Nitric oxide and peroxynitrite induce cellular death in bovine chromaffin cells: Evidence for a mixed necrotic and apoptotic mechanism with caspases activation
| Autor: | Rocío Pérez-Rodríguez, A.M. Oliván, M.P. González, A. Martínez Palacián, S. Vicente, María Jesús Oset-Gasque |
|---|---|
| Rok vydání: | 2006 |
| Předmět: |
endocrine system
Chromaffin Cells Fluorescent Antibody Technique Caspase 3 DNA Fragmentation Nitric Oxide Cell morphology Necrosis Cellular and Molecular Neuroscience chemistry.chemical_compound Superoxides Peroxynitrous Acid Animals Drug Interactions Nitric Oxide Donors Propidium iodide Enzyme Inhibitors Fragmentation (cell biology) Cells Cultured Heat-Shock Proteins Caspase Analysis of Variance Cell Death Dose-Response Relationship Drug L-Lactate Dehydrogenase biology Cell Cycle Penicillamine Cytochromes c Free Radical Scavengers Cell cycle Flow Cytometry Peptide Fragments Cell biology Enzyme Activation chemistry Apoptosis Caspases biology.protein DNA fragmentation Cattle |
| Zdroj: | Journal of Neuroscience Research. 84:78-96 |
| ISSN: | 1097-4547 0360-4012 |
| DOI: | 10.1002/jnr.20853 |
| Popis: | Treatment of chromaffin cells with nitric oxide (NO) donors (SNP and SNAP) and peroxynitrite produces a time- and dose-dependent necrotic and apoptotic cell death. Necrotic cell death was characterized by both an increase in lactate dehydrogenase and ATP release and changes in nuclei and cell morphology (as seen with fluorescence microscopy analysis with propidium iodide and Hoechst 33342). Apoptotic cell death was characterized by nuclear fragmentation and presence of apoptotic cell bodies, by a decrease in DNA content, and by an increase in DNA fragmentation. Treatment of chromaffin cells with lipopolysaccharide (LPS) or cytokines (interferon-γ, tumor necrosis factor-α) resulted only in apoptotic cell death. Apoptotic effects of NO-inducing compounds were specifically reversed, depending on the stimuli, by the NO scavenger carboxy-PTIO (CPTio) or by the NOS inhibitors L-NMA and thiocitrulline. NO-induced apoptotic death in chromaffin cells was concomitant to a cell cycle arrest in G0G1 phase and a decrease in the number of chromaffin cells in the G2M and S phases of cell cycle. All NO-producing compounds were able to induce activation of caspase 3 and cytochrome c release, and specific inhibitors of caspase 3 and 9, such as Ac-DEVD-CHO (CPP32) and Ac-Z-LEHD-FMK, respectively, prevented NO-induced apoptosis in chromaffin cells. These results suggest that chromaffin cells could be good models for investigating the molecular basis of degeneration in diseases showing death of catecholaminergic neurons, phenomenon in which NO plays an important role. © 2006 Wiley-Liss, Inc. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Plný text