Garcia-Rivas 2013 Abstract MiP2013: Difference between revisions
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{{Abstract | {{Abstract | ||
|title= | |title=Garcia-Rivas G,Morales JA, Vega-Sevilla L, Silva-Platas C, García N (2013) Regulation of mitochondrial permeability transition by Sirt3-catalyzed cyclophilin D deacetylation and its relevance for ventricular dysfunction in metabolic syndrome. Mitochondr Physiol Network 18.08. | ||
|authors= | |info=[[File:Garcia-Rivas.jpg|right|120px| Gerardo Garcia-Rivas]][[MiP2013]], [[Laner 2013 Mitochondr Physiol Network MiP2013|Book of Abstracts Open Access]] | ||
|authors=Garcia-Rivas G,Morales JA, Vega-Sevilla L, Silva-Platas C, Garcia N | |||
|year=2013 | |year=2013 | ||
|event= | |event=MiPNet18.08_MiP2013 | ||
|abstract= | |abstract=Metabolic syndrome (MS) can be defined as a group of signs that increases the risk of cardiovascular diseases (CVD). These signs include central obesity, hypertriglyceridemia and hypertension. We are interested in the mechanisms that trigger ventricular dysfunction in a MS murine model, as a way to understand how mitochondrial function fails in CVD. The sustained opening of the mitochondrial permeability transition pore (PTP) is a major event in the onset of irreversible myocardial injury. Several mitochondrial proteins modulate the PTP, including the cyclophilin D (CyD), the adenine nucleotide translocator (ANT) and the SIRTUINS. In this regard, SIRT-3 has emerged recently as a pivotal mediator of mitochondrial metabolism and PTP inductor in a knockout murine model. However, the precise role of SIRT-•3 in a pathophysiologic context remains indefinable. Male Wistar rats with sucrose-induced MS were subjected to cardiac echocardiography and ex-vivo contraction measurements at 6 and 12 months. Respiratory activity, calcium retention capacity and deacetylation profile were investigated in isolated mitochondria. The expression of SIRT-3, ANT and CyD was evaluated by qPCR or western blot. We observed differences in the E/A ratio (control 1.07±0.01 vs. MS 0.85±0.06, ''P''<0.029) and the ventricular deceleration time (0.029±0.002 vs. 0.034±0.003, ''P''<0.04) indicating an abnormal lusitropism. No significant differences were found in respiratory activity and respiratory control from isolated mitochondria. Nevertheless, calcium retention in MS mitochondria was reduced (0.83±0.03 vs 0.65±0.04 Abs.min-1, ''P''<0.004) indicating premature PTP opening. Proneness in PTP opening was associated with lower expression (60% p<0.001) of SIRT-3. These changes correlated with the MS heart´s mitochondrial acetylation profile. It appears that metabolic changes inherent to MS promote alterations in the expression of SIRT-3 and correlates with PTP opening sensibility. | ||
|mipnetlab=MX San Pedro Garcia-Rivas G | |||
}} | }} | ||
{{Labeling}} | {{Labeling | ||
|area=Respiration | |||
|diseases=Cardiovascular, Diabetes, Other | |||
|injuries=Permeability transition | |||
|organism=Rat | |||
|preparations=Isolated mitochondria | |||
|topics=Calcium | |||
|additional=MiP2013 | |||
}} | |||
== Affiliations and author contributions == | |||
1 - Cátedra de Cardiología y Medicina Vascular. Escuela de Medicina. Tecnológico de Monterrey. México. | |||
2 - Centro de Investigación Básica y Transferencia. Instituto de Cardiología y Medicina Vascular. Tec Salud del Sistema Tecnológico de Monterrey. San Pedro Garza García. México. | |||
Email: gdejesus@itesm.mx | |||
Latest revision as of 09:10, 18 July 2022
Garcia-Rivas G,Morales JA, Vega-Sevilla L, Silva-Platas C, García N (2013) Regulation of mitochondrial permeability transition by Sirt3-catalyzed cyclophilin D deacetylation and its relevance for ventricular dysfunction in metabolic syndrome. Mitochondr Physiol Network 18.08. |
Link:
MiP2013, Book of Abstracts Open Access
Garcia-Rivas G, Morales JA, Vega-Sevilla L, Silva-Platas C, Garcia N (2013)
Event: MiPNet18.08_MiP2013
Metabolic syndrome (MS) can be defined as a group of signs that increases the risk of cardiovascular diseases (CVD). These signs include central obesity, hypertriglyceridemia and hypertension. We are interested in the mechanisms that trigger ventricular dysfunction in a MS murine model, as a way to understand how mitochondrial function fails in CVD. The sustained opening of the mitochondrial permeability transition pore (PTP) is a major event in the onset of irreversible myocardial injury. Several mitochondrial proteins modulate the PTP, including the cyclophilin D (CyD), the adenine nucleotide translocator (ANT) and the SIRTUINS. In this regard, SIRT-3 has emerged recently as a pivotal mediator of mitochondrial metabolism and PTP inductor in a knockout murine model. However, the precise role of SIRT-•3 in a pathophysiologic context remains indefinable. Male Wistar rats with sucrose-induced MS were subjected to cardiac echocardiography and ex-vivo contraction measurements at 6 and 12 months. Respiratory activity, calcium retention capacity and deacetylation profile were investigated in isolated mitochondria. The expression of SIRT-3, ANT and CyD was evaluated by qPCR or western blot. We observed differences in the E/A ratio (control 1.07±0.01 vs. MS 0.85±0.06, P<0.029) and the ventricular deceleration time (0.029±0.002 vs. 0.034±0.003, P<0.04) indicating an abnormal lusitropism. No significant differences were found in respiratory activity and respiratory control from isolated mitochondria. Nevertheless, calcium retention in MS mitochondria was reduced (0.83±0.03 vs 0.65±0.04 Abs.min-1, P<0.004) indicating premature PTP opening. Proneness in PTP opening was associated with lower expression (60% p<0.001) of SIRT-3. These changes correlated with the MS heart´s mitochondrial acetylation profile. It appears that metabolic changes inherent to MS promote alterations in the expression of SIRT-3 and correlates with PTP opening sensibility.
• O2k-Network Lab: MX San Pedro Garcia-Rivas G
Labels: MiParea: Respiration Pathology: Cardiovascular, Diabetes, Other Stress:Permeability transition Organism: Rat
Preparation: Isolated mitochondria
Regulation: Calcium
MiP2013
Affiliations and author contributions
1 - Cátedra de Cardiología y Medicina Vascular. Escuela de Medicina. Tecnológico de Monterrey. México.
2 - Centro de Investigación Básica y Transferencia. Instituto de Cardiología y Medicina Vascular. Tec Salud del Sistema Tecnológico de Monterrey. San Pedro Garza García. México.
Email: gdejesus@itesm.mx