The mechanism of radiation-induced dysfunction in rat submandibular glands was investigated at the cellular level. After X irradiation (single dose, 15 Gy), a vacuolation in the acinar cells or an enlargement of the acinar lumen was observed as a typical morphological change for 2 weeks. As observed using a video-enhanced contrast differential interference contrast (VEC-DIC) microscope, exocytosis and shrinkage of the acinar cells induced by application of pilocarpine (100 microM) were markedly suppressed for 5 days and then recovered to 80% of the control levels. Using an immunohistochemical method, no significant change was observed in amylase distribution, but a marked loss of aquaporin 5 was found in the acinar cells after the irradiation. The extent and time course of pilocarpine-induced mobilization of intracellular Ca(2+) did not change after the irradiation. We conclude that radiation-induced dysfunction in the salivary glands is due to an impairment of exocytosis and a reduction of water secretion. The loss of aquaporin 5 and possibly other membrane-fusion proteins in acinar cells may be the major mechanism underlying such a dysfunction.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1667/0033-7587(2003)159[0351:sosixi]2.0.co;2 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Exploratory study on the efficacy of topical pan-JAK inhibitor in ocular and skin GVHD in a sclerodermatous GVHD mouse model.
Sci Rep
January 2025
Department of Ophthalmology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo, 160-0016, Japan.
Systemic administration of Janus kinase (JAK) inhibitors is effective in treating chronic graft-versus-host disease (cGVHD) but is associated with side effects. Topical drug administration effectively minimizes side effects. We aimed to investigate potential trends of the efficacy of topical delgocitinib administration in a mouse model.
View Article and Find Full Text PDFEZH2 deletion does not impact acinar regeneration but restricts progression to pancreatic cancer in mice.
JCI Insight
December 2024
Department of Physiology and Pharmacology, University of Western Ontario, London, Canada.
Enhancer of Zeste Homologue 2 (EZH2) is part of the Polycomb Repressor Complex 2, which promotes trimethylation of lysine 27 on histone 3 (H3K27me3) and genes repression. EZH2 is overexpressed in many cancers and studies in mice attributed both pro-oncogenic and tumor suppressive functions to EZH2 in pancreatic ductal adenocarcinoma (PDAC). EZH2 deletion enhances de novo KRAS-driven neoplasia following pancreatic injury, while increased EZH2 expression in PDAC patients is correlated to poor prognosis, suggesting a context-dependant effect for EZH2 in PDAC progression.
View Article and Find Full Text PDFImpact of acute schistosomiasis mansoni and concurrent type 1 diabetes on pancreatic architecture in mice.
Exp Parasitol
December 2024
Romero Lascasas Porto Laboratory of Helminthology, Department of Microbiology, Immunology and Parasitology, Medical Sciences College (FCM), Rio de Janeiro State University (UERJ), Rio de Janeiro, Brazil.
It is not well understood how type 1 diabetes (T1D) and concomitant acute schistosomiasis mansoni affect pancreatic architecture. Male Swiss mice were administered streptozotocin (single 100 mg/kg i.p.
View Article and Find Full Text PDFTuft cells transdifferentiate to neural-like progenitor cells in the progression of pancreatic cancer.
Dev Cell
December 2024
Department of Surgery, Henry Ford Health, Detroit, MI, USA; Department of Pharmacology and Toxicology, Michigan State University, Lansing, MI, USA. Electronic address:
Pancreatic ductal adenocarcinoma (PDA) is partly initiated through the transdifferentiation of acinar cells to metaplasia, which progresses to neoplasia and cancer. Tuft cells (TCs) are chemosensory cells not found in the normal pancreas but arise in cancer precursor lesions and diminish during progression to carcinoma. These metaplastic TCs (mTCs) suppress tumor progression through communication with the tumor microenvironment, but their fate during progression is unknown.
View Article and Find Full Text PDFHyperaminoacidemia from interrupted glucagon signaling increases pancreatic acinar cell proliferation and size via mTORC1 and YAP pathways.
iScience
December 2024
Department of Molecular Physiology & Biophysics, Vanderbilt University, Nashville, TN, USA.
Increased blood amino acid levels (hyperaminoacidemia) stimulate pancreas expansion by unclear mechanisms. Here, by genetic and pharmacological disruption of glucagon receptor (GCGR) in mice and zebrafish, we found that the ensuing hyperaminoacidemia promotes pancreatic acinar cell proliferation and cell hypertrophy, which can be mitigated by a low protein diet in mice. In addition to mammalian target of rapamycin complex 1 (mTORC1) signaling, acinar cell proliferation required , the most highly expressed amino acid transporter gene in both species.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!