Dissecting SNARE-Mediated Exocytosis in RBL-2H3 Mast Cells.

SNARE-dependent mast cell (MC) exocytosis causes the release of a wide variety of mediators with important physiological/pathological consequences. Unlike synaptic transmission in the brain, which relies primarily on one set of exocytic SNAREs (i.e.

Analysis of predictors of clinical pregnancy and live birth in patients with RIF treated with IVF-ET technology: a cohort study based on a propensity score approach.

Objective: To investigate the predictors of clinical pregnancy and live birth rate in patients with recurrent embryo implantation failure (RIF) treated with fertilization-embryo transfer (IVF-ET) technique.

Method: This retrospective cohort study was conducted in Jinjiang District Maternal and Child Health Hospital, Chengdu City, Sichuan Province, China. Patients were recruited who were enrolled at this hospital between November 1, 2019 and August 31, 2022, and who met the following criteria: a frozen embryo transfer (FET) at day 5 or 6 blastocyst stage was performed and the number of transfer cycles was not less than two.

Exocytic machineries differentially control mediator release from allergen-triggered RBL-2H3 cells.

Background: Mast cells utilize SNAREs (soluble-N-ethyl-maleimide sensitive factor attachment protein receptors) and SM (Sec1/Munc18) proteins to secrete/exocytose a variety of proinflammatory mediators. However, whether a common SNARE-SM machinery is responsible remains unclear.

Methods: Four vesicle/granule-anchored SNAREs (VAMP2, VAMP3, VAMP7, and VAMP8) and two Munc18 homologs (Munc18a and Munc18b) were systematically knocked down or knocked out in RBL-2H3 mast cells and antigen-induced release of β-hexosaminidase, histamine, serotonin, and TNF was examined.

TNFR1 links TNF exocytosis to TNF production in allergen-activated RBL-2H3 cells.

We previously reported that the maximal production of Tumor Necrosis Factor (TNF or TNFα) in antigen-activated RBL-2H3 cells (a tumor analog of mucosal mast cells) requires Munc13-4, a regulator of exocytic fusion. In this study, we investigated the involvement of various fusion catalysts in TNF production. We observed a strong correlation between the total TNF level and TNF exocytosis in RBL-2H3 cells.

TNF Production in Activated RBL-2H3 Cells Requires Munc13-4.

Mast cell activation triggers intricate signaling pathways that promote the expression and/or release of a wide range of mediators including tumor necrosis factor (TNF; also known as TNFα). In this study, we investigated the connection between TNF secretion and TNF production, exploiting RBL-2H3 cells (a tumor analog of mucosal mast cells) that are depleted of Munc13-4, a crucial component of the mast cell exocytic machinery. We showed that antigen/IgE elicited robust TNF production in RBL-2H3 cells, but not in Munc13-4 knockout cells.

Correction: Surveillance of Influenza A Virus and Its Subtypes in Migratory Wild Birds of Nepal.

[This corrects the article DOI: 10.1371/journal.pone.

Author Correction: PKC-dependent phosphorylation of Munc18a at Ser313 in activated RBL-2H3 cells.

Acknowledgements This work was supported by the University of Southern Mississippi Development Grant DE01475, the National Institute of Allergy and Infectious Diseases Grant 1R15AI133430-01, and by the Mississippi INBRE, which was funded by an Institutional Development Award (IDeA) from NIGMS under Grant no. P20GM103476.

PKC-dependent phosphorylation of Munc18a at Ser313 in activated RBL-2H3 cells.

Protein Kinase C (PKC) regulates the release of pro-inflammatory compounds from IgE/antigen-activated mast cells by unknown mechanisms. In this study, we show for the first time that PKC inhibitor Ro-03-0432, which inhibits RBL-2H3 exocytosis/degranulation in a concentration-dependent fashion, prevents the phosphorylation of membrane fusion factor Munc18a at Ser 313. Our study provides fresh evidence that PKC-dependent protein phosphorylation may contribute to the intricate regulation of mast cell degranulation by directly targeting the fusion factors.

Munc18a clusters SNARE-bearing liposomes prior to -SNARE zippering.

Sec1-Munc18 (SM) proteins co-operate with SNAREs {SNAP [soluble NSF (-ethylmaleimide-sensitive factor) attachment protein] receptors} to mediate membrane fusion in eukaryotic cells. Studies of Munc18a/Munc18-1/Stxbp1 in neurotransmission suggest that SM proteins accelerate fusion kinetics primarily by activating the partially zippered -SNARE complex. However, accumulating evidence has argued for additional roles for SM proteins in earlier steps in the fusion cascade.

Surveillance of Influenza A Virus and Its Subtypes in Migratory Wild Birds of Nepal.

Nepal boarders India and China and all three countries lie within the Central Asian Flyway for migratory birds. Novel influenza A H7N9 caused human fatalities in China in 2013. Subclinical infections of influenza A H7N9 in birds and the potential for virus dispersal by migratory birds prompted this study to assess avian H7N9 viral intrusion into Nepal.