Immortalized Human Gingival Keratinocytes-SV40
Cat.No.: CSC-I2301Z
Morphology: Polygonal
Culture Properties: Adherent
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Immortalized human gingival keratinocytes-SV40 (HGK/SV40) are generated by introducing the SV40 large T antigen into primary human gingival keratinocytes. This confers indefinite proliferative capacity while preserving key keratinocyte features. In low-calcium serum-free medium, HGK/SV40 maintain a basal/proliferative phenotype expressing p63, cytokeratin 5/14, and E-cadherin. Upon calcium switch or air-liquid interface culture, they can differentiate toward a stratified squamous phenotype with cytokeratin 13, involucrin, and junctional proteins such as ZO-1 and occludin, supporting studies of oral epithelial barrier formation and differentiation.
Compared with primary human gingival keratinocytes, HGK/SV40 offer a continuous, scalable, and cost-effective source with high batch-to-batch consistency and reduced donor variability. This enables reproducible high-throughput screening, long-term culture, and siRNA/CRISPR perturbation. They retain innate immune responsiveness through Toll-like receptors and respond to inflammatory stimuli such as IL-1β, TNF-α, and bacterial LPS, with cytokine and chemokine secretion relevant to periodontal immunity. They are widely used to model periodontal inflammation, peri-implantitis, oral mucositis, wound healing, and host–microbiome interactions, and to test dental materials, oral care products, and pharmaceuticals for biocompatibility and toxicity.
Fiber Architecture Directs Proliferation and Differentiation in Gingival Keratinocytes
This study systematically evaluated how electrospun polycaprolactone (PCL) scaffolds with defined fiber orientations (aligned vs. random) and diameters (600–800 nm, 1.2–1.7 µm, 2.0–2.5 µm) direct gingival keratinocyte fate. Using immortalized human gingival keratinocytes (ihGK), we assessed cell and nuclear morphology, proliferation dynamics, differentiation marker expression, and the effects of basal keratin (KRT5/KRT14) knockdown.
Quantitative morphological analysis revealed scaffold-dependent changes in cell shape: aligned medium-diameter fibers (with fiber diameters of 1.2–1.7 µm) induced pronounced cell and nuclear elongation, whereas random fibers (600–800 nm) promoted larger, more rounded cell and nuclear shapes. Time-resolved EdU assays indicated that aligned scaffolds supported sustained proliferation, whereas random scaffolds elicited a transient proliferative burst followed by a decline. Gene expression analysis (ddPCR) demonstrated that random scaffolds (especially 600–800 nm fibers) upregulated basal keratins (KRT5, KRT14) and early differentiation markers (KRT1, KRT10, KRT4, KRT13) relative to aligned scaffolds. At the protein level, differentiation markers involucrin (IVL) and filaggrin (FLG) were likewise elevated on random scaffolds, corroborating the mRNA findings. Collectively, these findings establish fiber orientation and diameter as key design parameters for controlling keratinocyte fate.
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