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Spinster homolog 2/S1P signaling ameliorates macrophage inflammatory response to bacterial infections by balancing PGE production.
Cell Commun Signal
September 2024
Department of Pharmacology, School of Pharmacy, Fourth Military Medical University, Xi'an, China.
Article Synopsis
- - Mitochondria are essential for how macrophages (a type of immune cell) respond to bacterial infections, and the protein Spns2, which regulates S1P secretion, influences mitochondrial functions in these cells.
- - Researchers isolated peritoneal macrophages from both normal and Spns2-deficient rats to explore how Spns2/S1P signaling affects mitochondrial functions and inflammation, using techniques like metabolomics, RNA sequencing, and various assays.
- - The study identifies prostaglandin E (PGE) as a key factor in the communication between Spns2/S1P signaling and mitochondria; a lack of Spns2 leads to high PGE levels that disrupt mitochondrial respiration and cause inflammation-related
SPHK1 promotes bladder cancer metastasis via PD-L2/c-Src/FAK signaling cascade.
Cell Death Dis
September 2024
Department of Life Sciences, National Chung Hsing University, Taichung, Taiwan.
SPHK1 (sphingosine kinase type 1) is characterized as a rate-limiting enzyme in sphingolipid metabolism to phosphorylate sphingosine into sphingosine-1-phosphate (S1P) that can bind to S1P receptors (S1PRs) to initiate several signal transductions leading to cell proliferation and survival of normal cell. Many studies have indicated that SPHK1 is involved in several types of cancer development, however, a little is known in bladder cancer. The TCGA database analysis was utilized for analyzing the clinical relevance of SPHK1 in bladder cancer.
View Article and Find Full Text PDFQuercetin Mitigates Lysophosphatidylcholine (LPC)-Induced Neutrophil Extracellular Traps (NETs) Formation through Inhibiting the P2X7R/P38MAPK/NOX2 Pathway.
Int J Mol Sci
August 2024
Xiangya School of Public Health, Central South University, Changsha 410013, China.
Neutrophil extracellular traps (NETs) are three-dimensional reticular structures that release chromatin and cellular contents extracellularly upon neutrophil activation. As a novel effector mechanism of neutrophils, NETs possess the capacity to amplify localized inflammation and have been demonstrated to contribute to the exacerbation of various inflammatory diseases, including cardiovascular diseases and tumors. It is suggested that lysophosphatidylcholine (LPC), as the primary active component of oxidized low-density lipoprotein, represents a significant risk factor for various inflammatory diseases, such as cardiovascular diseases and neurodegenerative diseases.
View Article and Find Full Text PDFFunctional determinants of lysophospholipid- and voltage-dependent regulation of TRPC5 channel.
Cell Mol Life Sci
August 2024
Department of Cellular Neurophysiology, Institute of Physiology, Czech Academy of Sciences, Videnska 1083, 142 20, Prague 4, Czech Republic.
Lysophosphatidylcholine (LPC) is a bioactive lipid present at high concentrations in inflamed and injured tissues where it contributes to the initiation and maintenance of pain. One of its important molecular effectors is the transient receptor potential canonical 5 (TRPC5), but the explicit mechanism of the activation is unknown. Using electrophysiology, mutagenesis and molecular dynamics simulations, we show that LPC-induced activation of TRPC5 is modulated by xanthine ligands and depolarizing voltage, and involves conserved residues within the lateral fenestration of the pore domain.
View Article and Find Full Text PDFLPA-induced expression of CCN2 in muscular fibro/adipogenic progenitors (FAPs): Unraveling cellular communication networks.
Matrix Biol
June 2024
Centro Científico y Tecnológico de Excelencia Ciencia & Vida, Santiago, Chile; Facultad de Medicina y Ciencia, Universidad San Sebastián, Santiago, Chile. Electronic address:
Cellular Communication Network Factor 2, CCN2, is a profibrotic cytokine implicated in physiological and pathological processes in mammals. The expression of CCN2 is markedly increased in dystrophic muscles. Interestingly, diminishing CCN2 genetically or inhibiting its function improves the phenotypes of chronic muscular fibrosis in rodent models.
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