Cryopreserved Human Keratinocytes

Cryopreserved Human Keratinocytes

Cat.No.: CSC-7677W

Species: Human

Source: Epidermis; Skin

Cell Type: Keratinocyte

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Cat.No.
CSC-7677W
Description
Bioarray epidermal keratinocytes are available from adult and neonatal donor tissue and are provided at the earliest passage without the use of a murine feeder layer. Keratinocytes are available from donors of varying ages, genders, and diabetes status. Donor matched epidermal keratinocytes, dermal fibroblasts, melanocytes and subcutaneous preadipocytes are available.
Species
Human
Source
Epidermis; Skin
Cell Type
Keratinocyte
Disease
Normal
Storage and Shipping
Store in liquid nitrogen and ship in dry ice.
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.

Cryopreserved human keratinocytes are primary epidermal keratinocytes, typically neonatal or adult, that are expanded, quality-controlled, and stored in liquid nitrogen. After thawing, they recover, attach, and proliferate in serum-free, low-calcium medium, retaining a basal phenotype marked by p63 and cytokeratin 5/14. Upon calcium switch or air-liquid interface culture, they differentiate into stratified epidermis expressing cytokeratin 1/10, involucrin, filaggrin, and loricrin, supporting cornified envelope formation and barrier development.

Their key advantage is readiness for use. Compared with freshly isolated keratinocytes, cryopreserved cells reduce lead time, logistical complexity, and culture failure risk, while enabling flexible scheduling and scalable experiments. Each lot can be qualified for viability, attachment, proliferation, marker expression, and differentiation capacity, improving reproducibility. Compared with immortalized lines such as HaCaT, cryopreserved primary keratinocytes better preserve donor genetic background, native receptor expression, and physiological signaling.

They are widely used in epidermal biology, wound healing, psoriasis, atopic dermatitis, contact dermatitis, photoaging, and skin carcinogenesis, as well as in safety and efficacy testing of drugs, cosmetics, irritants, sensitizers, and wound-care products. They are compatible with 2D monolayers, 3D organotypic skin equivalents, co-culture with fibroblasts or immune cells, and high-content imaging.

The Glycoprotein GPNMB Protects Against Oxidative Stress Through Enhanced PI3K/AKT Signaling in Epidermal Keratinocytes

This study aimed to determine the role of glycoprotein nonmetastatic melanoma protein B (GPNMB) in normal and vitiligo epidermis. First, we investigated the intracellular signaling changes after H2O2-induced oxidative stress in cultured normal human epidermal keratinocytes (NHEKs). Then, GPNMB was knocked down to mimic vitiligo keratinocytes (KCs) to investigate the role of GPNMB and its underlying mechanisms in cell susceptibility to H2O2 treatment.

GPNMB knockdown reduced the phosphorylation levels of AKTT308 and AKTS473 after H2O2 treatment, accompanied by reduced Dickkopf-1 (DKK1) mRNA and protein production and decreased FOXM1 mRNA expression. These results suggested that GPNMB protects KCs from H2O2-induced cell death through enhanced PI3K/AKT signaling, and WNT/β-catenin/FOXM1 and DKK1/CKAP4/AKT pathways. Furthermore, a significant increase in thioredoxin-interacting protein (TXNIP) following GPNMB knockdown was observed, indicating the enhanced phosphorylation of JNK and p38 and suppression of WNT/β-catenin signaling. These results suggest that the decreased expression of epidermal GPNMB in vitiligo lesions triggers increased sensitivity to H2O2-induced oxidative stress and decreased WNT/β-catenin signaling, consistent with the pathological features of the vitiligo epidermis.

H2O2 induces time-dependent signal activation in NHEKs.
Fig. 1. H2O2 induces time-dependent signal activation in NHEKs (Nishida, Natsuki, et al., 2025).
GPNMB knockdown attenuates Dickkopf-1 (DKK1) expression and secretion from NHEKs and suppresses the PI3K/AKT signaling pathway.
Fig. 2. GPNMB knockdown attenuates Dickkopf-1 (DKK1) expression and secretion from NHEKs and suppresses the PI3K/AKT signaling pathway (Nishida, Natsuki, et al., 2025).

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