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New mechanisms for oral epithelial basal stem cell plasticity during re-epithelialization after injury

ABSTRACT: New mechanisms for oral epithelial basal stem cell plasticity during re-epithelialization after injury

PROVIDER: PRJNA1183549 | ENA |

REPOSITORIES: ENA

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New mechanisms for oral epithelial basal stem cell plasticity during re-epithelialization after injury

Project description:The oral mucosa undergoes daily insults and stem cells in the epithelial basal cell layer are required to regenerate gingiva tissue to maintain oral health. The Iroquois Homeobox 1 (IRX1/Irx1) protein is expressed in the stem cell niches in human/mouse oral epithelium and mesenchyme under homeostasis. We found that Irx1+/- heterozygous (Het) mice have delayed wound closure, delayed morphological changes of regenerated epithelium, as well as defective keratinocyte proliferation and differentiation during wound healing. RNA-seq analyses between wildtype and Irx1+/- mice at 3 days post injury (dpi), found impaired epithelial migration and decreased keratinocyte-related genes upon injury. Irx1 expressing cells are found in the gingival epithelial basal cell layer, a stem cell niche for gingival maintenance. Irx1 expressing cells are also found in cell niches in the underlying stroma. Irx1 activates Sox9 in the transient amplifying layer to increase cell proliferation and EGF signaling is activated to induce cell migration. Krt14CreERT lineage tracing experiments reveal defects in the stratification of the Irx1+/- heterozygous mouse oral epithelium. Irx1 is primed at the base of the gingiva in the basal cell layer of the oral epithelium, facilitating rapid and scarless wound healing through activating Sox9 and the EGF signaling pathway.

2024-11-14 | GSE281359 | GEO

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

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. hRPTEC incubated with TGF-b for 48h and hRPTEC incubated with or without TGF-b for additional 24h were collected. Then, they were applied in this experiment.

2016-04-01 | E-GEOD-74436 | biostudies-arrayexpress

Expression data between migrating keratinocytes in diabetic mice against normal mice during re-epithelialization 3 days post wounding

Project description:During re-epithelialization, keratinocytes have to undergo specific gene expression changes that grant them increased motility. Diabetic keratinocytes have been observed to portray an impairment in this aspect. We used microarrays to identify the changes in the expression patterns of both normal and diabetic migrating keratinocytes during re-epithelialization.

2020-10-23 | GSE141956 | GEO

Lgr6 marks epidermal stem cells with a nerve-dependent role in wound re- epithelialization

Project description:Stem cells support the lifelong maintenance of adult organs but their specific roles during injury are poorly understood. Here, we demonstrate that Lgr6 marks a regionally restricted population of epidermal stem cells that interact with nerves and specialize in wound re-epithelialization. Diphtheria toxin-mediated ablation of Lgr6 stem cells delays wound healing, and skin denervation phenocopies this effect. Using intravital imaging to capture stem cell dynamics after injury, we show that wound re-epithelialization by Lgr6 stem cells is diminished following the loss of nerves. This induces the recruitment of other stem cell populations, including hair follicle stem cells, which partially compensate to mediate the wound closure. Single-cell lineage tracing and gene expression analysis reveal that the fate of Lgr6 stem cells is shifted towards differentiation following the loss of their niche. We conclude that Lgr6 epidermal stem cells are primed for injury response and interact with nerves to regulate their fate

2021-04-08 | GSE171662 | 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.

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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

Lgr6 marks epidermal stem cells with a nerve-dependent role in wound re- epithelialization

Project description:Lgr6 marks epidermal stem cells with a nerve-dependent role in wound re- epithelialization

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

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

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Inactivation of LATS1/2 drives luminal-basal plasticity to initiate basal-like mammary carcinomas

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