CCK1 and CCK2 receptors are expressed on pancreatic stellate cells and induce collagen production. (1/41)

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Pancreatic stellate cell models for transcriptional studies of desmoplasia-associated genes. (2/41)

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The effect of anti-hypertensive drugs on the obstructive pancreatitis in rats. (3/41)

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Role of pancreatic stellate cells in pancreatic cancer metastasis. (4/41)

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Roles of Smad3 and Smad7 in rat pancreatic stellate cells activated by transforming growth factor-beta 1. (5/41)

BACKGROUND: Pancreatic stellate cells (PSCs) play a major role in promoting pancreatic fibrosis. Transforming growth factor beta 1 (TGF-beta1) is a critical mediator of this process. This study aimed to determine the expression of the Smad3 and Smad7 genes in the process of PSC activation, and explore the mechanisms of chronic pancreatitis. METHODS: The expressions of Smad3 and Smad7 in PSCs before and after TGF-beta1 treatment were detected by reverse transcription-polymerase chain reaction and Western blotting analysis. Smad3 expression was detected in PSCs after treatment with 5 ng/ml of TGF-beta1 for 24 hours. RESULTS: Smad7 expression was decreased in TGF-beta1-activated PSCs (P<0.05) in a dose-dependent manner. When TGF-beta1 concentration reached 10 ng/ml, the expression of p-Smad3, Smad3, and Smad7 was inhibited (P<0.05). CONCLUSIONS: TGF-beta1 promotes the expression of Smad3 and inhibits the expression of Smad7 during the activation of PSCs. In contrast, high-dose TGF-beta1 downregulates the expression of Smad3 in completely activated PSCs.  (+info)

Phenotypic changes in mouse pancreatic stellate cell Ca2+ signaling events following activation in culture and in a disease model of pancreatitis. (6/41)

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Studies on mechanisms of interferon-gamma action in pancreatic cancer using a data-driven and model-based approach. (7/41)

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Pancreatic stellate cells radioprotect pancreatic cancer cells through beta1-integrin signaling. (8/41)

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