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Topical application of an irreversible small molecule inhibitor of Lysyl Oxidases ameliorates skin scarring and fibrosis

ABSTRACT: Topical application of an irreversible small molecule inhibitor of Lysyl Oxidases ameliorates skin scarring and fibrosis

PROVIDER: PRJNA685738 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13258900.fastq.gz	Fastqsanger.gz
	SRR13258901.fastq.gz	Fastqsanger.gz
	SRR13258902.fastq.gz	Fastqsanger.gz
	SRR13258903.fastq.gz	Fastqsanger.gz
	SRR13258904.fastq.gz	Fastqsanger.gz

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Topical application of an irreversible small molecule inhibitor of Lysyl Oxidases ameliorates skin scarring and fibrosis

Project description:Next-generation sequencing (NGS) has been performed to investigate the effect of Lysyl oxidase inhibition by PXS-4787A on transcriptome of normal skin derived fibroblasts and keratinocytes. Fibroblasts and keratinocytes of low passage (p2-5) were cultured onto T25 flasks until ~70% confluence was reached. Fibroblasts were treated with or without 10 µM PXS-4787A in complete fibroblast growth media for 48 hours at 37°C. Keratinocytes were treated with 10 µM PXS-4787A with basal keratinocyte medium supplemented with 1.2 mM calcium chloride for 48 hours at 37°C. Cells were then collected using 0.05% trypsin and washed in Phosphate Buffered Saline (PBS). RNA was extracted using the RNeasy Mini kit protocol. Samples were then sent to the Australian Genome Research Facility (AGRF) where 1μg of RNA was submitted for next-generation sequencing. Once raw data returned, bioinformatics analyses were conducted. This study found that the exposure of PXS-4787A only had minor impact on gene expression in both fibroblasts and keratinocytes. In fibroblasts, 3 genes were significantly upregulated and only one gene was significantly downregulated. Besides, There were only two upregulated genes in the whole genome analysis after LOX inhibition in keratinocytes. In conclusion, this study highlights the safety of LOX-inhibition through PXS-4787A on primary human epidermal cells. The results of the transcriptome analysis intimate that PXS-4787A treatment has no adverse effects on the healthy keratinocytes. Taken together, this study suggests that LOX-inhibition has no potential effects on the epidermal differentiation in human skin.

2020-12-17 | GSE163309 | GEO

Topical application of an irreversible small molecule inhibitor of lysyl oxidases ameliorates skin scarring and fibrosis.

Project description: Not available

| S-EPMC9500072 | biostudies-literature

Lysyl Oxidases are Necessary for Myometrial Contractility and On-Time Parturition in Mice

Project description:The extracellular matrix (ECM) plays a pivotal role in the maintenance of tissue mechanical homeostasis. Collagens and elastic fibers are the most predominant fibrous ECM proteins providing tissue mechanical function through covalent cross-linking, which is mediated by the lysyl oxidase family of enzymes. In this study, the function of lysyl oxidases in maintaining the integrity of the extracellular matrix in the myometrium and its impact on parturition-timing was investigated. Gene and protein expression analyses demonstrate that a subset of the lysyl oxidase family of enzymes are highly induced in pregnant myometrium. Inhibition of the activity of the lysyl oxidase family of enzymes through β-aminopropionitrile (BAPN) delays parturition in mice, in part because of myometrial dysfunction. In BAPN-treated mice, the expression of genes encoding contraction-associated proteins such as connexin 43, oxytocin receptor, and prostaglandin synthase 2, is significantly reduced in the myometrium compared to the untreated control mice. Proteomic analysis revealed that the composition of the ECM is altered in response to BAPN treatment, which demonstrates that the inhibition of the activity of lysyl oxidases disrupted the integrity of the myometrial ECM. Our findings demonstrate that the lysyl oxidases-mediated ECM function is necessary for the myometrium to transition from a quiescent to a contractile phenotype at term for on-time parturition.

