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Related Concept Videos

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion01:27

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion

The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
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Multicellular organisms contain a variety of structurally and functionally distinct cell types, but the DNA in all the cells originated from the same parent cells. The differences in the cells can be attributed to the differential gene expression. Liver cells, whose functions include detoxification of blood, production of bile to metabolize fats, and synthesis of proteins essential for metabolism, must express a specific set of genes to perform their functions. Gene expression also varies with...
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Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular uptake of...
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Chronic pancreatitis is a progressive and irreversible inflammation of the pancreas, most often caused by long-term alcohol abuse, but it can also be related to ductal obstruction, smoking, or genetic factors.Chronic pancreatitis occurs when the pancreas is repeatedly exposed to harmful agents like alcohol, smoking, ductal obstruction, or genetic predisposition. These factors lead to the release of toxic metabolites and inflammatory cytokines, sustaining chronic inflammation in the pancreatic...
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Related Experiment Video

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Isolated Pancreatic Islet Treatment and Apoptosis Measurement
09:36

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Published on: May 2, 2025

Interleukin-32 expression in the pancreas.

Atsushi Nishida1, Akira Andoh, Osamu Inatomi

  • 1Department of Medicine, Shiga University of Medical Science, Seta-Tukinowa, Otsu 520-2192, Japan.

The Journal of Biological Chemistry
|April 24, 2009
PubMed
Summary

Interleukin-32 (IL-32) is upregulated in chronic pancreatitis and pancreatic cancer. This proinflammatory cytokine promotes cancer cell growth and survival, suggesting its role in pancreatic ductal adenocarcinoma progression.

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Area of Science:

  • Immunology
  • Oncology
  • Gastroenterology

Background:

  • Interleukin-32 (IL-32) is a proinflammatory cytokine.
  • IL-32 induces nuclear factor-kappaB (NF-kappaB) activation.
  • The role of IL-32 in pancreatic inflammation and cancer is not well understood.

Purpose of the Study:

  • To investigate IL-32 expression in human pancreatic tissue and cancer cell lines.
  • To elucidate the regulatory mechanisms of IL-32 expression.
  • To determine the functional role of IL-32 in pancreatic cancer cell growth and apoptosis.

Main Methods:

  • Immunohistochemistry, Northern blotting, and real-time PCR were used to analyze IL-32 expression.
  • Pancreatic cancer cell lines were treated with IL-1beta, interferon-gamma (IFN-gamma), and tumor necrosis factor-alpha (TNF-alpha).
  • Inhibitors of phosphatidylinositol 3-kinase (PI3K) and NF-kappaB/activator protein-1 (AP-1) pathways were used.
  • Small interfering RNA (siRNA) targeting IL-32 was employed to assess its functional role.

Main Results:

  • IL-32 was weakly expressed in normal pancreatic duct cells but markedly increased in chronic pancreatitis lesions.
  • Pancreatic cancer cells showed strong IL-32alpha expression.
  • IL-1beta, IFN-gamma, and TNF-alpha enhanced IL-32 expression in cancer cell lines.
  • PI3K, NF-kappaB, and AP-1 pathways regulate IL-32 expression.
  • IL-32 knockdown reduced proliferation and increased apoptosis in PANC-1 cells, suppressing antiapoptotic protein expression.

Conclusions:

  • Pancreatic duct cells are a local source of IL-32.
  • IL-32 plays a significant role in pancreatic inflammation and cancer progression.
  • Targeting IL-32 may offer a therapeutic strategy for pancreatic cancer.