Immortalized Human Pancreatic Stellate Cells-SV40

Cat.No.: CSC-I2291Z

Species: homo sapiens

Morphology: Polygonal

Culture Properties: Adherent

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Cat.No.
CSC-I2291Z
Description
Immortalized Human Pancreatic Stellate Cells-SV40 provided by Creative Bioarray have been developed by immortalizing primary human pancreatic stellate cells with SV40 Large T antigen. The cell line was continuously cultured for more than 20 passages without showing signs of growth retardation or replicative senescence.
Species
homo sapiens
Recommended Medium
SuperCult® Immortalized Human Pancreatic Stellate Cell Medium (Cat No.: CM-I2291Z)
Freezing Medium
Complete medium supplemented with 10% (v/v) DMSO
Culture Properties
Adherent
Morphology
Polygonal
Immortalization Method
SV40 large T antigen
Application
For Research Use Only
Growth Properties
Cells are cultured as a monolayer at 37°C in a humidified atmosphere with 5% CO2.
Shipping
Dry Ice.
Quality Control
Real Time PCR was used to quantify SV40T gene expression in immortalized cell line.
free from contaminations (bacteria incl. mycoplasma, fungi, HIV, HAV, HBV, HCV, Parvo-B19) and cross-contaminations
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.

Pancreatic stellate cells (PSCs) play a key role in the pathogenesis of pancreatic fibrosis and the deposition of large amounts of insoluble extracellular matrix (ECM). In a normal pancreas, stellate cells are quiescent and, like their counterparts in the liver, store vitamin A in lipid droplets in their cytoplasm. When exposed to injury, inflammation or after prolonged cultivation in vitro, the cells transform to an activated myofibroblast-like state. In this activated state, PSCs begin to proliferate and synthesize ECM components like collagen type I and III (Col I and Col III), fibronectin (FN) and laminin. This state is accompanied by a gradual loss of lipid droplets and the expression of the proteins desmin, vimentin, αSMA and glial fibrillary acidic protein (GFAP).

Several methods for isolation of these cells have been published; however, these methods need fairly large amounts of tissue to obtain a sufficient number of cells. Furthermore, due to the finite lifespan of PSCs and the phenotypic changes observable with time in culture, researchers need to analyze different preparations of PSCs, making a direct comparison of results difficult. Immortalized Human Pancreatic Stellate Cells-SV40 retain key phenotypic features of primary pancreatic stellate cells while possessing the extended lifespan and reproducibility required for robust experimental studies. They are ideal for research in pancreatic biology, fibrosis, tumor-stroma interactions, and extracellular matrix regulation.

Key characteristics of the immortalized human pancreatic stellate cell line

Fig. 1. Key characteristics of the immortalized human pancreatic stellate cell line (Sun, L. et al., 2020).

Collagen Signaling via DDR1 Exacerbates Barriers to Macromolecular Drug Delivery in a 3D Model of Pancreatic Cancer Fibrosis

Fibrosis is a significant barrier to drug delivery in pancreatic ductal adenocarcinoma (PDAC) and contributes to its dismal prognosis. Pancreatic stellate cells (PSCs) drive fibrosis by excessively secreting extracellular matrix proteins such as collagen I. Collagen I is thought to physically obstruct the delivery of macromolecules, such as albumin, antibodies, and nanomedicines. Apart from its structural role, collagen signals through dedicated cell surface receptors, such as the discoidin domain receptors (DDR) 1/2. However, whether and how collagen signaling contributes to fibrotic barrier generation remains uncharacterized.

Here, a 3D culture model of PDAC fibrosis constructed from patient PSCs is used to assess the contribution of DDR1/2-mediated collagen signaling. DDR1/2 inhibition diminishes collagen I expression in PSCs to enhance macromolecular delivery. Moreover, MEK inhibitors exacerbate the fibrotic barrier by up-regulating collagen I, an effect reversed by inhibiting DDR1/2. Through isoform-specific targeting, inhibiting DDR1, but not DDR2, is shown to be effective. Altogether, the results show in vitro that DDR1-mediated collagen signaling exacerbates the fibrotic barrier and may be targeted to enhance macromolecular drug delivery in PDAC.

Thickness and permeability to 2000 kDa FITC-dextran of 3D-PDAC fibrotic tissues treated with the DDR1 inhibitor DDR1-IN-1, DDR2 inhibitor WRG-28, siRNA targeting DDR1 (siDDR1), DDR2 (siDDR2), or a 1:1 mixture of the two (siDDR1+2).

Fig. 1. Targeting of DDR1 is sufficient to enhance macromolecular permeability of 3D-PDAC fibrotic tissues (Ohira, Mayu, et al., 2025).

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