Fusion or Fission: The Destiny of Mitochondria In Traumatic Brain Injury of Different Severities

Abstract Mitochondrial dynamics are regulated by a complex system of proteins representing the mitochondrial quality control (MQC). MQC balances antagonistic forces of fusion and fission determining mitochondrial and cell fates. In several neurological disorders, dysfunctional mitochondria show sign...

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Autores principales:	Valentina Di Pietro, Giacomo Lazzarino, Angela Maria Amorini, Stefano Signoretti, Lisa J. Hill, Edoardo Porto, Barbara Tavazzi, Giuseppe Lazzarino, Antonio Belli
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/b1100553362f423f9877f3894a059508
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spelling	oai:doaj.org-article:b1100553362f423f9877f3894a0595082021-12-02T12:32:14ZFusion or Fission: The Destiny of Mitochondria In Traumatic Brain Injury of Different Severities10.1038/s41598-017-09587-22045-2322https://doaj.org/article/b1100553362f423f9877f3894a0595082017-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-09587-2https://doaj.org/toc/2045-2322Abstract Mitochondrial dynamics are regulated by a complex system of proteins representing the mitochondrial quality control (MQC). MQC balances antagonistic forces of fusion and fission determining mitochondrial and cell fates. In several neurological disorders, dysfunctional mitochondria show significant changes in gene and protein expression of the MQC and contribute to the pathophysiological mechanisms of cell damage. In this study, we evaluated the main gene and protein expression involved in the MQC in rats receiving traumatic brain injury (TBI) of different severities. At 6, 24, 48 and 120 hours after mild TBI (mTBI) or severe TBI (sTBI), gene and protein expressions of fusion and fission were measured in brain tissue homogenates. Compared to intact brain controls, results showed that genes and proteins inducing fusion or fission were upregulated and downregulated, respectively, in mTBI, but downregulated and upregulated, respectively, in sTBI. In particular, OPA1, regulating inner membrane dynamics, cristae remodelling, oxidative phosphorylation, was post-translationally cleaved generating differential amounts of long and short OPA1 in mTBI and sTBI. Corroborated by data referring to citrate synthase, these results confirm the transitory (mTBI) or permanent (sTBI) mitochondrial dysfunction, enhancing MQC importance to maintain cell functions and indicating in OPA1 an attractive potential therapeutic target for TBI.Valentina Di PietroGiacomo LazzarinoAngela Maria AmoriniStefano SignorettiLisa J. HillEdoardo PortoBarbara TavazziGiuseppe LazzarinoAntonio BelliNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-13 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Valentina Di Pietro Giacomo Lazzarino Angela Maria Amorini Stefano Signoretti Lisa J. Hill Edoardo Porto Barbara Tavazzi Giuseppe Lazzarino Antonio Belli Fusion or Fission: The Destiny of Mitochondria In Traumatic Brain Injury of Different Severities
description	Abstract Mitochondrial dynamics are regulated by a complex system of proteins representing the mitochondrial quality control (MQC). MQC balances antagonistic forces of fusion and fission determining mitochondrial and cell fates. In several neurological disorders, dysfunctional mitochondria show significant changes in gene and protein expression of the MQC and contribute to the pathophysiological mechanisms of cell damage. In this study, we evaluated the main gene and protein expression involved in the MQC in rats receiving traumatic brain injury (TBI) of different severities. At 6, 24, 48 and 120 hours after mild TBI (mTBI) or severe TBI (sTBI), gene and protein expressions of fusion and fission were measured in brain tissue homogenates. Compared to intact brain controls, results showed that genes and proteins inducing fusion or fission were upregulated and downregulated, respectively, in mTBI, but downregulated and upregulated, respectively, in sTBI. In particular, OPA1, regulating inner membrane dynamics, cristae remodelling, oxidative phosphorylation, was post-translationally cleaved generating differential amounts of long and short OPA1 in mTBI and sTBI. Corroborated by data referring to citrate synthase, these results confirm the transitory (mTBI) or permanent (sTBI) mitochondrial dysfunction, enhancing MQC importance to maintain cell functions and indicating in OPA1 an attractive potential therapeutic target for TBI.
format	article
author	Valentina Di Pietro Giacomo Lazzarino Angela Maria Amorini Stefano Signoretti Lisa J. Hill Edoardo Porto Barbara Tavazzi Giuseppe Lazzarino Antonio Belli
author_facet	Valentina Di Pietro Giacomo Lazzarino Angela Maria Amorini Stefano Signoretti Lisa J. Hill Edoardo Porto Barbara Tavazzi Giuseppe Lazzarino Antonio Belli
author_sort	Valentina Di Pietro
title	Fusion or Fission: The Destiny of Mitochondria In Traumatic Brain Injury of Different Severities
title_short	Fusion or Fission: The Destiny of Mitochondria In Traumatic Brain Injury of Different Severities
title_full	Fusion or Fission: The Destiny of Mitochondria In Traumatic Brain Injury of Different Severities
title_fullStr	Fusion or Fission: The Destiny of Mitochondria In Traumatic Brain Injury of Different Severities
title_full_unstemmed	Fusion or Fission: The Destiny of Mitochondria In Traumatic Brain Injury of Different Severities
title_sort	fusion or fission: the destiny of mitochondria in traumatic brain injury of different severities
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/b1100553362f423f9877f3894a059508
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Fusion or Fission: The Destiny of Mitochondria In Traumatic Brain Injury of Different Severities

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