Merely touching the pancreas can lead to premature zymogen activation and pancreatitis but the mechanism is not completely understood. Here we demonstrate that pancreatic acinar cells express the mechanoreceptor Piezo1 and application of pressure within the gland produces pancreatitis. To determine if this effect is through Piezo1 activation, we induce pancreatitis by intrapancreatic duct instillation of the Piezo1 agonist Yoda1. Pancreatitis induced by pressure within the gland is prevented by a Piezo1 antagonist. In pancreatic acinar cells, Yoda1 stimulates calcium influx and induces calcium-dependent pancreatic injury. Finally, selective acinar cell-specific genetic deletion of Piezo1 protects mice against pressure-induced pancreatitis. Thus, activation of Piezo1 in pancreatic acinar cells is a mechanism for pancreatitis and may explain why pancreatitis develops following pressure on the gland as in abdominal trauma, pancreatic duct obstruction, pancreatography, or pancreatic surgery. Piezo1 blockade may prevent pancreatitis when manipulation of the gland is anticipated.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5928090 | PMC |
http://dx.doi.org/10.1038/s41467-018-04194-9 | DOI Listing |
BMC Pediatr
January 2025
Department of Pediatric, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Background: Pediatric pancreatic acinar cell carcinoma (PACC) is an exceptionally rare and poorly understood malignancy with a challenging prognosis. Its clinical presentation is often atypical, and standardized treatment guidelines are currently unavailable. While genetic alterations in adult PACC have been studied to some extent, knowledge of genetic abnormalities in pediatric cases remains limited.
View Article and Find Full Text PDFPharmacol Res
January 2025
Department of Integrated Traditional Chinese and Western Medicine, West China Hospital of Sichuan University, Chengdu, China. Electronic address:
The necrosis of pancreatic acinar cells is a key molecular event in the progression of acute pancreatitis (AP), with disturbances in mitochondrial energy metabolism considered to be a direct causative factor of acinar cell necrosis. Histidine triad nucleotide-binding protein 2 (HINT2) has been implicated in the development of various diseases, whereas its involvement in the progression of AP remains unclear. This study aims to investigate the role of HINT2 in AP.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Translational Research and Cellular Therapeutics, Arthur Riggs Diabetes and Metabolism Research Institute, Duarte, USA.
Lectins are produced in almost all life forms, can interact with targets (glycans) in a cross-kingdom manner and have served as valuable tools for studying glycobiology. Previously, a bacterial lectin, named Streptomyces hemagglutinin (SHA), was found to agglutinate human type B erythrocytes. However, the binding of SHA to mammalian cell types other than human erythrocytes has not been explored.
View Article and Find Full Text PDFFront Nutr
January 2025
Department of Ultrasound, Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian, China.
Background: Hyperuricemia and non-alcoholic fatty pancreas disease (NAFPD) are prevalent metabolic diseases, but the relationship between them remains underexplored.
Methods: Eighteen Sprague-Dawley rats were randomly assigned to three groups: normal (CON), high-fat (PO), and high-fat high-uric acid (PH). After 12 weeks, serum uric acid (SUA) and triacylglycerol levels were measured.
Ann Surg Treat Res
January 2025
Center for Liver and Pancreatobiliary Cancer, National Cancer Center, Goyang, Korea.
Purpose: This study investigated epidemiologic features of patients with pancreatic cancer in Korea, according to the histologic subtypes.
Methods: The Korea Central Cancer Registry data on patients with pancreatic cancer from 1999 to 2019 were reviewed. The 101,446 patients with pancreatic cancer (C25 based on the International Classification of Diseases, 10th revision) were allocated according to the following morphological codes: A, endocrine; B, carcinoma excluding cystic and mucinous; C, cystic or mucinous; D, acinar cell; and E, sarcoma and soft tissue tumor.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!