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Content of mitochondrial calcium uniporter (MCU) in cardiomyocytes is regulated by microRNA-1 in physiologic and pathologic hypertrophy

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العنوان:	Content of mitochondrial calcium uniporter (MCU) in cardiomyocytes is regulated by microRNA-1 in physiologic and pathologic hypertrophy
المؤلفون:	Diego De Stefani, Tullio Pozzan, Marco Mongillo, Giulia Borile, Giovanni Stellin, Fabio Di Lisa, Daniele Catalucci, Raffaele Coppini, V Prando, Elisabetta Cerbai, Rosario Rizzuto, Giuseppe Faggian, Vladimiro L. Vida, Marco Sandri, Wisløff Ulrik, Pierluigi Carullo, Tania Zaglia, Tomas Stølen, Antonio Campo, Andrea Armani, Paola Ceriotti
بيانات النشر:	National Academy of Sciences, 2017.
سنة النشر:	2017
مصطلحات موضوعية:	0301 basic medicine, medicine.medical_specialty, Cardiomyocyte calcium, Heart, MicroRNA, Mitochondrial calcium uniporter, Myocardial hypertrophy, Multidisciplinary, Cardiomegaly, Stimulation, Biology, Muscle hypertrophy, Rats, Sprague-Dawley, Mice, 03 medical and health sciences, Physical Conditioning, Animal, cardiomyocyte calcium, heart, microRNA, mitochondrial calcium uniporter, myocardial hypertrophy, Internal medicine, Receptors, Adrenergic, beta, medicine, Animals, Humans, Myocytes, Cardiac, Uniporter, Aorta, Ion channel, Pressure overload, Heart development, Voltage-dependent calcium channel, Rats, MicroRNAs, 030104 developmental biology, Endocrinology, PNAS Plus, Mitochondrial matrix, Calcium Channels, Energy Metabolism
الوصف:	The mitochondrial Ca2+ uniporter complex (MCUC) is a multimeric ion channel which, by tuning Ca2+ influx into the mitochondrial matrix, finely regulates metabolic energy production. In the heart, this dynamic control of mitochondrial Ca2+ uptake is fundamental for cardiomyocytes to adapt to either physiologic or pathologic stresses. Mitochondrial calcium uniporter (MCU), which is the core channel subunit of MCUC, has been shown to play a critical role in the response to β-adrenoreceptor stimulation occurring during acute exercise. The molecular mechanisms underlying the regulation of MCU, in conditions requiring chronic increase in energy production, such as physiologic or pathologic cardiac growth, remain elusive. Here, we show that microRNA-1 (miR-1), a member of the muscle-specific microRNA (myomiR) family, is responsible for direct and selective targeting of MCU and inhibition of its translation, thereby affecting the capacity of the mitochondrial Ca2+ uptake machinery. Consistent with the role of miR-1 in heart development and cardiomyocyte hypertrophic remodeling, we additionally found that MCU levels are inversely related with the myomiR content, in murine and, remarkably, human hearts from both physiologic (i.e., postnatal development and exercise) and pathologic (i.e., pressure overload) myocardial hypertrophy. Interestingly, the persistent activation of β-adrenoreceptors is likely one of the upstream repressors of miR-1 as treatment with β-blockers in pressure-overloaded mouse hearts prevented its down-regulation and the consequent increase in MCU content. Altogether, these findings identify the miR-1/MCU axis as a factor in the dynamic adaptation of cardiac cells to hypertrophy.
اللغة:	English
الوصول الحر:	https://explore.openaire.eu/search/publication?articleId=doi_dedup___::b0c184091657ef849f7e4a6573c3a2baTest http://hdl.handle.net/11577/3246295Test
حقوق:	OPEN
رقم الانضمام:	edsair.doi.dedup.....b0c184091657ef849f7e4a6573c3a2ba
قاعدة البيانات:	OpenAIRE

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In the heart, this dynamic control of mitochondrial Ca2+ uptake is fundamental for cardiomyocytes to adapt to either physiologic or pathologic stresses. Mitochondrial calcium uniporter (MCU), which is the core channel subunit of MCUC, has been shown to play a critical role in the response to β-adrenoreceptor stimulation occurring during acute exercise. The molecular mechanisms underlying the regulation of MCU, in conditions requiring chronic increase in energy production, such as physiologic or pathologic cardiac growth, remain elusive. Here, we show that microRNA-1 (miR-1), a member of the muscle-specific microRNA (myomiR) family, is responsible for direct and selective targeting of MCU and inhibition of its translation, thereby affecting the capacity of the mitochondrial Ca2+ uptake machinery. Consistent with the role of miR-1 in heart development and cardiomyocyte hypertrophic remodeling, we additionally found that MCU levels are inversely related with the myomiR content, in murine and, remarkably, human hearts from both physiologic (i.e., postnatal development and exercise) and pathologic (i.e., pressure overload) myocardial hypertrophy. Interestingly, the persistent activation of β-adrenoreceptors is likely one of the upstream repressors of miR-1 as treatment with β-blockers in pressure-overloaded mouse hearts prevented its down-regulation and the consequent increase in MCU content. 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