The action of two potent store operated Ca2+ entry (SOCE) inhibitors, ML-9 and GdCl3 on Ca2+ fluxes induced by the pro-inflammatory agonists FMLP, PAF, LTB(4) as well as the receptor-independent stimulus thapsigargin has not been documented in human neutrophils. In this study, ML-9 enhanced both release and subsequent Ca2+ influx in response to agonists whereas it enhanced Ca2+ release by thapsigargin, but inhibited Ca2+ influx. In contrast, 1muM GdCl3 completely inhibited Ca2+ influx in response to thapsigargin, but only partially blocked Ca2+ influx after agonist stimulation. These results strongly suggest a major role for receptor-operated Ca2+ influx in human neutrophils.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.cellimm.2010.02.001 | DOI Listing |
FASEB J
January 2025
Department of Urology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Acute Kidney Injury (AKI) is a significant medical condition characterized by the abrupt decline in kidney function.Low-intensity pulsed ultrasound (LIPUS), a non-invasive therapeutic technique employing low-intensity acoustic wave pulses, has shown promise in promoting tissue repair and regeneration. A novel LIPUS system was developed and evaluated in rat AKI models, focusing on its effects on glomerular filtration rate (GFR), blood urea nitrogen (BUN), serum creatinine (SCr), and the Notch1-Akt-eNOS signaling pathway.
View Article and Find Full Text PDFJ Integr Plant Biol
January 2025
State Key Laboratory of Crop Genetics & Germplasm Enhancement and Utilization, College of Agriculture, Nanjing Agricultural University, Nanjing, 210095, China.
Members of the cyclic nucleotide-gated channel (CNGC) proteins are reportedly involved in a variety of biotic and abiotic responses and stomatal movement. However, it is unknown if and how a single member could regulate multiple responses. Here we characterized three closely related CNGC genes in rice, OsCNGC14, OsCNGC15 and OsCNGC16, to determine whether they function in multiple abiotic stresses.
View Article and Find Full Text PDFBMC Med
January 2025
Physiological Institute, University of Regensburg, University Street 31, 93053, Regensburg, Germany.
Background: Dystonia is a common neurological hyperkinetic movement disorder that can be caused by mutations in anoctamin 3 (ANO3, TMEM16C), a phospholipid scramblase and ion channel. We previously reported patients that were heterozygous for the ANO3 variants S651N, V561L, A599D and S651N, which cause dystonia by unknown mechanisms.
Methods: We applied electrophysiology, Ca measurements and cell biological methods to analyze the molecular mechanisms that lead to aberrant intracellular Ca signals and defective activation of K channels in patients heterozygous for the ANO3 variants.
Proc Natl Acad Sci U S A
January 2025
Department of Microbiology and Immunology, Center for Molecular Parasitology, Drexel University College of Medicine, Philadelphia, PA 19129.
Among new antimalarials discovered over the past decade are multiple chemical scaffolds that target P-type ATPase (ATP4). This essential protein is a Na pump responsible for the maintenance of Na homeostasis. ATP4 belongs to the type two-dimensional (2D) subfamily of P-type ATPases, for which no structures have been determined.
View Article and Find Full Text PDFAm J Physiol Lung Cell Mol Physiol
January 2025
Smooth Muscle Research Centre, Dundalk Institute of Technology, Dublin Road, Dundalk, Co. Louth, Ireland.
Cholinergic tone is elevated in obstructive lung conditions such as COPD and asthma, but the cellular mechanisms underlying cholinergic contractions of airway smooth muscle (ASM) are still unclear. Some studies report an important role for L-type Ca channels (LTCC) and Ano1 Ca-activated Cl™ channels (CACC) in these responses, but others dispute their importance. Cholinergic contractions of ASM involve activation of M3Rs, however stimulation of M2Rs exerts a profound hypersensitisation of these responses.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!