C57BL/6 Mouse Gingival Epithelial Cells

Cat.No.: CSC-C9083J

Species: Mouse

Source: Gingiva; Periodontium

Cell Type: Epithelial Cell

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Cat.No.
CSC-C9083J
Description
C57BL/6 Mouse Gingival Epithelial Cells from Creative Bioarray are isolated from gingival tissue of pathogen-free laboratory mice. C57BL/6 Mouse Gingival Epithelial Cells are grown in a T25 tissue culture flask pre-coated with gelatin-based coating solution for 2 min and incubated in Creative Bioarray’s Culture Complete Growth Medium for 3-5 days. Cells are detached from flasks and immediately cryo-preserved in vials. Each vial contains at least 0.5x10^6 cells per ml and is delivered frozen. Cells can be expanded for 3-7 passages at a split ratio of 1:2 under the cell culture conditions specified by Creative Bioarray. Repeated freezing and thawing of cells is not recommended.
Species
Mouse
Source
Gingiva; Periodontium
Recommended Medium
Complete Epithelial Cell Medium
Cell Type
Epithelial Cell
Disease
Normal
Storage and Shipping
We ship frozen cells on dry ice. Upon receiving, directly and immediately transfer the cells from dry ice to liquid nitrogen and keep the cells in liquid nitrogen until they are needed for experiments. Never can primary cells be kept at -20 °C.
Citation Guidance
If you use this products in your scientific publication, it should be cited in the publication as: Creative Bioarray cat no. If your paper has been published, please click here to submit the PubMed ID of your paper to get a coupon.

C57BL/6 Mouse Gingival Epithelial Cells (GECs) are primary cells that have been isolated from the gingival mucosa of C57BL/6 mice. C57BL/6 mice are a common inbred strain used in immunological and periodontal studies. The gingiva is composed of stratified epithelium which can be divided into the keratinized oral epithelium, the semi-permeable sulcular epithelium, and the non-keratinized junctional epithelium (JE). The JE forms a tight seal with the tooth surface and is responsible for regulating the entry of bacteria into the gingival crevice. GECs in vitro show a typical epithelial cobblestone morphology and express epithelial markers including cytokeratins and E-cadherin. They require specialized media with added growth factors to proliferate in vitro and maintain their physiological properties. In their physiological context, GECs serve as a barrier to oral pathogens and are involved in innate immune responses, such as the production of antimicrobial peptides (e.g. β-defensins) and the secretion of cytokines (e.g. IL-6, IL-8). Dysregulation of GECs is thought to contribute to the pathogenesis of periodontitis, with increased inflammatory signaling and tissue destruction observed.

GECs are commonly used in research to study periodontal disease, host-microbe interactions (e.g. in the context of Porphyromonas gingivalis infection), and screening of potential therapeutic agents. They are also used in tissue engineering approaches for gingival regeneration studies. Their genetic background (C57BL/6) allows for reproducibility between experiments and translational relevance for studying epithelial immunity and developing new treatments for periodontal diseases.

Activation of Canonical Wnt Signaling Induced TNF-α Expression in the Macrophages but Not in GEC In Vitro

Wnt signaling is involved in homeostasis and inflammation, but its role in periodontitis macrophages is unknown. Here, Chen's team induced periodontitis in mice with P.g-associated ligature and examined TNF-α, β-catenin, and F4/80 expression. They assessed Wnt signaling's effect on TNF-α in Raw 264.7 macrophages and compared it with gingival epithelial cells (GECs).

Wnt signaling is vital for macrophage recruitment. They found similar expression patterns of F4/80, activated β-catenin, and TNF-α in gingiva during periodontitis, suggesting that Wnt pathway activation is linked to macrophage recruitment and activation. They treated GEC and Raw 264.7 cells with Wnt3a-conditioned medium, observing nuclear β-catenin accumulation, confirming Wnt pathway activation (Fig. 1A-E). TNF-α significantly increased in Raw 264.7 cells but not in GEC (Fig. 1C, F), indicating that Wnt pathway activation mainly affects macrophages. Blocking Wnt3a with an antibody reduced β-catenin accumulation and significantly decreased TNF-α in Raw 264.7 cells, with no significant change in GEC (Fig. 1A-D, F). This shows that Wnt pathway activation directly promotes TNF-α production in macrophages. Overall, Wnt pathway activation is associated with macrophage recruitment and activation in gingiva during periodontitis, contributing to inflammation in periodontal diseases.

Activation of Wnt signaling induced the secretion of TNF-α in the GEC and macrophages.

Fig. 1. Activation of Wnt signaling induced the secretion of TNF-α in the GEC and macrophages (Chen Y and Hu Y, 2023).

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