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Mechanisms by which Ganglioside GM1, a specific type of glycosphingolipid, ameliorates BMAA-induced neurotoxicity in early-life stage of zebrafish embryos.
Food Res Int
January 2025
State Key Laboratory of Marine Food Processing & Safety Control, College of Food Science and Engineering, Ocean University of China, Qingdao 266404, China; Qingdao Marine Science and Technology Center, Qingdao, Shandong Province 266235, China.
The neurotoxin β-methylamino-L-alanine (BMAA) produced by cyanobacteria is widely present in foods and dietary supplements, posing a significant threat to human health. Ganglioside GM1 (GM1) has demonstrated potential for treating neurodegenerative diseases; however, its ability to prevent BMAA-induced neurotoxicity remains uncertain. In this study, zebrafish embryos were treated with Ganglioside GM1 to investigate its neuroprotective effects against BMAA exposure and the underlying mechanisms.
View Article and Find Full Text PDFGYY4137 protects against type 2 diabetes mellitus-associated myocardial autophagy by suppressing FOXO1 signal pathway.
Anim Cells Syst (Seoul)
December 2024
Yunkang School of Medicine and Health, Nanfang College, Guangzhou, People's Republic of China.
Diabetic cardiomyopathy (DCM) is a major complication of type 2 diabetes mellitus (T2DM), but its effective prevention and treatment are still limited. We investigated the effects of GYY4137, a slow-releasing hydrogen sulfide donor, and its downstream mediator forkhead box protein O1 (FOXO1) on T2DM-associated DCM. , T2DM mice were induced by a high-fat diet coupled with streptozotocin injection.
View Article and Find Full Text PDFGPR68 Mediates Lung Endothelial Dysfunction Caused by Bacterial Inflammation and Tissue Acidification.
Cells
December 2024
Division of Pulmonary and Critical Care, Department of Medicine, UMSOM Lung Biology Program, University of Maryland School of Medicine, 20 Penn Street, HSF-2, Room S143, Baltimore, MD 21201, USA.
Tissue acidification resulting from dysregulated cellular bioenergetics accompanies various inflammatory states. GPR68, along with other members of proton-sensing G protein-coupled receptors, responds to extracellular acidification and has been implicated in chronic inflammation-related diseases such as ischemia, cancer, and colitis. The present study examined the role of extracellular acidification on human pulmonary endothelial cell (EC) permeability and inflammatory status per se and investigated potential synergistic effects of acidosis on endothelial dysfunction caused by bacterial lipopolysaccharide (LPS, ).
View Article and Find Full Text PDFDiabetes is associated with the dysfunction of glucagon-producing pancreatic islet α-cells, although the underlying mechanisms regulating glucagon secretion and α-cell dysfunction remain unclear. While insulin secretion from pancreatic β-cells has long been known to be partly controlled by intracellular phospholipid signaling, very little is known about the role of phospholipids in glucagon secretion. Here we show that TMEM55A, a lipid phosphatase that dephosphorylates phosphatidylinositol-4,5-bisphosphate (PIP2) to phosphatidylinositol-5-phosphate (PI5P), regulates α-cell exocytosis and glucagon secretion.
View Article and Find Full Text PDFCell wall components of gut commensal bacteria stimulate peritrophic matrix formation in malaria vector mosquitoes through activation of the IMD pathway.
PLoS Biol
January 2025
State Key Laboratory of Genetic Engineering, School of Life Sciences, Department of Infectious Diseases, Zhongshan Hospital, Fudan University, Shanghai, China.
The peritrophic matrix (PM) acts as a physical barrier that influences the vector competence of mosquitoes. We have previously shown that gut microbiota promotes PM formation in Anopheles stephensi, although the underlying mechanisms remain unclear. In this study, we identify that the cell wall components of gut commensal bacteria contribute to PM formation.
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