Figure 2.
(A) Cyclic AMP nanodomains in inflammatory and structural cells diverse such as eosinophils, macrophages, neutrophils, lymphocytes, monocytes, epithelial cells, airway smooth muscle cells, fibroblasts, cardiomyocytes, endothelial cells and myofibroblasts. (B) Cellular effects caused by diesel exhaust particles (DEP) in inflammatory cells and structural cells. DEP induces the production of reactive oxygen species (ROS). Subsequently, ROS production induces changes in mitochondrial membrane potential leading to mitochondria dysfunction and mitochondria damage. Mitochondrial cAMP is generated from ATP by soluble adenylyl cyclase (sAC) present in the mitochondria matrix. Levels of cAMP are regulated by phosphodiesterase (PDE) degrading cAMP to 5′AMP. A-kinase anchoring protein (AKAP) 1 recruits macromolecules to mitochondria. Shown are the mitochondrial respiratory chain complexes I–V localized in the inner membrane of mitochondria. See text for further details.
Cyclic AMP Nanodomains.

(A) Cyclic AMP nanodomains in inflammatory and structural cells diverse such as eosinophils, macrophages, neutrophils, lymphocytes, monocytes, epithelial cells, airway smooth muscle cells, fibroblasts, cardiomyocytes, endothelial cells and myofibroblasts. (B) Cellular effects caused by diesel exhaust particles (DEP) in inflammatory cells and structural cells. DEP induces the production of reactive oxygen species (ROS). Subsequently, ROS production induces changes in mitochondrial membrane potential leading to mitochondria dysfunction and mitochondria damage. Mitochondrial cAMP is generated from ATP by soluble adenylyl cyclase (sAC) present in the mitochondria matrix. Levels of cAMP are regulated by phosphodiesterase (PDE) degrading cAMP to 5′AMP. A-kinase anchoring protein (AKAP) 1 recruits macromolecules to mitochondria. Shown are the mitochondrial respiratory chain complexes I–V localized in the inner membrane of mitochondria. See text for further details.

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