The cellular mechanisms regulating secretion of the peptide hormone atrial natriuretic factor (ANF) differ in neonatal atrial and ventricular cardiocytes. We demonstrate that although both cell types synthesize and secrete ANF, only atrial cells store peptide in abundant secretory granules. Neonatal ventricular cells secrete ANF rapidly after synthesis and lack secretory granules. We propose that ventricular ANF is released by a constitutive secretory pathway whereas atrial ANF is stored and released by a regulated pathway. Furthermore, ventricular ANF mRNA and hormone concentrations decrease during the first week of life. Developmental variation in the use of ANF secretory pathways may reflect changing requirements for maintenance of intravascular volume and pressure. Tissue-specific modulation of hormone secretory pathways appears to be a novel response to developmentally induced changes in the requirements for a peptide hormone.
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BMC Gastroenterol
January 2025
Department of Pediatrics, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi Province, 710061, China.
Background: The increased apoptosis of bile duct epithelial cells (BECs) due to some damage factors is considered the initiating factor in the occurrence and progression of biliary atresia (BA). Vitamin D receptor (VDR) is thought to play a crucial role in maintaining the intrinsic immune balance and integrity of bile duct epithelial cells (BECs). To investigate the role of VDRs in the pathogenesis and progression of BA using in vitro and in vivo models.
View Article and Find Full Text PDFJ Lipid Res
January 2025
Department of Biological Sciences, Kent State University, P.O. Box 5190, Kent, OH 44242, USA. Electronic address:
Phosphatidic acid (PA) through its unique negatively charged phosphate headgroup binds to various proteins to modulate multiple cellular events. To perform such diverse signaling functions, the ionization and charge of PA's headgroup relies on the properties of vicinal membrane lipids and changes in cellular conditions. Cholesterol has conspicuous effects on lipid properties and membrane dynamics.
View Article and Find Full Text PDFmBio
January 2025
Department of Microbiology and Immunology, University of Rochester Medical Center, Rochester, New York, USA.
Unlabelled: Pathogenic strains cause cholera using different mechanisms. O1 and O139 serogroup strains use the toxin-co-regulated pilus (TCP) and cholera toxin (CT) for intestinal colonization and to promote secretory diarrhea, while non-O1/non-O139 serogroup strains are typically non-toxigenic and use alternate virulence factors to cause a clinically similar disease. An O39 serogroup, TCP/CT-negative strain, named AM-19226, uses a type III secretion system (T3SS) to translocate more than 10 effector proteins into the host cell cytosol.
View Article and Find Full Text PDFPlant Physiol
January 2025
State Key Laboratory of Microbial Metabolism & Joint International Research Laboratory of Metabolic and Developmental Sciences, School of Life Sciences and Biotechnology, Shanghai Jiao Tong University, Shanghai, 200240, China, P. R.
Mitochondria have generated the bulk of ATP to fuel cellular activities, including membrane trafficking, since the beginning of eukaryogenesis. How inhibition of mitochondrial energy production will affect the form and function of the endomembrane system and whether such changes are specific in today's cells remain unclear. Here, we treated Arabidopsis thaliana with antimycin A (AA), a potent inhibitor of the mitochondrial electron transport chain (mETC), as well as other mETC inhibitors and an uncoupler.
View Article and Find Full Text PDFLife Metab
February 2025
New Cornerstone Science Laboratory, State Key Laboratory of Membrane Biology, Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Institute of Molecular Medicine, National Biomedical Imaging Center, The Beijing Laboratory of Biomedical Imaging, Peking-Tsinghua Center for Life Sciences, School of Future Technology, Peking University, Beijing 100871, China.
Glucose-stimulated insulin release from pancreatic β-cells is critical for maintaining blood glucose homeostasis. An abrupt increase in blood glucose concentration evokes a rapid and transient rise in insulin secretion followed by a prolonged, slower phase. A diminished first phase is one of the earliest indicators of β-cell dysfunction in individuals predisposed to develop type 2 diabetes.
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