2025-04-18 | PXD055537 | Pride

Transcriptome-guided development of a fibrosis-reversal compound reduces skin scarring and allows regeneration via mitochondrial uncoupling [DRUG-seq2]

Project description:Skin scarring impairs function and aesthetics. Current therapies show limited efficacy and cause iatrogenic dermal disruption (e.g., triamcinolone acetonide, a first-line corticosteroid for keloids), with topical medications demonstrating inferior outcomes. Through transcriptome-guided evaluation, we develop FR-1 (fibrosis-reversal compound 1), a small molecule that reverses fibrosis in vitro by inhibiting fibroblast proliferation, suppressing α-SMA, and remodeling the ECM via collagen downregulation and MMP1 induction. In a murine linear excisional wound model, daily topical FR-1 application progressively reduces scar area. Notably, unlike triamcinolone acetonide, FR-1 avoids skin atrophy and hair follicle damage. Comprehensive safety evaluations, druggability and skin permeation assessments, and studies utilizing patient-derived keloid ex vivo explants and in vivo xenografts demonstrate its translational potential. Mechanistically, FR-1 induces mitochondrial uncoupling, lowering ATP levels in profibrotic myofibroblasts. Other uncouplers similarly attenuate fibrosis. This work identifies a topical small molecule that attenuates scarring, highlighting the therapeutic potential of mitochondrial uncouplers in resolving fibrosis.

2026-05-18 | GSE303486 | GEO

Transcriptome-guided development of a fibrosis-reversal compound reduces skin scarring and allows regeneration via mitochondrial uncoupling [RNA-seq]

2026-05-18 | GSE303487 | GEO

Small molecule inhibitors of lysyl oxidases synergize with 5-azacytidine to restore erythropoiesis in myeloid neoplasms

Project description:In this study, we assessed the effects of lysyl oxidase (LOX/LOXL) inhibition on the composition of extracellular matrix (ECM) produced by in vitro expanded bone marrow derived mesenchymal stromal cells (MSCs) of n=3 patients with myelodysplastic syndromes (MDS) and myeloproliferative neoplasms (MPN).

2023-02-17 | PXD031217 | Pride

Human Scarring Project

Project description:Full thickness and deep partial thickness burn injuries heal by scarring. There are several mechanisms thought to be essential for the development of burn scars, but a challenge to studying the skin response to burn injury is that there are few animal models of burn scarring that are either clinically similar to human burn scars or are practical for most investigators to use. The purpose of this study was to examine the changes in RNA expression in human skin to burn injury. This was done by comparing pre-injury tissue from otherwise healthy adults undergoing aesthetic scarification created by branding with a hot metal object to serial samples of untreated wounds in the same subjects.

2014-01-22 | E-MTAB-1323 | biostudies-arrayexpress

Origin and evolution of lysyl oxidases.

Project description: Not available

| S-EPMC4448552 | biostudies-literature

JUN promotes hypertrophic skin scarring via CD36

Project description:Hypertrophic skin scarring following dermal injury causes extreme pain and psychological trauma for patients. Unfortuately, we do not have effective treatments to prevent or reverse skin scarring. Using RNA and ATAC sequencing of mouse and human fibroblasts, we show that JUN expressing fibroblasts are responsible for skin scarring by regulating CD36 expression. In summary, we show that CD36 antagonism by represent a therapeutic target to overcome JUN hypertrophic skin scarring.

2021-06-22 | GSE178562 | GEO

Treatment of C3H/HeJ grafted mice with baricitinib [topical]

Project description:The C3H/HeJ grafted model of alopecia areata was used to determine the efficacy of systemic baricitinib at preventing alopecia or treating established disease. The efficacy of topical baricitinib at treating established alopecia in the C3H/HeJ grafted model was also assessed. Microarrays were performed on skin RNA at week 0 and week 12 after starting treatment in all models. Baricitinib was administered in topical form after disease establishement. Skin samples were taken at the start of treatment and after 12 weeks.

2015-05-01 | E-GEOD-61554 | biostudies-arrayexpress

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