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| Campo DC | Valor | Lengua/Idioma |
|---|---|---|
| dc.provenance | Universidad Nacional de Rosario.RepHipUNR | - |
| dc.creator | Toledo, Flavia D. | - |
| dc.creator | Pérez, Leonardo M. | - |
| dc.creator | Basiglio, Cecilia Lorena | - |
| dc.creator | Ochoa, Justina E. | - |
| dc.creator | Sánchez Pozzi, Enrique J. | - |
| dc.creator | Roma, Marcelo G. | - |
| dc.date | 2014-03-11 | - |
| dc.date | 2014-03-11 | - |
| dc.date.accessioned | 2019-07-15T19:04:41Z | - |
| dc.date.available | 2019-07-15T19:04:41Z | - |
| dc.date.issued | 2014-03-11 | - |
| dc.date.issued | 2014-03-11 | - |
| dc.identifier | 0340-5761 | - |
| dc.identifier | http://hdl.handle.net/2133/10485 | - |
| dc.identifier | http://hdl.handle.net/2133/10485 | - |
| dc.identifier.uri | http://rodna.bn.gov.ar/jspui/handle/bnmm/570797 | - |
| dc.description | Oxidative stress is a common event in most hepatopathies, leading to mitochondrial permeability transition pore (MPTP) formation and further exacerbation of both oxidative stress from mitochondrial origin and cell death. Intracellular Ca2+ elevations play a permissive role in these events, but the underlying mechanisms are poorly known. We examined in primary cultured rat hepatocytes whether the Ca2+/calmodulin (CaM)-dependent protein kinase II (CaMKII) signalling pathway is involved in this process, by using tert-butyl hydroperoxide (tBOOH) as a pro-oxidizing, model compound. tBOOH (500 µM, 15 min) induced MPTP formation, as assessed by measuring mitochondrial membrane depolarization as a surrogate marker, and increased lipid peroxidation in a clyclosporin A (CsA)-sesitive manner, revealing the involvement of MPTPs in tBOOH-induced ROS formation. Intracellular Ca2+ sequestration with BAPTA/AM, CaM blockage with W7 or trifluoperazine, and CaMKII inhibition with KN-62 all fully prevented tBOOH-induced MPTP opening and reduced tBOOH-induced lipid peroxidation to a similar extent to CsA, suggesting that Ca2+/CaM/CaMKII signaling pathway fully mediates MPTP-mediated mitochondrial ROS generation. tBOOH induced apoptosis, as shown by flow cytometry of annexin V/propidium iodide, mitochondrial release of cytochrome c, activation of caspase-3 and increase in the Bax-to-Bcl-xL ratio, and the Ca2+/CaM/CaMKII signaling antagonists fully prevented these effects. Intramitochondrial CaM and CaMKII were partially involved in tBOOH-induced MPTP formation, since W7 and KN-62 both attenuated the tBOOH-induced, MPTP-mediated swelling of isolated mitochondria. We concluded that Ca2+/CaM/CaMKII signaling pathway is a key mediator of oxidative stress-induced induced MPTP formation, and the subsequent exacerbation of oxidative stress from mitochondrial origin and apoptotic cell death. | - |
| dc.description | Fil: Toledo, Flavia D. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Fisiología Experimental (IFISE-CONICET); Argentina. | - |
| dc.description | Fil: Pérez, Leonardo M. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Fisiología Experimental (IFISE-CONICET); Argentina. | - |
| dc.description | Fil: Basiglio, Cecilia Lorena. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Fisiología Experimental (IFISE-CONICET); Argentina. | - |
| dc.description | Fil: Ochoa, Justina E. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Fisiología Experimental (IFISE-CONICET); Argentina. | - |
| dc.description | Fil: Sánchez Pozzi, Enrique J. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Fisiología Experimental (IFISE-CONICET); Argentina. | - |
| dc.description | Fil: Roma, Marcelo G. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Fisiología Experimental (IFISE-CONICET); Argentina. | - |
| dc.format | application/pdf | - |
| dc.language | eng | - |
| dc.publisher | Springer | - |
| dc.relation | https://link.springer.com/article/10.1007%2Fs00204-014-1219-5 | - |
| dc.relation | 10.1002/hep.2675210.1007/s00204-014-1219-5 | - |
| dc.rights | info:eu-repo/semantics/openAccess | - |
| dc.source | reponame:RepHipUNR (UNR) | - |
| dc.source | instname:Universidad Nacional de Rosario | - |
| dc.source | instacron:UNR | - |
| dc.source.uri | http://hdl.handle.net/2133/10485 | - |
| dc.subject | Oxidative Stress | - |
| dc.subject | tert-Butyl Hydroperoxide | - |
| dc.subject | Ca2+/calmodulin-dependent Protein Kinase II | - |
| dc.subject | Mitochondrial Permeability Transition Pore | - |
| dc.subject | Apoptosis | - |
| dc.subject | Cytochrome c | - |
| dc.subject | Caspasas | - |
| dc.title | The Ca2+-calmodulin-Ca2+/calmodulin-dependent protein kinase II pathway is involved in oxidative stress-induced mitochondrial permeability transition and apoptosis in rat hepatocytes | - |
| dc.type | info:eu-repo/semantics/article | - |
| dc.type | info:eu-repo/semantics/publishedVersion | - |
| dc.type | artículo | - |
| dc.type | info:ar-repo/semantics/articulo | - |
| Aparece en las colecciones: | Universidad Nacional de Rosario. RepHipUNR | |
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