Helicobacter Pylori Virulence Factor Cytotoxin-Associated Gene A (CagA) Induces Vascular Calcification in Coronary Artery Smooth Muscle Cells.
Martin O SundqvistJonatan WärmeRobin HofmannSven-Christian PawelzikMagnus BäckPublished in: International journal of molecular sciences (2023)
Helicobacter pylori ( H. pylori ) has been associated with cardiovascular diseases. The pro-inflammatory H. pylori virulence factor cytotoxin-associated gene A (CagA) has been detected in serum exosomes of H. pylori -infected subjects and may exert systemic effects throughout the cardiovascular system. The role of H. pylori and CagA in vascular calcification was hitherto unknown. The aim of this study was to determine the vascular effects of CagA through human coronary artery smooth muscle cell (CASMC) osteogenic and pro-inflammatory effector gene expression as well as interleukin 1β secretion and cellular calcification. CagA upregulated bone morphogenic protein 2 (BMP-2) associated with an osteogenic CASMC phenotype switch and induced increased cellular calcification. Furthermore, a pro-inflammatory response was observed. These results support that H. pylori may contribute to vascular calcification through CagA rendering CASMCs osteogenic and inducing calcification.
Keyphrases
- helicobacter pylori
- mesenchymal stem cells
- coronary artery
- chronic kidney disease
- helicobacter pylori infection
- gene expression
- smooth muscle
- bone marrow
- inflammatory response
- cardiovascular disease
- escherichia coli
- pseudomonas aeruginosa
- endothelial cells
- staphylococcus aureus
- cell therapy
- type diabetes
- dna methylation
- coronary artery disease
- copy number
- genome wide
- biofilm formation
- stem cells
- dendritic cells
- metabolic syndrome
- cystic fibrosis
- single cell
- high glucose
- lipopolysaccharide induced
- protein protein
- oxidative stress
- diabetic rats
- postmenopausal women
- immune response
- cardiovascular risk factors
- lps induced
- small molecule
- regulatory t cells
- amino acid
- pluripotent stem cells