Prospective clinical biomarkers of caspase-mediated apoptosis associated with neuronal and neurovascular damage following stroke and other severe brain injuries: Implications for chronic neurodegeneration

Glushakova, Olena; Glushakov, Andriy A; Wijesinghe, Dayanjan S.; Valadka, Alex B.; Hayes, Ronald L.; Glushakov, Alexander V.

doi:10.4103/bc.bc_27_16

Cited by 44 publications

(25 citation statements)

References 238 publications

(397 reference statements)

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“…Apoptosis involving caspase-3 is one of the most common mechanisms implicated in the etiopathology of both acute and chronic neurological and neurodegenerative diseases . Even group I mGluRs could have a neuroprotective role mediated by caspase modulation .…”

Section: Resultsmentioning

confidence: 99%

“…Apoptosis involving caspase-3 is one of the most common mechanisms implicated in the etiopathology of both acute and chronic neurological and neurodegenerative diseases. 35 Even group I mGluRs could have a neuroprotective role mediated by caspase modulation. 36 Therefore, we measured the caspase-3 activity in all experimental groups, which was not significantly modified by age or RSV treatment (Figure 7).…”

Section: ■ Results and Discussionmentioning

confidence: 99%

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Resveratrol Differently Modulates Group I Metabotropic Glutamate Receptors Depending on Age in SAMP8 Mice

Sánchez-Melgar

Albasanz

Pallàs

et al. 2020

ACS Chem. Neurosci.

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Glutamate homeostasis is critical for neurotransmission as this excitatory neurotransmitter has a relevant role in cognition functions through ionotropic and metabotropic glutamate receptors in the central nervous system. During the last years, the role of the group I metabotropic glutamate receptors (mGluRs) in neurodegenerative diseases such as Alzheimer's disease has been intensely investigated. Resveratrol (RSV) is a natural polyphenolic compound that is thought to have neuroprotective properties for human health. However, little is known about the action of this compound on mGluR signaling. Therefore, the aim of this study was to investigate the possible modulation of group I mGluRs in SAMP8 mice five and seven months of age supplemented with RSV in the diet. Data reported herein show that RSV plays a different modulatory action on group I mGluRs: mGluR 5 is downregulated as age increases, independently of RSV presence, and mGluR 1 is upregulated or downregulated by RSV treatment depending on age (i.e., depending on mGluR 5 levels). In addition, a neuroprotective role can be inferred for RSV as lower glutamate levels, higher synapsin levels, and unchanged caspase-3 activity were detected after RSV treatment. In conclusion, our findings indicate that RSV treatment modifies the group I mGluR-mediated glutamatergic system in SAMP8 mice, which could contribute to the beneficial effects of this natural polyphenol.

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Section: Resultsmentioning

confidence: 99%

Section: ■ Results and Discussionmentioning

confidence: 99%

Resveratrol Differently Modulates Group I Metabotropic Glutamate Receptors Depending on Age in SAMP8 Mice

Sánchez-Melgar

Albasanz

Pallàs

et al. 2020

ACS Chem. Neurosci.

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“…The ratio of Bax/Bcl-2 is a useful index for determining apoptotic state [ 30 ]. The anti-apoptotic property of Ramelteon was further confirmed by the decreased Bax/Bcl-2 ratio and the downregulation of cleaved caspase-3, another pro-apoptotic protein [ 31 ].…”

Section: Discussionmentioning

confidence: 99%

Ramelteon ameliorated 1-methyl-4-phenylpyridinium (MPP+)-induced neurotoxicity in neuronal cells in a mitochondrial-dependent pathway

