Expression data between migrating keratinocytes in diabetic mice against normal mice during re-epithelialization 3 days post wounding
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ABSTRACT:
PROVIDER: PRJNA595379 | ENA |
REPOSITORIES: ENA
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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
Project description:Dendritic epidermal T cells (DETC) reside in murine skin and participate in homeostasis and wound repair. Upon wounding, DETC become activated through the recognition of an unidentified ligand expressed by keratinocytes proximal to sites of injury. Such DETC activation is mediated through a monoclonal T cell receptor (TCR). Using a soluble form of this monoclonal TCR, we have shown that keratinocytes upregulate DETC TCR ligands in wounded tissue within 2 hours following wounding. Down-modulation of the ligand is seen 3 hours following wounding, and no expression is evident in non-wounded skin. In vitro studies on cell lines which express this unknown ligand indicate that antigen recognition by the DETC TCR is dependent upon N-linked glycosylation of the ligand. Given the glycosylation sensitivity of the ligand and the restricted expression following wounding, we are interested in pursuing microarray analysis to identify genes that are modulated in keratinocytes in response to wounding.
2011-09-06 | GSE31926 | GEO
Project description:identify an underlying mechanism a new pathway where GRHL3 activates the Fscn1 gene to effect cell-cell loosening in the migrating wound front
2021-10-13 | GSE172161 | GEO
Project description:Dendritic epidermal T cells (DETC) reside in murine skin and participate in homeostasis and wound repair. Upon wounding, DETC become activated through the recognition of an unidentified ligand expressed by keratinocytes proximal to sites of injury. Such DETC activation is mediated through a monoclonal T cell receptor (TCR). Using a soluble form of this monoclonal TCR, we have shown that keratinocytes upregulate DETC TCR ligands in wounded tissue within 2 hours following wounding. Down-modulation of the ligand is seen 3 hours following wounding, and no expression is evident in non-wounded skin. In vitro studies on cell lines which express this unknown ligand indicate that antigen recognition by the DETC TCR is dependent upon N-linked glycosylation of the ligand. Given the glycosylation sensitivity of the ligand and the restricted expression following wounding, we are interested in pursuing microarray analysis to identify genes that are modulated in keratinocytes in response to wounding. Keratinocytes represent 90% of the cells in the epidermis (DETC and Langerhan’s cells make up the remaining 10%). As such, we propose to isolate RNA from whole epidermis under either wounded or resting conditions. In addition to comparing RNA from wounded and non-wounded epidermis, we would like to compare RNA from tissue that has been wounded for different times. Initially, we would like to analyze 4 sampes (non-wounded epidermis, and epidermal cells isolated 30 minutes, 2 hours, and 4 hours following wounding). These time points would correlate to a period prior to cell surface expression of ligand (30 minutes), during cell surface expression (2 hours), and following down regulation of cell surface expression (4 hours). In addition to providing possible identification of the unknown DETC TCR ligand, such analysis would provide novel information about early responses by keratinocytes in response to physical wounding in vivo. We propose to isolate RNA from whole epidermis under either wounded or resting conditions. In addition to comparing RNA from wounded and non-wounded epidermis, we would like to compare RNA from tissues that has been wounded for different times.
2011-09-05 | E-GEOD-31926 | biostudies-arrayexpress
Project description:Re-epithelialization is a crucial process to reestablish the protective barrier upon wounding of the skin. Although this process is well described for wounds where the complete epidermis and dermis is damaged, little is known about the re-epithelialization strategy in more frequently occurring smaller scratch wounds in which structures such as the hair follicles and sweat glands stay intact. To study this, we established a scratch wound model to follow individual keratinocytes in all epidermal layers in the back skin of mice by intravital microscopy. We discover that keratinocytes adopt a re-epithelialization strategy that enables them to bypass immobile obstacles such as hair follicles. Wound-induced cell loss is replenished by proliferation in a distinct zone away from the wound and this proliferation does not affect overall migration pattern. Whereas suprabasal keratinocytes are rather passive, basal keratinocytes move as a sheet of independently migrating cells into the wound, thereby constantly changing their direct neighboring cells enabling them to bypass intact obstacles. This re-epithelialization strategy results in a fast re-establishment of the protective skin barrier upon wounding.
| S-EPMC7723264 | biostudies-literature
Project description:Mammalian injury responses are characterized by fibrosis and scarring rather than the functional regeneration observed in other phyla. Limited regenerative capacity in mammals could reflect a loss of pro-regeneration programs or active suppression by genes functioning akin to tumor suppressors. To uncover programs governing regeneration in mammals, we investigated Wound Induced Hair Neogenesis (WIHN), a rare example of regeneration in adult mammals1,2. Through comprehensive screening of transcripts associated with both WIHN and human facial rejuvenation after laser treatment, we found the endoribonuclease RNase L to be a powerful suppressor of regeneration. Rnasel-/- mice exhibit remarkable regenerative capacity and accelerated wound healing following injury through the production of IL-36α. Consistent with the known role of RNase L to stimulate caspase-1 signaling, we find that pharmacologic inhibition of caspases promotes regeneration in an IL-36-dependent manner. These responses are not limited to skin but occur following intestinal injury as well, suggesting that suppression of regeneration is a general characteristic of mammalian wound healing. Taken together, this work suggests a therapeutic strategy to uncover latent regenerative capacity and promote functional response to injury. Biopsies of re-epithelialized tissue were recovered from wild-type or Rnasel KO mice approximately 10 days after wounding. Total RNA was extracted and sent for microarray analysis.
2021-11-18 | GSE164003 | GEO
Project description:REDD1 KO affects basal global gene expression profile and transcriptomic response to wounding and glucocorticoid treatment in HaCaT human keratinocytes
2021-08-10 | GSE177061 | GEO
Project description:Expression profiles of wild type migratory border cells (WTBC), non-migrating slbo mutant border cells (slboBC) and non-migrating follicle cells (FC)
2006-04-01 | E-MEXP-493 | biostudies-arrayexpress
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