Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Alcaligenes faecalis corrects aberrant matrix metalloproteinase expression to promote re-epithelialization of diabetic wounds

ABSTRACT: Alcaligenes faecalis corrects aberrant matrix metalloproteinase expression to promote re-epithelialization of diabetic wounds

PROVIDER: PRJNA1086913 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR28305570_1.fastq.gz	Fastqsanger.gz
	SRR28305570_2.fastq.gz	Fastqsanger.gz
	SRR28305571_1.fastq.gz	Fastqsanger.gz
	SRR28305571_2.fastq.gz	Fastqsanger.gz
	SRR28305572_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

Alcaligenes faecalis corrects aberrant matrix metalloproteinase expression to promote re-epithelialization of diabetic wounds

Project description:Chronic wounds are a common and costly complication of diabetes, where multifactorial defects contribute to dysregulated skin repair, inflammation, tissue damage, and infection. We previously showed that aspects of the diabetic foot ulcer microbiota were correlated with poor healing outcomes, but many microbial species recovered remain uninvestigated with respect to wound healing. Here we focused onAlcaligenes faecalis, a Gram-negative bacterium that is frequently recovered from chronic wounds but rarely causes infection. Treatment of diabetic wounds withA. faecalisaccelerated healing during early stages. We investigated the underlying mechanisms and found thatA. faecalistreatment promotes re-epithelialization of diabetic keratinocytes, a process which is necessary for healing but deficient in chronic wounds. Overexpression of matrix metalloproteinases in diabetes contributes to failed epithelialization, and we found thatA. faecalistreatment balances this overexpression to allow proper healing. This work uncovers a mechanism of bacterial-driven wound repair and provides a foundation for the development of microbiota-based wound interventions.

2024-03-30 | GSE261418 | GEO

<i>Alcaligenes faecalis</i> corrects aberrant matrix metalloproteinase expression to promote reepithelialization of diabetic wounds.

Project description:Chronic wounds are a common and costly complication of diabetes, where multifactorial defects contribute to dysregulated skin repair, inflammation, tissue damage, and infection. We previously showed that aspects of the diabetic foot ulcer microbiota were correlated with poor healing outcomes, but many microbial species recovered remain uninvestigated with respect to wound healing. Here, we focused on Alcaligenes faecalis, a Gram-negative bacterium that is frequently recovered from chronic wounds but rarely causes infection. Treatment of diabetic wounds with A. faecalis accelerated healing during early stages. We investigated the underlying mechanisms and found that A. faecalis treatment promotes reepithelialization of diabetic keratinocytes, a process that is necessary for healing but deficient in chronic wounds. Overexpression of matrix metalloproteinases in diabetes contributes to failed epithelialization, and we found that A. faecalis treatment balances this overexpression to allow proper healing. This work uncovers a mechanism of bacterial-driven wound repair and provides a foundation for the development of microbiota-based wound interventions.

| S-EPMC11204295 | biostudies-literature

Gene expression profiling of negative-pressure-treated split-thickness skin graft donor site wounds reveals novel effects on epithelialization

Project description:Negative-pressure wound therapy (NPWT) is widely used to improve skin wound healing and to accelerate wound bed preparation. Although NPWT has been extensively studied as a treatment for deep wounds, its effect on epithelialization of superficial dermal wounds remains unclear. To clarify the effect of NPWT on reepithelialization, we applied NPWT on split- thickness skin graft donor sites from the first postoperative day (POD) to the seventh POD. Six patients took part in the study and two samples were obtained from each. The first biopsy sample was taken at elective surgery before split-thickness skin grafting and the second one during reepithelialization on the seventh POD. In all 12 samples (eight from four NPWT patients, and four from two control patients) were collected for this study. From each sample, we carried out a comprehensive genome-wide microarray analysis. Data from patients receiving NPWT were compared groupwise with data from those not receiving NPWT. Overall 12 samples were analyzed

2011-10-24 | E-GEOD-33169 | biostudies-arrayexpress

Gene expression profiling of negative-pressure-treated split-thickness skin graft donor site wounds reveals novel effects on epithelialization

2011-10-25 | GSE33169 | GEO

Novel epoxy-tiglianes stimulate keratinocyte wound healing responses and re-epithelialization via protein kinase C activation

Project description:Impaired re-epithelialization is a hallmark of non-healing, chronic skin wounds. These represent major causes of patient morbidity, particularly amongst ever-increasing ageing and diabetic populations, posing significant challenges to healthcare providers worldwide. Despite many treatment options being available, these often offer limited benefits to healing outcomes. We address the need for more efficacious treatments through evaluation of novel epoxy-tigliane compounds as chronic wound pharmaceuticals, based on their effectiveness in promoting keratinocyte healing responses and re-epithelialization in vivo. Here, we identify that prototype epoxy-tigliane (EBC-46) and analogue (EBC-211), accelerate G1/S and S/G2 cell cycle transitions and proliferation in a normal human keratinocyte cell line of skin origin (HaCaTs). EBC-46 and EBC-211 further induce HaCaT migration/wound repopulation, even with mitomycin C treatment, suggesting epoxy-tiglianes can promote migration/repopulation independently of proliferation. Epoxy-tiglianes modulate keratin, DNA synthesis/replication, cell cycle/proliferation, motility/migration, differentiation, proteinase; and cytokine/chemokine gene expression, to facilitate enhanced responses. Although epoxy-tiglianes down-regulate cytokine/chemokine agonists of keratinocyte proliferation/migration, we demonstrate that enhanced HaCaT responses are mediated through protein kinase C (PKC) phosphorylation and abrogated by inhibition of PKC activation with bisindolylmaleimide-1 (BIM-1). By identifying how epoxy-tiglianes stimulate keratinocyte healing responses, we highlight their potential as novel therapeutics for impaired re-epithelialization associated with non-healing, chronic wounds.

2019-08-01 | GSE122297 | GEO

Alcaligenes

Project description:Alcaligenes sp. overview

| PRJNA182074 | ENA

Identification of genes involved in re-epithelialization

Project description:To identify candidate genes involved in re-epithelialization of TGF-b induced dedifferentiated hRPTEC, this experiment was designed.

2016-04-01 | GSE74436 | GEO

Transcriptome data of Alcaligenes sp. HO-1 in response to ammonium stimulation at several time points.

Project description:A heterotrophic ammonia-oxidizing bacterium Alcaligenes sp. HO-1 was isolated from the activated sludge of a bioreactor treating ammonia-rich piggery wastewater. The goal and objectives of this experiment are to analyze the transcriptome profiles of nitrogen-metabolism-related genes of Alcaligenes sp. HO-1 in response to ammonium stimulation over time and to find out potential genes involved in ammonia oxidation process. So the RNA-seq anaylsis was performed by setting up each time points (0, 3.5, 10, 22 hours) when strain HO-1 were exposed to ammonia. HO-1 was cultured with 83 mM succinate and 14 mM ammonium sulfate until ammonia was completely consumed and then another 14 mM of ammonium sulfate was added to the culture. Cells were harvested at 0 h, 3.5 h, 10 h and 22 h after the addition of ammonium sulfate. The sequencing data of RNAs obtained from strain HO-1 cells at each time was analyzed.

2022-05-20 | GSE174685 | GEO

Alcaligenes faecalis

Project description:Alcaligenes faecalis

| PRJNA1079921 | ENA

Alcaligenes faecalis

Project description:Alcaligenes faecalis

| PRJNA1081340 | ENA