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The Complexity and Multiplicity of the Specific cAMP Phosphodiesterase Family: PDE4, Open New Adapted Therapeutic Approaches.
Int J Mol Sci
September 2022
Section de Structures Biologiques, Pharmacologie et Enzymologie, CNRS/Unistra, CRBS, UR 3072, CEDEX, 67084 Strasbourg, France.
Cyclic nucleotides (cAMP, cGMP) play a major role in normal and pathologic signaling. Beyond receptors, cyclic nucleotide phosphodiesterases; (PDEs) rapidly convert the cyclic nucleotide in its respective 5'-nucleotide to control intracellular cAMP and/or cGMP levels to maintain a normal physiological state. However, in many pathologies, dysregulations of various PDEs (PDE1-PDE11) contribute mainly to organs and tissue failures related to uncontrolled phosphorylation cascade.
View Article and Find Full Text PDFMethods to Investigate Signal Transduction Pathways in Trypanosoma cruzi: Cyclic Nucleotide Phosphodiesterases Assay Protocols.
Methods Mol Biol
February 2021
Laboratorio de Señalización y Mecanismos Adaptativos en Tripanosomátidos, Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres" (INGEBI), Buenos Aires, Argentina.
Intracellular levels of cyclic nucleotide second messengers are regulated predominantly by a large superfamily of phosphodiesterases (PDEs). Most of the different PDE variants play specific physiological functions; in fact, PDEs can associate with other proteins allowing them to be strategically anchored throughout the cell. In this regard, precise cellular expression and compartmentalization of these enzymes produce the specific control of cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) gradients in cells and enable their integration with other signaling pathways.
View Article and Find Full Text PDFEffects of cyclic nucleotide phosphodiesterases (PDEs) on mitochondrial skeletal muscle functions.
Cell Mol Life Sci
May 2017
EA 3072 "Mitochondrie, Stress Oxydant et Protection Musculaire", Fédération de Médecine Translationnelle, Faculté de Médecine, Institut de Physiologie, Université de Strasbourg, 4, Rue Kirschleger, 67085, Strasbourg Cedex, France.
Mitochondria play a critical role in skeletal muscle metabolism and function, notably at the level of tissue respiration, which conduct muscle strength as well as muscle survival. Pathological conditions induce mitochondria dysfunctions notably characterized by free oxygen radical production disturbing intracellular signaling. In that way, the second messengers, cyclic AMP and cyclic GMP, control intracellular signaling at the physiological and transcription levels by governing phosphorylation cascades.
View Article and Find Full Text PDFSildenafil potentiates bone morphogenetic protein signaling in pulmonary arterial smooth muscle cells and in experimental pulmonary hypertension.
Arterioscler Thromb Vasc Biol
January 2013
Division of Respiratory Medicine, Department of Medicine, University of Cambridge School of Clinical Medicine, Box 157, Addenbrooke's Hospital, Hills Road, Cambridge CB2 0QQ, UK.
Objective: Mutations in the bone morphogenetic protein type II receptor (BMPR-II) are responsible for the majority of cases of heritable pulmonary arterial hypertension (PAH), and BMPR-II deficiency contributes to idiopathic and experimental forms of PAH. Sildenafil, a potent type-5 nucleotide-dependent phosphodiesterase inhibitor, is an established treatment for PAH, but whether sildenafil affects bone morphogenetic protein (BMP) signaling in the pulmonary circulation remains unknown.
Methods And Results: Studies were undertaken in human pulmonary arterial smooth muscle cells (PASMCs) and in vivo in the monocrotaline rat model of PAH.
[5'-nucleotide phosphodiesterase isozyme -V (5' -NPD-V)].
Nihon Rinsho
July 2010
Department of Surgery, Teikyo University School of Medicine.
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