Calpains and neuronal damage in the ischemic brain: The swiss knife in synaptic injury

Curcio, M. Joan; Salazar, Ivan L.; Mele, Miranda; Canzoniero, Lorella M.T.; Duarte, Carlos B.

doi:10.1016/j.pneurobio.2016.06.001

Cited by 81 publications

(69 citation statements)

References 479 publications

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“…According to calcium overload hypothesis 24, 25 , the accumulated high Ca 2+ levels lead to mitochondrial dysfunction and generation of reactive oxygen species (ROS), and over activate Ca 2+ -dependent enzymes such as proteases, phospholipases and endonucleases. The breakdown of proteins, lipids and nucleic acids by these enzymes contribute to cell death.…”

Section: Discussionmentioning

confidence: 99%

The Role of TRPC6 in the Neuroprotection of Calycosin Against Cerebral Ischemic Injury

Guo

et al. 2017

Sci Rep

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Our previous studies have provided evidences that calycosin can protect the brain from ischemia/reperfusion injury, but its mechanisms is not fully understand. Transient receptor potential canonical 6 (TRPC6) has a critical role in promoting neuronal survival against cerebral ischemic injury. The aim of the present study is to test whether calycosin protects against cerebral ischemic injury through TRPC6-CREB pathway. In vivo, rats were subjected to transient middle cerebral artery occlusion (MCAO) for 2 h and then treated with different doses of calycosin at the onset of reperfusion. In vitro, primary cultured neurons were treated by calycosin, then exposed to 2 h oxygen glucose deprivation (OGD) followed by 24 h reoxygenation. Our results showed that treatment with calycosin protected against ischemia-induced damages by increasing TRPC6 and P-CREB expression and inhibiting calpain activation. The neuroprotection effect of calycosin was diminished by inhibition or knockdown of TRPC6 and CREB. These findings indicated that the potential neuroprotection mechanism of calycosin was involved with TRPC6-CREB pathway.

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Section: Discussionmentioning

confidence: 99%

The Role of TRPC6 in the Neuroprotection of Calycosin Against Cerebral Ischemic Injury

Guo

et al. 2017

Sci Rep

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“…Intracellular concentration of Ca 2+ is tightly regulated by ion channels and transporters because of its broad involvement in cellular processes ranging from enzyme activity to programmed cell death (Cai and Patel, 2010; Curcio et al, 2016). Mitochondria and ER are both capable of sequestrating Ca 2+ .…”

Section: Impact Of Aging On the Components Of The Nvumentioning

confidence: 99%

Dysfunction of the neurovascular unit in ischemic stroke and neurodegenerative diseases: An aging effect

Cai

Zhang

et al. 2017

Ageing Research Reviews

229

184

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Current understanding on the mechanisms of brain injury and neurodegeneration highlights an appreciation of multicellular interactions within the neurovascular unit (NVU), which include the evolution of blood-brain barrier (BBB) damage, neuronal cell death or degeneration, glial reaction, and immune cell infiltration. Aging is an important factor that influences the integrity of the NVU. The age-related physiological or pathological changes in the cellular components of the NVU have been shown to increase the vulnerability of the NVU to ischemia/reperfusion injury or neurodegeneration, and to result in deteriorated brain damage. This review describes the impacts of aging on each NVU component and discusses the mechanisms by which aging increases NVU sensitivity to stroke and neurodegenerative diseases. Prophylactic or therapeutic perspectives that may delay or diminish aging and thus prevent the incidence of these neurological disorders will also be reviewed.

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“…the proteasome) can, in some cases, elevate activity in other pathways (e.g. autophagy; 135 , but see 137 ); and, finally, because of the existence of additional routes for synaptic protein degradation which involve calpains 138 and extracellular acting proteases (e.g. tissue plasminogen activator, β-site amyloid precursor protein-cleaving enzyme 1, and matrix metalloproteinases; reviewed in 139, 140 among others 141 ).…”

Section: Discussionmentioning

confidence: 99%

Recent insights on principles of synaptic protein degradation

Cohen

Ziv

2017

F1000Res

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Maintaining synaptic integrity and function depends on the continuous removal and degradation of aged or damaged proteins. Synaptic protein degradation has received considerable attention in the context of synaptic plasticity and growing interest in relation to neurodegenerative and other disorders. Conversely, less attention has been given to constitutive, ongoing synaptic protein degradation and the roles canonical degradation pathways play in these processes. Here we briefly review recent progress on this topic and new experimental approaches which have expedited such progress and highlight several emerging principles. These include the realization that synaptic proteins typically have unusually long lifetimes, as might be expected from the remote locations of most synaptic sites; the possibility that degradation pathways can change with time from synthesis, cellular context, and physiological input; and that degradation pathways, other than ubiquitin-proteasomal-mediated degradation, might play key roles in constitutive protein degradation at synaptic sites. Finally, we point to the importance of careful experimental design and sufficiently sensitive techniques for studying synaptic protein degradation, which bring into account their slow turnover rates and complex life cycles.

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Calpains and neuronal damage in the ischemic brain: The swiss knife in synaptic injury

Cited by 81 publications

References 479 publications

The Role of TRPC6 in the Neuroprotection of Calycosin Against Cerebral Ischemic Injury

The Role of TRPC6 in the Neuroprotection of Calycosin Against Cerebral Ischemic Injury

Dysfunction of the neurovascular unit in ischemic stroke and neurodegenerative diseases: An aging effect

Recent insights on principles of synaptic protein degradation

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