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Mechanistic connections among epithelial plasticity, skin barrier, inflammation, and whole-body metabolism [ChIP-seq]

ABSTRACT: We found that epitheilial-specific Ovol1/2 iDKO mice develop spontaneous barrier defects and whole body physiological alterations. To investigate the mechanism behind these changes, we compared gene expression changes between homeostatic iDKO epidermis compared with control at "early" 25 days post injection (DPI) and at 52 DPI

ORGANISM(S): Mus musculus

PROVIDER: GSE211893 | GEO | 2023/04/07

REPOSITORIES: GEO

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Mechanistic connections among epithelial plasticity, skin barrier, inflammation, and whole-body metabolism [RNA-seq]

Project description:We found that epitheilial-specific Ovol1/2 iDKO mice develop spontaneous barrier defects and whole body physiological alterations. To investigate the mechanism behind these changes, we compared gene expression changes between homeostatic iDKO epidermis compared with control at "early" 25 days post injection (DPI) and at 52 DPI

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Mechanistic connections among epithelial plasticity, skin barrier, inflammation, and whole-body metabolism

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Expression data from isolated E17.5 mouse skin with or without Ovol2 overexpression

Project description:During epithelial tissue morphogenesis, developmental progenitor cells undergo dynamic adhesive and cytoskeletal remodeling to trigger proliferation and migration. Transcriptional mechanisms that restrict such mild form of epithelial plasticity to maintain lineage-restricted differentiation in committed epithelial tissues are poorly understood. Here we report that simultaneous ablation of transcriptional repressor-encoding Ovol1 and Ovol2 results in expansion and blocked terminal differentiation of embryonic epidermal progenitor cells. Conversely, mice overexpressing Ovol2 in their skin epithelia exhibit precocious differentiation accompanied by smaller progenitor cell compartments. We show that Ovol1/2-deficient epidermal cells fail to undertake alpha-catenin–driven actin cytoskeletal reorganization and adhesive maturation, and exhibit changes that resemble epithelial-to-mesenchymal transition (EMT). Remarkably, these alterations as well as defective terminal differentiation are reversed upon depletion of EMT-promoting transcriptional factor Zeb1. Collectively, our findings reveal Ovol-Zeb1-a-catenin sequential repression and highlight novel functions of Ovol as gatekeepers of epithelial adhesion and differentiation by inhibiting progenitor-like traits and epithelial plasticity. Skin from control and Ovol2 overexpression (Ovol2 BT) were physically isolated for RNA extraction and hybridization on Affymetrix microarrays. In order to identify changes in differentiation of the epidermis, we analyzed skin from E17.5 mice, when differentiation of the epidermis was more advanced.

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Mosaic deletion of claudin-5 reveals rapid non-cell-autonomous consequences of blood-brain barrier leakage

Project description:Claudin-5 (CLDN5) is an endothelial tight junction protein essential for blood-brain barrier (BBB) formation. Abnormal CLDN5 expression is common in brain disease, and knockdown of Cldn5 at the BBB has been proposed to facilitate drug delivery to the brain. To study the consequences of CLDN5 loss in the mature brain, we induced mosaic endothelial-specific Cldn5 gene ablation in adult mice (Cldn5iECKO). These mice displayed increased BBB permeability to tracers up to 10 kDa in size from 7 days post induction (dpi) and ensuing lethality from 11 dpi. Single-cell RNA sequencing at 12 dpi revealed profound transcriptomic differences in brain endothelial cells regardless of their Cldn5 status in mosaic mice, suggesting major non-cell-autonomous responses. Reactive microglia and astrocytes suggested rapid cellular responses to BBB leakage. Our study demonstrates a critical role for CLDN5 in the adult BBB and provides molecular insight into the consequences and risks associated with CLDN5 inhibition.

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