Zhang

Liu

et al. 2021

Bioengineered

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Parkinson's disease (PD) is a common neurodegenerative disease with global health and economic impact. 1-methyl-4-phenylpyridinium (MPP+)-induced mitochondrial dysfunction and oxidative stress are reported to participate in the pathological mechanism of PD. Ramelteon is a novel oral hypnotic agent that has recently been reported to display neuronal protective effects. However, it is unknown whether Ramelteon possesses a beneficial effect in PD. In this study, we aimed to examine the potential function of Ramelteon in MPP+-challenged neurons. We found that Ramelteon rescued the cell viability reduced by MPP+-stimulation. Further, oxidative stress in MPP+-challenged SH-SY5Y cells was mitigated by Ramelteon as verified by the upregulated levels of mitochondrial reactive oxygen species (ROS) and protein carboxyl, and the upregulation of NADPH oxidase 4 (NOX-4). Furthermore, the declined mitochondrial membrane potential ( Δ Ψ m ) caused by MPP+ was reversed by Ramelteon. Importantly, Ramelteon attenuated MPP+-induced apoptosis, accompanied by a decreased ratio of Bax/Bcl-2, inhibition of cytochrome C release, and downregulation of cleaved caspase-3. For the first time, we conclude that Ramelteon might ameliorate MPP+-induced neurotoxicity in neuronal cells in a mitochondrial-dependent pathway.

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“…Apoptosis occurs via two approaches: endogenous apoptosis, which occurs in and is mediated by the mitochondria, and exogenous apoptosis, which occurs outside the mitochondria and is induced by death receptors called the exogenous apoptotic cell death pathway [ 21 , 22 ]. The expression of caspase-1 leads to the induction of pathways that result in a type of regulated cell death (RCD), distinct from apoptosis, called pyroptosis, which is associated with the influence of inflammatory cytokines [ 23 ]. Caspase-1, caspase-4, caspase-5, and caspase-11 are collectively referred to as inflammatory caspases owing to their functions in these processes.…”

Section: Pathways Associated With Caspase Activation In Ebi After Sahmentioning

confidence: 99%

“…Activated caspase-8 can cleave the Bcl-2 interacting domain (BID) into a truncated active form (tBid), affecting caspase-3 by participating in mitochondria-mediated endogenous apoptosis. Collectively, the above pathways can ultimately induce the apoptotic pathway by activating caspase-3 [ 1 , 23 ].…”

Section: Extrinsic Mechanisms Of Classic Apoptosismentioning

confidence: 99%

Biological Effects and Mechanisms of Caspases in Early Brain Injury after Subarachnoid Hemorrhage

Liu

Zhou

et al. 2022

Oxidative Medicine and Cellular Longevity

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Caspases are an evolutionarily conserved family of proteases responsible for mediating and initiating cell death signals. In the past, the dysregulated activation of caspases was reported to play diverse but equally essential roles in neurodegenerative diseases, such as brain injury and neuroinflammatory diseases. A subarachnoid hemorrhage (SAH) is a traumatic event that is either immediately lethal or induces a high risk of stroke and neurological deficits. Currently, the prognosis of SAH after treatment is not ideal. Early brain injury (EBI) is considered one of the main factors contributing to the poor prognosis of SAH. The mechanisms of EBI are complex and associated with oxidative stress, neuroinflammation, blood-brain barrier disruption, and cell death. Based on mounting evidence, caspases are involved in neuronal apoptosis or death, endothelial cell apoptosis, and increased inflammatory cytokine-induced by apoptosis, pyroptosis, and necroptosis in the initial stages after SAH. Caspases can simultaneously mediate multiple death modes and regulate each other. Caspase inhibitors (including XIAP, VX-765, and Z-VAD-FMK) play an essential role in ameliorating EBI after SAH. In this review, we explore the related pathways mediated by caspases and their reciprocal regulation patterns after SAH. Furthermore, we focus on the extensive crosstalk of caspases as a potential area of research on therapeutic strategies for treating EBI after SAH.

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Prospective clinical biomarkers of caspase-mediated apoptosis associated with neuronal and neurovascular damage following stroke and other severe brain injuries: Implications for chronic neurodegeneration

Cited by 44 publications

References 238 publications

Resveratrol Differently Modulates Group I Metabotropic Glutamate Receptors Depending on Age in SAMP8 Mice

Resveratrol Differently Modulates Group I Metabotropic Glutamate Receptors Depending on Age in SAMP8 Mice

Ramelteon ameliorated 1-methyl-4-phenylpyridinium (MPP+)-induced neurotoxicity in neuronal cells in a mitochondrial-dependent pathway

Biological Effects and Mechanisms of Caspases in Early Brain Injury after Subarachnoid Hemorrhage

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