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Tytuł pozycji:

Abnormal Mitochondrial cAMP/PKA Signaling Is Involved in Sepsis-Induced Mitochondrial and Myocardial Dysfunction.

Tytuł :
Abnormal Mitochondrial cAMP/PKA Signaling Is Involved in Sepsis-Induced Mitochondrial and Myocardial Dysfunction.
Autorzy :
Nevière, Rémi
Delguste, Florian
Durand, Arthur
Inamo, Jocelyn
Boulanger, Eric
Preau, Sebastien
Pokaż więcej
Temat :
mitochondria respiration
cyclic adenosine monophosphate (cAMP)
protein kinase A
soluble adenylyl cyclase
phosphodiesterase
isolated heart
sepsis
MESH: 1-Methyl-3-isobutylxanthine/pharmacology
MESH: Animals
MESH: Cyclic Nucleotide Phosphodiesterases, Type 2/metabolism
MESH: Electron Transport/drug effects
MESH: Mice
MESH: Electron Transport Complex I/metabolism
MESH: Imidazoles/pharmacology
MESH: Mitochondria/metabolism
MESH: Mitochondrial Proteins/metabolism
MESH: Myocardial Contraction/drug effects
MESH: Myocardium/metabolism
MESH: Myocardium/pathology
MESH: Phosphoserine/metabolism
MESH: Phosphodiesterase Inhibitors/pharmacology
MESH: Phosphorylation/drug effects
MESH: Sepsis/metabolism
MESH: Blotting, Western
MESH: Signal Transduction*/drug effects
MESH: Triazines/pharmacology
MESH: Cell Respiration/drug effects
MESH: Cyclic AMP/metabolism
MESH: Cyclic AMP-Dependent Protein Kinases/metabolism
[SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology
[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system
Źródło :
International Journal of Molecular Sciences
International Journal of Molecular Sciences, MDPI, 2016, 17 (12), pp.2075. ⟨10.3390/ijms17122075⟩
Wydawca :
MDPI, 2016.
Rok publikacji :
2016
Kolekcja :
Hyper_Article_en_Ligne
Język :
English
ISSN :
1422-0067
DOI :
10.3390/ijms17122075
Numer akcesji :
edsair.od.......166..5171fd02f0bcc72bd46b11d47d048473
International audience; Adrenergic receptors couple to Gs-proteins leading to transmembrane adenylyl cyclase activation and cytosolic cyclic adenosine monophosphate (cAMP) production. Cyclic AMP is also produced in the mitochondrial matrix, where it regulates respiration through protein kinase A (PKA)-dependent phosphorylation of respiratory chain complexes. We hypothesized that a blunted mitochondrial cAMP-PKA pathway would participate in sepsis-induced heart dysfunction. Adult male mice were subjected to intra-abdominal sepsis. Mitochondrial respiration of cardiac fibers and myocardial contractile performance were evaluated in response to 8Br-cAMP, PKA inhibition (H89), soluble adenylyl cyclase inhibition (KH7), and phosphodiesterase inhibition (IBMX; BAY60-7550). Adenosine diphosphate (ADP)-stimulated respiratory rates of cardiac fibers were reduced in septic mice. Compared with controls, stimulatory effects of 8Br-cAMP on respiration rates were enhanced in septic fibers, whereas inhibitory effects of H89 were reduced. Ser-58 phosphorylation of cytochrome c oxidase subunit IV-1 was reduced in septic hearts. In vitro, incubation of septic cardiac fibers with BAY60-7550 increased respiratory control ratio and improved cardiac MVO2 efficiency in isolated septic heart. In vivo, BAY60-7550 pre-treatment of septic mice have limited impact on myocardial function. Mitochondrial cAMP-PKA signaling is impaired in the septic myocardium. PDE2 phosphodiesterase inhibition by BAY60-7550 improves mitochondrial respiration and cardiac MVO2 efficiency in septic mice.

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