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Related Concept Videos

Acute Pancreatitis II: Pathophysiology01:21

Acute Pancreatitis II: Pathophysiology

The pathophysiology of acute pancreatitis centers on injury to pancreatic acinar cells, which initiates a cascade of harmful intracellular events.This injury leads to premature activation of trypsinogen to trypsin in the pancreas. Trypsin then activates other digestive enzymes, such as chymotrypsin, elastase, and phospholipase A2, which begin breaking down pancreatic tissue. The resulting autodigestion causes local inflammation, tissue swelling, hemorrhage, and fat necrosis.Injured acinar cells...
Chronic Pancreatitis II: Pathophysiology01:21

Chronic Pancreatitis II: Pathophysiology

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...
Chronic Pancreatitis I: Introduction01:24

Chronic Pancreatitis I: Introduction

The pancreas, an elongated and flat gland situated behind the stomach, serves a vital function in digesting food and managing blood sugar levels.
Pancreatitis is the inflammation of the pancreas, which occurs when the immune system becomes active and causes swelling, pain, and disruptions in organ function. Pancreatitis can manifest as either an acute or chronic condition.
Acute pancreatitis arises suddenly and lasts for a brief duration, while chronic pancreatitis is a long-term affliction...
Chronic Pancreatitis I: Introduction01:25

Chronic Pancreatitis I: Introduction

Chronic pancreatitis is a long-standing, relapsing inflammation of the pancreas, characterized by irreversible damage to the gland. It results in progressive destruction of the pancreatic parenchyma, fibrosis, and eventual loss of both exocrine and endocrine function. The disease may evolve gradually after multiple episodes of acute pancreatitis or develop independently.EtiologyChronic pancreatitis can arise from a variety of causes:Alcohol use is the leading cause, accounting for 70–80% of...
Cellular Adaptation IV: Dysplasia and Metaplasia01:24

Cellular Adaptation IV: Dysplasia and Metaplasia

DysplasiaDysplasia refers to abnormal changes in the size, shape, and organization of mature cells, characterized by pleomorphism, nuclear abnormalities, and increased mitotic activity. It commonly affects epithelial tissues, including the cervix, gastrointestinal tract, respiratory mucosa, and endometrium. Although it may occur alongside hyperplasia, dysplasia is not a true adaptive response but a preneoplastic change with potential to progress to cancer.When confined above the basement...
Cellular Adaptation II: Hypertrophy01:26

Cellular Adaptation II: Hypertrophy

Hypertrophy is the increase in the size of individual cells, resulting in the enlargement of a tissue or organ. Unlike hyperplasia, which involves an increase in cell number, hypertrophy is characterized by an increase in cell volume. This process often occurs in response to higher functional demand or hormonal stimulation, leading to the production of more structural proteins and organelles, thereby enhancing the cells' work capacity.There are two primary types of hypertrophy: physiological...

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Related Experiment Video

Updated: May 8, 2026

Mimicking and Manipulating Pancreatic Acinar-to-Ductal Metaplasia in 3-dimensional Cell Culture
08:16

Mimicking and Manipulating Pancreatic Acinar-to-Ductal Metaplasia in 3-dimensional Cell Culture

Published on: February 11, 2019

Increased Protein Synthesis With Reduced Endoplasmic Reticulum Stress Defines a Specific Adaptation in Pancreatic

Maxime Libert1, Sophie Quiquempoix1, Leyre López-Muneta1,2

  • 1Université catholique de Louvain, de Duve Institute, Brussels, Belgium.

Gastro Hep Advances
|May 7, 2026
PubMed
Summary

Pancreatic cancer cells increase protein synthesis and modify ribosomes, while decreasing endoplasmic reticulum stress. This adaptation in acinar cells highlights unique translational machinery changes during tumorigenesis.

Keywords:
ER StressPancreatic TumorigenesisRibosomeTranslation Initiation

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Isolating and Analyzing Cells of the Pancreas Mesenchyme by Flow Cytometry
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Last Updated: May 8, 2026

Mimicking and Manipulating Pancreatic Acinar-to-Ductal Metaplasia in 3-dimensional Cell Culture
08:16

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Published on: February 11, 2019

Preparation of Pancreatic Acinar Cells for the Purpose of Calcium Imaging, Cell Injury Measurements, and Adenoviral Infection
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Preparation of Pancreatic Acinar Cells for the Purpose of Calcium Imaging, Cell Injury Measurements, and Adenoviral Infection

Published on: July 5, 2013

Isolating and Analyzing Cells of the Pancreas Mesenchyme by Flow Cytometry
05:38

Isolating and Analyzing Cells of the Pancreas Mesenchyme by Flow Cytometry

Published on: January 28, 2017

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cellular Biology

Background:

  • Tumorigenesis often involves elevated protein synthesis and endoplasmic reticulum (ER) stress.
  • Pancreatic acinar cells possess high basal protein synthesis rates, posing unique challenges during tumor development.
  • Pancreatic ductal adenocarcinoma (PDAC) arises from precursor lesions, necessitating an understanding of cellular adaptations.

Purpose of the Study:

  • To investigate how pancreatic acinar cells alter protein synthesis rates during tumorigenesis.
  • To characterize the modulation of translation and ER stress in precursor lesions of PDAC.
  • To explore the role of ribosomal RNA methylation in adaptive protein synthesis.

Main Methods:

  • Puromycin incorporation assays to measure protein synthesis rates.
  • Transcriptomic analysis and mouse models to study translation control and ER stress.
  • RiboMethSeq (deep sequencing) to assess ribosomal RNA methylation patterns.

Main Results:

  • Protein synthesis rates significantly increased in acinar-to-ductal metaplasia compared to normal acinar cells.
  • Enhanced translation initiation factors, ribosomal components, and assembly factors were observed.
  • Differential ribosomal RNA methylation occurred near key functional sites, potentially impacting translation and protein folding.
  • Despite increased synthesis, ER stress decreased, linked to reduced N-linked glycosylation and increased proteasome activity.

Conclusions:

  • Pancreatic tumorigenesis involves a unique adaptation of the translational machinery in acinar cells.
  • This adaptation includes the generation of differentially modified ribosomes.
  • The study reveals a combination of increased protein synthesis and decreased ER stress, showcasing adaptive plasticity in transforming tissues.