WI-38

Cat.No.: CSC-C9261W

Species: Human

Source: Lung

Morphology: fibroblast

Cell Type: Fibroblast

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Cat.No.

CSC-C9261W

Description

The WI-38 human diploid cell line was derived by Leonard Hayflick from normal embryonic (3 months gestation) lung tissue.

Species

Human

Source

Lung

Recommended Medium

EMEM, 90%; h.i. FBS, 10%

Morphology

fibroblast

Cell Type

Fibroblast

Disease

Normal

Storage and Shipping

liquid nitrogen vapor phase

Citation Guidance

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The WI-38 human embryonic lung cell line, recognized as a milestone in the field of biomedical research, was successfully isolated and established in 1960 by Leonard Hayflick from the lung tissue of a 14-week female fetus. WI-38 cells exhibit typical fibroblast morphology; they adhere to the substrate, have relatively indistinct cell boundaries, and possess large, round nuclei, making them easily identifiable among numerous cell lines. Notably, the WI-38 cell line lacks differentiation potential, which simplifies its application and study in experiments to some extent. Despite being a finite cell line, WI-38 has an in vitro culture lifespan of approximately 50±10 passages. The addition of growth-promoting factors such as tumor necrosis factor-α (TNF-α) to the culture medium can significantly extend the growth period and viability of WI-38 cells.

As the first human diploid cell line used for human vaccine production, WI-38 is highly valued for its stable diploid characteristics and susceptibility to viruses. It not only supports the replication and propagation of various viruses but also provides a platform closely mirroring human physiological conditions for in-depth research on viral infection mechanisms, virus-host cell interactions, and vaccine development and assessment. Vaccines produced using the WI-38 cell line are diverse and widely applied globally, including but not limited to those for rubella, rabies, adenovirus, poliovirus (polio), measles, varicella (chickenpox), and herpes zoster (shingles). Additionally, WI-38 cells are frequently used for establishing cellular senescence models to study the molecular mechanisms of cell aging and to identify potential anti-aging targets.

Laser confocal microscopy captured images of WI-38 cells grown in BEGM. The intermediate filaments labeled with anti-vimentin appear green, the nuclei are stained blue. Fig. 1. Laser confocal images of WI-38 cells cultured in fresh bronchial epithelial growth medium (BEGM). Green: anti-vimentin labeled intermediate filaments; Blue: nuclei (Boublil L, Martinon L, et al., 2013).

Shikonin Alleviates LPS-Induced WI-38 Cell Injury

Pneumonia is an inflammatory disease induced by infection with different pathogens. Currently, multiple preclinical studies have revealed that shikonin, a natural naphthoquinone, can mitigate lipopolysaccharide (LPS)-induced inflammation, but its underlying mechanism in pneumonia remains unknown. Wang et al. constructed an in vitro model of pneumonia by co-treating WI-38 cells with LPS and investigated the role of shikonin in LPS-induced WI-38 cell injury.

To assess the impact of LPS on WI-38 cell viability, an MTT assay showed a clear time-dependent inhibition (Fig. 1A). Apoptosis increased in LPS-treated WI-38 cells, indicated by elevated Bax, cleaved-caspase-3 (C-caspase-3) levels, and apoptosis rate, alongside reduced Bcl-2 expression (Fig. 1B and C). Pro-inflammatory cytokines (IL-6, IL-1β, IL-18, TNF-α) were elevated in LPS-treated WI-38 cells compared to controls, indicating a severe inflammatory response (Fig. 1D). Figure 2A revealed that Shikonin markedly improved cell viability. LPS elevated the expression levels of Bax and C-caspase-3, but shikonin treatment reversed these effects. Conversely, shikonin restored the reduced expression of Bcl-2 caused by LPS (Fig. 2B). Shikonin countered the increased cell apoptosis rate induced by LPS (Fig. 2C). Shikonin suppressed LPS-induced productions of IL-6, IL-1β, IL-18, and TNF-a (Fig. 2D). In summary, shikonin alleviates LPS-induced WI-38 cell injury by enhancing cell viability and inhibiting cell apoptosis and inflammatory response.

Shikonin mitigates lipopolysaccharide (LPS)-induced damage in WI-38 cells. Fig. 1. Lipopolysaccharide (LPS) contributes to WI-38 cell damage and inflammatory response (Wang J, Chen Z, et al., 2021).

Lipopolysaccharide (LPS) induces damage and triggers an inflammatory response in WI-38 cells. Fig. 2. Shikonin alleviates lipopolysaccharide (LPS)-induced cell injury on WI-38 cells (Wang J, Chen Z, et al., 2021).

Histamine-Evoked Elevation in [Ca²⁺]_i in WI-38 was Mainly Mediated by H1R

Histamine, an inflammatory mediator released from mast cells, induces airway remodeling and persistent airflow limitation in asthma. Histamine receptor 1 (H1R) mediates histamine's effects by increasing intracellular Ca²⁺ concentration in human pulmonary fibroblasts, but the signaling mechanisms are unclear. Therefore, Berra-Romani et al. aimed to examined the mechanisms underlying histamine-induced increase in [Ca²⁺]_i in fetal human pulmonary WI-38 fibroblasts.

The results showed that histamine elicited various intracellular Ca²⁺ responses that were blocked by pyrilamine (H1R inhibitor) and reduced by ranitidine (H2R inhibitor). The Ca²⁺ signals were triggered by Ca²⁺ release from the endoplasmic reticulum via InsP3 receptors and maintained by store-operated Ca²⁺ channels (SOCs). Specific HR antagonists were used to determine which histamine receptor (HR) isoform triggered intracellular Ca²⁺ signaling in WI-38 (pyrilamine: H1R, ranitidine: H2R, clobenpropit: H3R, NJ7777120: H4R). Following a preincubation period with these antagonists, histamine was applied. Arachidonic acid (AA) was used to confirm cell viability in cases where histamine did not induce a [Ca²⁺]_i increase. The results revealed that H1R blockage completely abolished the histamine-evoked Ca²⁺ signal (Fig. 3A), H2R blockage significantly decreased the amplitude of the Ca²⁺ signal (Fig. 3B), while H3R (Fig. 3C) and H4R blockage (Fig. 3D) had no significant effect. Statistical comparisons (Fig. 3E) confirmed that H1R and, to a lesser extent, H2R are essential for Ca²⁺ elevation in WI-38 cells, whereas H3R and H4R are not involved.

Fig. 3. Histamine-evoked Ca²⁺ signals in WI-38 human lung fibroblasts do not involve Gα_i/o activation but require PLC and ER Ca²⁺ release (Berra-Romani R, Vargaz-Guadarrama A, et al., 2022).

What is WI-38?

WI-38, derived from the embryonic lung tissue of a 3-month-gestation female in 1962, is the first human diploid cell line used in the preparation of human vaccines.

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10 Feb 2023