samples.
2023-11-08 | PXD046800 |
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
Project description:To explore the functional difference between CD90+CD39+ and CD90+CD39- fibroblasts in human hypertrophic scar and normal skin, the gene expresson microarray was performed on Live CD49f- E-Cadherin- Lin- CD45- CD31- CD90+ CD39+ and Live CD49f- E-Cadherin- Lin- CD45- CD31- CD90+ CD39- cells sorted from suspension disgested from three human hypertrophic scar samples; and Live CD49f- E-Cadherin- Lin- CD45- CD31- CD90+ CD39+ cells sorted from suspension disgested from three human normal skin samples
2021-07-05 | GSE158766 | GEO
Project description:Hypertrophic scars, which result from aberrant fibrosis and disorganized collagen synthesis by skin fibroblasts, emerge due to disrupted wound healing processes. These scars present significant psychosocial and functional challenges to affected individuals. The current treatment limitations largely arise from an incomplete understanding of the underlying mechanisms of hypertrophic scar development. Recent studies, however, have shed light on the potential of exosomal non-coding RNAs interventions to mitigate hypertrophic scar proliferation. This research assesses the impact of exosomes derived from adipose-derived stem cells (ADSCs-Exos) on hypertrophic scar formation using a rabbit ear model. We employed Hematoxylin and Eosin staining, Masson’s Trichrome staining, and Immunohistochemical staining techniques to track scar progression. Our comprehensive analysis encompassed the differential expression of non-coding RNAs, enrichment analyses of functional pathways, protein-protein interaction studies, and miRNA-mRNA interaction investigations. The results reveal a marked alteration in the expression levels of long non-coding RNAs and microRNAs following ADSCs-Exos treatment, with little changes observed in circular RNAs. Notably, miR-194 emerges as a critical regulator within the signaling pathways that govern hypertrophic scar formation. Dual-luciferase assays indicated a significant reduction in the promoter activity of TGF-β1 after miR-194 overexpression. Quantitative reverse transcription PCR and Western blotting assays further validated the decrease in TGF-β1 expression in the treated samples. Moreover, the treatment resulted in diminished levels of inflammatory markers IL-1β, TNF-α, and IL-10. In vivo evidence strongly supports the role of miR-194 in attenuating hypertrophic scar formation through the suppression of TGF-β1. Our findings endorse the strategic use of ADSCs-Exos, particularly through miR-194 modulation, as an effective strategy for reducing scar formation and lowering pro-inflammatory and fibrotic indicators like TGF-β1. Therefore, this study advocates for the targeted application of ADSCs-Exos, with an emphasis on miR-194 modulation, as a promising approach to managing proliferative scarring.
2024-07-24 | GSE271671 | GEO
Project description:Hypertrophic scars, which result from aberrant fibrosis and disorganized collagen synthesis by skin fibroblasts, emerge due to disrupted wound healing processes. These scars present significant psychosocial and functional challenges to affected individuals. The current treatment limitations largely arise from an incomplete understanding of the underlying mechanisms of hypertrophic scar development. Recent studies, however, have shed light on the potential of exosomal non-coding RNAs interventions to mitigate hypertrophic scar proliferation. This research assesses the impact of exosomes derived from adipose-derived stem cells (ADSCs-Exos) on hypertrophic scar formation using a rabbit ear model. We employed Hematoxylin and Eosin staining, Masson’s Trichrome staining, and Immunohistochemical staining techniques to track scar progression. Our comprehensive analysis encompassed the differential expression of non-coding RNAs, enrichment analyses of functional pathways, protein-protein interaction studies, and miRNA-mRNA interaction investigations. The results reveal a marked alteration in the expression levels of long non-coding RNAs and microRNAs following ADSCs-Exos treatment, with little changes observed in circular RNAs. Notably, miR-194 emerges as a critical regulator within the signaling pathways that govern hypertrophic scar formation. Dual-luciferase assays indicated a significant reduction in the promoter activity of TGF-β1 after miR-194 overexpression. Quantitative reverse transcription PCR and Western blotting assays further validated the decrease in TGF-β1 expression in the treated samples. Moreover, the treatment resulted in diminished levels of inflammatory markers IL-1β, TNF-α, and IL-10. In vivo evidence strongly supports the role of miR-194 in attenuating hypertrophic scar formation through the suppression of TGF-β1. Our findings endorse the strategic use of ADSCs-Exos, particularly through miR-194 modulation, as an effective strategy for reducing scar formation and lowering pro-inflammatory and fibrotic indicators like TGF-β1. Therefore, this study advocates for the targeted application of ADSCs-Exos, with an emphasis on miR-194 modulation, as a promising approach to managing proliferative scarring.
2024-07-24 | GSE271672 | GEO