Novel cellular mechanisms for neuroprotection in ischemic preconditioning: a view from inside organelles
Ischemic preconditioning (IPC) represents an important adaptation mechanism of CNS, which results in its increased tolerance to the lethal cerebral ischemia. The molecular mechanisms responsible for the induction and maintenance of ischemic tolerance in the brain are complex and not yet completely c...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2015-05-01
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| Series: | Frontiers in Neurology |
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| Online Access: | http://journal.frontiersin.org/Journal/10.3389/fneur.2015.00115/full |
| _version_ | 1818245870491009024 |
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| author | Maria Josè eSisalli Lucio eAnnunziato Lucio eAnnunziato Antonella eScorziello |
| author_facet | Maria Josè eSisalli Lucio eAnnunziato Lucio eAnnunziato Antonella eScorziello |
| author_sort | Maria Josè eSisalli |
| collection | DOAJ |
| description | Ischemic preconditioning (IPC) represents an important adaptation mechanism of CNS, which results in its increased tolerance to the lethal cerebral ischemia. The molecular mechanisms responsible for the induction and maintenance of ischemic tolerance in the brain are complex and not yet completely clarified. In the last ten years great attention has been devoted to unravel the intracellular pathways activated by preconditioning, and responsible for the establishing of the tolerant phenotype. Indeed, recent papers have been published supporting the hypothesis that mitochondria might act as master regulators of preconditioning-triggered endogenous neuroprotection due to their ability to control cytosolic calcium homeostasis. More interestingly, the demonstration that functional alterations in the ability of mitochondria and Endoplasmic Reticulum (ER) managing calcium homeostasis during ischemia, opened a new line of research focused to the role played by mitochondria and ER cross-talk in the pathogenesis of cerebral ischemia in order to identify new molecular mechanisms involved in the ischemic tolerance. In line with these findings, and considering that the expression of the three isoforms of the sodium calcium exchanger (NCX), NCX1, NCX2 and NCX3, mainly responsible for the regulation of Ca2+ homeostasis, was reduced during cerebral ischemia, it was investigated whether these proteins, might play a role in neuroprotection induced by ischemic tolerance. In the present review evidence supporting the involvement of ER and mitochondria interaction within the preconditioning paradigm will be provided. In particular, the key role played by NCXs in the regulation of Ca2+-homeostasis at the different subcellular compartments, will be discussed as new molecular mechanism proposed for the establishing of ischemic tolerant phenotype . |
| first_indexed | 2024-12-12T14:39:47Z |
| format | Article |
| id | doaj.art-4b0bd864ac074b559b13979f0d668b4f |
| institution | Directory Open Access Journal |
| issn | 1664-2295 |
| language | English |
| last_indexed | 2024-12-12T14:39:47Z |
| publishDate | 2015-05-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Neurology |
| spelling | doaj.art-4b0bd864ac074b559b13979f0d668b4f2022-12-22T00:21:17ZengFrontiers Media S.A.Frontiers in Neurology1664-22952015-05-01610.3389/fneur.2015.00115136647Novel cellular mechanisms for neuroprotection in ischemic preconditioning: a view from inside organellesMaria Josè eSisalli0Lucio eAnnunziato1Lucio eAnnunziato2Antonella eScorziello3Federico II University of NaplesFederico II University of NaplesFondazione IRCSS SDN, Naples, ItalyFederico II University of NaplesIschemic preconditioning (IPC) represents an important adaptation mechanism of CNS, which results in its increased tolerance to the lethal cerebral ischemia. The molecular mechanisms responsible for the induction and maintenance of ischemic tolerance in the brain are complex and not yet completely clarified. In the last ten years great attention has been devoted to unravel the intracellular pathways activated by preconditioning, and responsible for the establishing of the tolerant phenotype. Indeed, recent papers have been published supporting the hypothesis that mitochondria might act as master regulators of preconditioning-triggered endogenous neuroprotection due to their ability to control cytosolic calcium homeostasis. More interestingly, the demonstration that functional alterations in the ability of mitochondria and Endoplasmic Reticulum (ER) managing calcium homeostasis during ischemia, opened a new line of research focused to the role played by mitochondria and ER cross-talk in the pathogenesis of cerebral ischemia in order to identify new molecular mechanisms involved in the ischemic tolerance. In line with these findings, and considering that the expression of the three isoforms of the sodium calcium exchanger (NCX), NCX1, NCX2 and NCX3, mainly responsible for the regulation of Ca2+ homeostasis, was reduced during cerebral ischemia, it was investigated whether these proteins, might play a role in neuroprotection induced by ischemic tolerance. In the present review evidence supporting the involvement of ER and mitochondria interaction within the preconditioning paradigm will be provided. In particular, the key role played by NCXs in the regulation of Ca2+-homeostasis at the different subcellular compartments, will be discussed as new molecular mechanism proposed for the establishing of ischemic tolerant phenotype .http://journal.frontiersin.org/Journal/10.3389/fneur.2015.00115/fullIschemic PreconditioningMitochondriaNeuronsCalcium.Sodium calcium exchanger |
| spellingShingle | Maria Josè eSisalli Lucio eAnnunziato Lucio eAnnunziato Antonella eScorziello Novel cellular mechanisms for neuroprotection in ischemic preconditioning: a view from inside organelles Frontiers in Neurology Ischemic Preconditioning Mitochondria Neurons Calcium. Sodium calcium exchanger |
| title | Novel cellular mechanisms for neuroprotection in ischemic preconditioning: a view from inside organelles |
| title_full | Novel cellular mechanisms for neuroprotection in ischemic preconditioning: a view from inside organelles |
| title_fullStr | Novel cellular mechanisms for neuroprotection in ischemic preconditioning: a view from inside organelles |
| title_full_unstemmed | Novel cellular mechanisms for neuroprotection in ischemic preconditioning: a view from inside organelles |
| title_short | Novel cellular mechanisms for neuroprotection in ischemic preconditioning: a view from inside organelles |
| title_sort | novel cellular mechanisms for neuroprotection in ischemic preconditioning a view from inside organelles |
| topic | Ischemic Preconditioning Mitochondria Neurons Calcium. Sodium calcium exchanger |
| url | http://journal.frontiersin.org/Journal/10.3389/fneur.2015.00115/full |
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