Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.arbres.2009.12.009 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Impact 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 PDFLow expression of CCKBR in the acinar cells is associated with insufficient starch hydrolysis in ruminants.
Commun Biol
December 2024
CAS Key Laboratory for Agro-Ecological Processes in Subtropical Region, National Engineering Laboratory for Pollution Control and Waste Utilization in Livestock and Poultry Production, Hunan Provincial Key Laboratory of Animal Nutritional Physiology and Metabolic Process, Institute of Subtropical Agriculture, The Chinese Academy of Sciences, Changsha, Hunan, 410125, China.
Unlike monogastric animals, ruminants exhibit significantly lower starch digestibility in the small intestine. A better understanding of the physiological mechanisms that regulate digestion patterns in ruminants could lead to an increased use of starch concentrates. Here we show more robust pancreatic exocrine function in adult goats (AG) than in neonatal goats (NG) by combining scRNA-seq and proteomic analysis.
View Article and Find Full Text PDFGlobal versus local matrix remodeling drives rotational versus invasive collective migration of epithelial cells.
Dev Cell
December 2024
Department of Bioengineering, University of California, San Diego, La Jolla, CA 92093, USA. Electronic address:
The coordinated movement of cell collectives is essential for normal epithelial tissue development, maintenance, and cancer progression. Here, we report on a minimal 3D extracellular matrix (ECM) system wherein both invasive collective migration (ICM) and rotational collective migration (RCM) arise spontaneously from individually seeded epithelial cells of mammary and hepatic origin, regardless of whether they express adherens junctions, and lead to ductal-like and acinar-like structures, respectively. Quantitative microscopy and cellular Potts modeling reveal that initial differences in cell protrusion dynamics and matrix-remodeling localization generate RCM and ICM behavior in confining 3D ECM.
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!