Efeito da descelularização com SDS na prevenção da calcificação em pericárdio bovino fixado em glutaraldeído

Collatusso, Claudinei; Roderjan, João Gabriel; Vieira, Eduardo; Costa, Francisco Diniz Affonso da; Noronha, Lúcia de; Fornazari, Daniele de Fátima

doi:10.5935/1678-9741.20120013

Cited by 6 publications

(1 citation statement)

References 14 publications

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“…The hydrolyzed samples were then sent for spectrometry analysis (PERKIN ELMER 4100, LACTEC-PR, Brazil), and the results were expressed in microgram of calcium per microgram of tissue mitochondrial proteins. 44 …”

Section: Methodsmentioning

confidence: 99%

MICU1 protects against myocardial ischemia/reperfusion injury and its control by the importer receptor Tom70

et al. 2017

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Mitochondrial Ca2+ overload is a main contributor to mitochondrial damage hence cardiomyocyte death in myocardial ischemia/reperfusion (MI/R) injury. MICU1 has been recently identified as an important regulator of mitochondrial Ca2+ homeostasis. Here we try to identify the role of MICU1 in MI/R, and to investigate whether the mitochondrial importer receptor Tom70 possesses critical roles in the mitochondrial translocation of MICU1 and MI/R. Specific small interfering RNA (20 μg) against MICU1 and Tom70, and lentivirus vectors carrying the Tom70a sequences (3.3 × 107 TU) were delivered through intramyocardial injection. Seventy-two hours after injection, mice were subjected to 30 min of MI followed by 3 h (for cell apoptosis and mitochondrial damage assessment) or 24 h (for cardiac function and infarct size determination) of reperfusion. MI/R had no significant effect on total MICU1 expression, but caused significant reduction of MICU1 in mitochondria. Knockdown of MICU1 significantly aggravated MI/R injury, as evidenced by enlarged infarct size, depressed cardiac function and increased myocardial apoptosis. Moreover, MICU1 deficiency resulted in markedly aggravated mitochondrial Ca2+ overload, consequently destructed mitochondrial morphology and suppressed mitochondrial function (evidenced by decreased ATP production). Interestingly, mitochondrial Tom70 was also decreased in MI/R. Genetic loss-function study revealed that mitochondrial MICU1 expression was depressed by Tom70 ablation. Furthermore, Tom70 deficiency significantly aggravated MI/R injury and worsened mitochondrial Ca2+ overload. However, supplementation of Tom70 significantly attenuated MI/R injury, preserved mitochondrial morphology and function, and inhibited mitochondrial Ca2+ overload, all of which were abolished by MICU1 suppression. Mitochondrial Tom70/MICU1 pathway protects against MI/R injury, in which mitochondrial localization of MICU1 is governed by Tom70, and MICU1 serves as an indispensable factor in Tom70’s cardioprotection.

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Section: Methodsmentioning

confidence: 99%