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Deciphering the impact of NOS-derived NO on nitrogen metabolism and carbon flux in the heterocytous cyanobacterium Aphanizomenon flos-aquae 2012/KM1/D3.
Plant Physiol Biochem
January 2025
Laboratory of Microbial Genetics, Department of Botany, Institute of Science, Banaras Hindu University, Varanasi, 221005, India. Electronic address:
Nitric oxide synthases (NOSs) are heme-based monooxygenases that catalyze the NADPH-dependent oxidation of L-arginine to produce NO and L-citrulline. Over the past five years, the identification and characterization of NOS homologs in cyanobacteria have significantly advanced our understanding of these enzymes. However, the precise mechanisms through which NOS-derived NO influences nitrogen metabolism remain incompletely elucidated.
View Article and Find Full Text PDFThe P2X7-Mediated Mitochondrial ROS as an Emerging Core Target of Tuftsin Nanoparticles in Severe Acute Pancreatitis Therapy via Regulating Mitophagy.
ACS Appl Mater Interfaces
January 2025
Department of Gerontology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, People's Republic of China.
20% acute pancreatitis (AP) develops into severe AP (SAP), a global health crisis, with an increased mortality rate to 30%-50%. Mitochondrial damage and immune disorders are direct factors, which exacerbate the occurrence and progression of AP. So far, mitochondrial and immunity injury in SAP remains largely elusive, with no established treatment options available.
View Article and Find Full Text PDFIslet NO-Synthases, extracellular NO and glucose-stimulated insulin secretion: Possible impact of neuronal NO-Synthase on the pentose phosphate pathway.
PLoS One
January 2025
Department of Clinical Science, SUS, Division of Islet Cell Physiology, University of Lund, Malmö, Sweden.
The impact of islet neuronal nitric oxide synthase (nNOS) on glucose-stimulated insulin secretion (GSIS) is less understood. We investigated this issue by performing simultaneous measurements of the activity of nNOS versus inducible NOS (iNOS) in GSIS using isolated murine islets. Additionally, the significance of extracellular NO on GSIS was studied.
View Article and Find Full Text PDFMutant KRAS and CK2 Cooperatively Stimulate SLC16A3 Activity to Drive Intrahepatic Cholangiocarcinoma Progression.
Cancer Res
January 2025
Shanghai Institute of Biochemistry and Cell Biology, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China.
Intrahepatic cholangiocarcinoma (iCCA) is a lethal malignancy affecting the liver and biliary system. Enhanced understanding of the pathogenic mechanisms underlying iCCA tumorigenesis and the discovery of appropriate therapeutic targets are imperative to improve patient outcomes. Here, we investigated the functions and regulations of solute carrier family 16 member 3 (SLC16A3), which has been reported to be a biomarker of poor prognosis in iCCA.
View Article and Find Full Text PDFMiRNA-223-5p inhibits hypoxia-induced apoptosis of BMSCs and promotes repair in Legg-Calvé-Perthes disease by targeting CHAC2 and activating the Wnt/β-catenin signaling pathway.
PLoS One
January 2025
School of Clinical Medicine, Guizhou Medical University, Guiyang, China.
Legg-Calvé-Perthes disease (LCPD) involves femoral head osteonecrosis caused by disrupted blood supply, leading to joint deformity and early osteoarthritis. This study investigates the role of miRNA-223-5p in regulating hypoxia-induced apoptosis and enhancing osteogenesis in bone marrow mesenchymal stem cells (BMSCs). Utilizing a juvenile New Zealand white rabbit model of LCPD established through femoral neck ligation, we transfected BMSCs with miR-223-5p mimics, inhibitors, and controls, followed by hypoxic exposure.
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