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Your search keyword '"Carlos E. Pedraza"' showing total 2 results
Start Over Author "Carlos E. Pedraza" Journal neurobiology of disease
2 results on '"Carlos E. Pedraza"'

1. β-Amyloid Peptides Decrease Soluble Guanylyl Cyclase Expression in Astroglial Cells

Author

Marı́a Antonia Baltrons, Carlos E. Pedraza, Michael T. Heneka, and Agustina Garcı́a

Subjects
astroglial, β-amyloid peptides, Cyclic GMP, soluble guanylyl cyclase, nitric oxide, Neurosciences. Biological psychiatry. Neuropsychiatry, RC321-571
Abstract

In astroglial cells β-amyloid peptides (βA) induce a reactive phenotype and increase expression of NO synthase. Here we show that treatment of rat brain astrocytes with βA decreases their capacity to accumulate cyclic GMP (cGMP) in response to NO as a result of a decreased expression of soluble guanylyl cyclase (sGC) at the protein and mRNA levels. Potentiation of βA-induced NO formation by interferon-γ did not result in a larger decrease in cGMP formation and inhibition of NO synthase failed to reverse down-regulation of sGC, indicating that NO is not involved. The βA effect was prevented by the protein synthesis inhibitor cycloheximide. Intracerebral βA injection also decreased sGC β1 subunit mRNA levels in adult rat hippocampus and cerebellum. A loss of sGC in reactive astrocytes surrounding β-amyloid plaques could be a mechanism to prevent excess signalling via cGMP at sites of high NO production.

Published
2002
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2. β-Amyloid Peptides Decrease Soluble Guanylyl Cyclase Expression in Astroglial Cells

Author

María Antonia Baltrons, Carlos E Pedraza, Michael T. Heneka, and Agustina García

Subjects
Nitroprusside, medicine.medical_specialty, Cerebellum, Receptors, Cytoplasmic and Nuclear, Hippocampus, Nerve Tissue Proteins, Cycloheximide, Biology, β-amyloid peptides, Nitric oxide, lcsh:RC321-571, Rats, Sprague-Dawley, chemistry.chemical_compound, 3',5'-Cyclic-GMP Phosphodiesterases, nitric oxide, Internal medicine, medicine, Animals, Nitric Oxide Donors, RNA, Messenger, astroglial, Cyclic GMP, lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry, Cells, Cultured, Nitrites, Protein Synthesis Inhibitors, Amyloid beta-Peptides, Protein synthesis inhibitor, soluble guanylyl cyclase, Long-term potentiation, Phenotype, Peptide Fragments, Rats, Cell biology, Isoenzymes, Protein Subunits, medicine.anatomical_structure, Endocrinology, Solubility, Neurology, chemistry, Guanylate Cyclase, Astrocytes, Enzyme Induction, Soluble guanylyl cyclase
Abstract

In astroglial cells beta-amyloid peptides (betaA) induce a reactive phenotype and increase expression of NO synthase. Here we show that treatment of rat brain astrocytes with betaA decreases their capacity to accumulate cyclic GMP (cGMP) in response to NO as a result of a decreased expression of soluble guanylyl cyclase (sGC) at the protein and mRNA levels. Potentiation of betaA-induced NO formation by interferon-gamma did not result in a larger decrease in cGMP formation and inhibition of NO synthase failed to reverse down-regulation of sGC, indicating that NO is not involved. The betaA effect was prevented by the protein synthesis inhibitor cycloheximide. Intracerebral betaA injection also decreased sGC beta1 subunit mRNA levels in adult rat hippocampus and cerebellum. A loss of sGC in reactive astrocytes surrounding beta-amyloid plaques could be a mechanism to prevent excess signalling via cGMP at sites of high NO production.

Published
2002

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