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

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Fusion or Fission : The Destiny of Mitochondria In Traumatic Brain Injury of Different Severities. / Di Pietro, Valentina; Lazzarino, Giacomo; Amorini, Angela Maria; Signoretti, Stefano; Porto, Edoardo; Hill, Lisa Jayne; Tavazzi, Barbara; Lazzarino, Giuseppe; Belli, Antonio.

In: Scientific Reports, Vol. 7, 9189, 2017.

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Di Pietro, Valentina ; Lazzarino, Giacomo ; Amorini, Angela Maria ; Signoretti, Stefano ; Porto, Edoardo ; Hill, Lisa Jayne ; Tavazzi, Barbara ; Lazzarino, Giuseppe ; Belli, Antonio. / Fusion or Fission : The Destiny of Mitochondria In Traumatic Brain Injury of Different Severities. In: Scientific Reports. 2017 ; Vol. 7.

Bibtex

@article{55c8663a43424727a6c3bc4740bc4a08,
title = "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 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.",
keywords = "Brain injuries, Molecular neuroscience",
author = "{Di Pietro}, Valentina and Giacomo Lazzarino and Amorini, {Angela Maria} and Stefano Signoretti and Edoardo Porto and Hill, {Lisa Jayne} and Barbara Tavazzi and Giuseppe Lazzarino and Antonio Belli",
year = "2017",
doi = "10.1038/s41598-017-09587-2",
language = "English",
volume = "7",
journal = "Scientific Reports",
issn = "2045-2322",
publisher = "Nature Publishing Group",

}

RIS

TY - JOUR

T1 - Fusion or Fission

T2 - The Destiny of Mitochondria In Traumatic Brain Injury of Different Severities

AU - Di Pietro, Valentina

AU - Lazzarino, Giacomo

AU - Amorini, Angela Maria

AU - Signoretti, Stefano

AU - Porto, Edoardo

AU - Hill, Lisa Jayne

AU - Tavazzi, Barbara

AU - Lazzarino, Giuseppe

AU - Belli, Antonio

PY - 2017

Y1 - 2017

N2 - 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.

AB - 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.

KW - Brain injuries

KW - Molecular neuroscience

U2 - 10.1038/s41598-017-09587-2

DO - 10.1038/s41598-017-09587-2

M3 - Article

VL - 7

JO - Scientific Reports

JF - Scientific Reports

SN - 2045-2322

M1 - 9189

ER -