Metabolism of cyclic GMP in peritoneal macrophages of rat and guinea pig.

Kobiałka, Marcin; Witwicka, Hanna; Siednienko, Jakub; Gorczyca, Wojciech

doi:10.18388/abp.2003_3675

Cited by 10 publications

(3 citation statements)

References 45 publications

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“…Formation of both cAMP and cGMP involves activation of CREB by phosphorylation, generating the transcription of several genes. As previously mentioned, both cAMP and cGMP are neutralized through the hydrolysis performed by phosphodiesterases …”

Section: Molecular Mechanism Of Pdes Functionmentioning

confidence: 95%

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Inhibition of phosphodiesterases as a strategy to achieve neuroprotection in Huntington's disease

Cardinale

Fusco

2018

CNS Neurosci Ther

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Huntington's disease (HD) is a fatal neurodegenerative condition, due to a mutation in the IT15 gene encoding for huntingtin. Currently, disease-modifying therapy is not available for HD, and only symptomatic drugs are administered for the management of symptoms. In the last few years, preclinical and clinical studies have indicated that pharmacological strategies aimed at inhibiting cyclic nucleotide phosphodiesterase (PDEs) may develop into a novel therapeutic approach in neurodegenerative disorders. PDEs are a family of enzymes that hydrolyze cyclic nucleotides into monophosphate isoforms. Cyclic nucleotides are second messengers that transduce the signal of hormones and neurotransmitters in many physiological processes, such as protein kinase cascades and synaptic transmission. An alteration in their balance results in the dysregulation of different biological mechanisms (transcriptional dysregulation, immune cell activation, inflammatory mechanisms, and regeneration) that are involved in neurological diseases. In this review, we discuss the action of phosphodiesterase inhibitors and their role as therapeutic agents in HD.

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Section: Molecular Mechanism Of Pdes Functionmentioning

confidence: 95%

“…As previously mentioned, both cAMP and cGMP are neutralized through the hydrolysis performed by phosphodiesterases. [36][37][38][39][40][41][42]…”

Section: Molecul Ar Mechanis M Of Pde S Fun C Tionmentioning

confidence: 99%

Inhibition of phosphodiesterases as a strategy to achieve neuroprotection in Huntington's disease

Cardinale

Fusco

2018

CNS Neurosci Ther

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“…Cells were incubated for 10 min at 37°C and then GC-A activator (0.1 µM ANP) was added. After 30 min incubation, the reaction was terminated, the cells were disintegrated and intracellular concentration of cGMP was determined using an immunoenzymatic assay (ELISA) based on rabbit polyclonal antibodies highly specific to cGMP (Kobiałka et al, 2003).…”

Section: Methodsmentioning

confidence: 99%

Sp1 mediates phorbol ester (PMA)-induced expression of membrane-bound guanylyl cyclase GC-A in human monocytic cells*

et al. 2018

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Cyclic guanosine monophosphate (cGMP) is synthesized by two types of enzymes: particulate (membrane-bound) guanylyl cyclases (pGCs) and soluble (cytosolic) guanylyl cyclases (sGCs). sGCs are primarily activated by binding of nitric oxide to their prosthetic heme group while pGCs are activated by binding of peptide ligands to their extracellular domains. One of them, pGC type A (GC-A) is activated by atrial and brain natriuretic peptides (ANP and BNP, respectively). Human monocytes isolated from peripheral blood mononuclear cells have been found to display sGC expression without concomitant expression of GC-A. However, GC-A activity appears in monocytes under certain conditions but a molecular mechanism of GC-A expression is still poorly understood. In this report we show that phorbol ester (PMA) induces transcription of a gene encoding GC-A in human monocytic THP-1 cells. Moreover, we find that PMA-treated THP-1 cells raise cGMP content following treatment with ANP. Studies using pharmacological inhibitors of protein kinases suggest involvement of protein kinase C (PKC), mitogen extracellular kinases (MEK1/2), and extracellular signal-regulated kinases (ERK1/2) in PMA-induced expression of the GC-A encoding gene in THP-1 cells. Finally, we show that PMA stimulates binding of Sp1 transcription factor to GC-rich DNA sequences and mithramycin A (a selective Sp1 inhibitor) inhibits expression of the GC-A mRNA in PMA-treated THP-1 cells. Taken together, our findings suggest that the PMA-stimulated PKC and MEK/ERK signaling pathways induce Sp1-mediated transcription of the GC-A encoding gene in human monocytic THP-1 cells.

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Can proline‐rich polypeptide complex mimic the effect of nerve growth factor?

et al. 2014

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Naturally occurring compounds that can act as prosurvival factors and neurite formation stimulants in the conditions of reduced neurotrophins production are important both in neuronal protection and therapy of neurodegenerative disorders. Therefore, the role of proline-rich polypeptide complex (PRP) and its nonapeptide fragment (NP) in the promotion of pheochromocytoma cell line (PC12) survival and neurite outgrowth pathway is presented. It was shown that PRP/NP did not affect the neuronal nitric oxide synthase (nNOS) at the transcriptional and protein level. However, the activity of nNOS and intracellular nitric oxide (NO) concentration was markedly increased after treatment of PC12 cells with peptides. This reaction was inhibited by L-NAME-nNOS inhibitor. It was shown that PRP and NP induce the soluble guanylyl cyclase to release higher amount of cyclic GMP (cGMP), and subsequently, the increased phosphorylation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) is observed. This effect was abolished by both U0126 (inhibitor of ERK1/2) and also by L-NAME. Reduction of ERK1/2 activity observed in the presence of nNOS inhibitor suggests that its activation is NO-dependent. The presented results shed some light on the mechanism of action of PRP complex. PRP and NP can activate NO/cGMP/ERK1/2 signaling pathway, similarly to nerve growth factor (NGF). The prosurvival action and short fibers formation suggest the role of PRP and NP in neuroprotection and the initiation of neuritogenesis. They can also participate in the amplification of signals controlling the survival and differentiation of neurons effect when the deficit of NGF takes place.

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Metabolism of cyclic GMP in peritoneal macrophages of rat and guinea pig.

Cited by 10 publications

References 45 publications

Inhibition of phosphodiesterases as a strategy to achieve neuroprotection in Huntington's disease

Inhibition of phosphodiesterases as a strategy to achieve neuroprotection in Huntington's disease

Sp1 mediates phorbol ester (PMA)-induced expression of membrane-bound guanylyl cyclase GC-A in human monocytic cells*

Can proline‐rich polypeptide complex mimic the effect of nerve growth factor?

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