Appearance of Nuclear-sorted Caspase-12 Fragments in Cerebral Cortical and Hippocampal Neurons in Rats Damaged by Autologous Blood Clot Embolic Brain Infarctions

Shimoke, Koji; Matsuki, Yoshinori; Fukunaga, Kohji; Matsumura, Yoshitaka; Fujita, Eriko; Sugihara, Kensuke; Nobuhara, Masamichi; Maruoka, Hiroki; Ikeuchi, Toshihiko; Kudo, Motoshige

doi:10.1007/s10571-011-9687-0

Cited by 10 publications

(9 citation statements)

References 32 publications

(36 reference statements)

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“…The processing of caspase-12 is at the N-terminal region, either by caspases or by calpains (10). Similar to this study, Shimoke et al found translocated caspase-12 in nuclei in cortical and hippocampal neurons in the case of an experimental blood clot model (38). We particularly found nuclear immunreactivity of caspase-12 in the radiation group in our study.…”

Section: █ Acknowledgementsupporting

confidence: 90%

Melatonin modulates nmda-receptor 2b/calpain-1/caspase-12 pathways in rat brain after long time exposure to gsm radiation

Seymen

Ilgaz²,

Erdoğan³

et al. 2019

Turkish Neurosurgery

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AIM: To investigate the potential protective effects of melatonin on the chronic radiation emitted by third generation mobile phones on the brain. MATERIAL and METHODS: A total of 24 male Wistar albino rats were divided into four equal groups. Throughout a 90-day experiment, no application was performed on the control group. The second group was exposed to 2100 MHz radiation for 30 minutes. Subcutaneous melatonin was injected into the third group. Subcutaneous melatonin injection was applied 40 minutes before radiation and then the fourth group was exposed to radiation for 30 minutes. At the end of the experiment, brain (cerebrum and cerebellum) tissues were taken from the subjects. Histochemical, immunohistochemical, ultrastructural and western blot analyses were applied. In addition to brain weight, Purkinje cells' number, immunohistochemical H Score analyses and the results of the Western blot were examined statistically. RESULTS: With the application of radiation, neuronal edema, relatively-decreased numbers of neurons on hippocampal CA1 and CA3 regions, displacement of the Purkinje neurons and dark neurons findings were observed as a result of histochemical stainings. Radiation also activated the NMDA-receptor 2B/Calpain-1/Caspase-12 pathway, NMDA-receptor 2B and Calpain-1 with the findings being supported by western blot analyses. Pre-increased protein synthesis before apoptosis was identified by electron microscopy. CONCLUSION: Mobile phone radiation caused certain (ultra) structural changes on the brain and activated the NMDA-receptor 2B/ Calpain-1/Caspase-12 pathway; in addition, melatonin was found to be effective, but insufficient in demonstrating the protective effects.

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Section: █ Acknowledgementsupporting

confidence: 90%

Melatonin modulates nmda-receptor 2b/calpain-1/caspase-12 pathways in rat brain after long time exposure to gsm radiation

Seymen

Ilgaz²,

Erdoğan³

et al. 2019

Turkish Neurosurgery

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“…International Publisher activation of caspase-3 and ERS-induced cell apoptosis in astrocytes following ischemic stroke [5][6][7]. Caspase-12 is classified in the group I family of caspases, which are characterized as inflammatory caspases [8,9].…”

Section: Ivyspringmentioning

confidence: 99%

Inhibiting Caspase-12 Mediated Inflammasome Activation protects against Oxygen-Glucose Deprivation Injury in Primary Astrocytes

Liu¹,

Chen²,

Lin³

et al. 2020

Int. J. Med. Sci.

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Stroke is one of the leading causes of death worldwide. Accumulating evidence suggests that NLRP3 inflammasome activation plays an important role in ischemic stroke injury. However, the existence of the NLRP3 inflammasome in astrocytes remains controversial. In this study, we demonstrated the presence of the NLRP3 inflammasome in primary mouse astrocytes and investigated the role of caspase-12 in NLRP3 inflammasome activation and cell injury in an in vitro astrocyte oxygen-glucose deprivation (OGD) model. Astrocytes exposed to 2, 3, and 4 h of OGD exhibited increased cell injury and apoptosis, and the protein levels of caspase-12, cleaved caspase-3, NLRP3 inflammasome components, and IL-1β were also significantly elevated. Interestingly, pretreatment with the caspase-12-specific inhibitor Z-ATAD-FMK attenuated cell injury and apoptosis and decreased the levels of NLRP3, caspase-1, IL-1β, and cleaved caspase-3 in the OGD group. In conclusion, Z-ATAD-FMK protected astrocytes against OGD-induced cell death and inhibited NLPR3-inflammasome activation. Our results indicate that caspase-12 and its potential regulation of NLRP3 inflammasome activation might be a promising target for treatment of ischemic stroke.

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“…Accordingly, in their active form, UPR transducers serve as ER stress markers. Critically, cumulative evidence suggests that all three signalling arms of the UPR are activated following ischemia [28,[60][61][62][63][64][65][66][67][68][69][70][71] .…”

Section: Er Response To Ischemiamentioning

confidence: 99%

Loss of endoplasmic reticulum Ca2+ homeostasis: contribution to neuronal cell death during cerebral ischemia

Bodalia

Jackson

2012

Acta Pharmacol Sin

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The loss of Ca 2+ homeostasis during cerebral ischemia is a hallmark of impending neuronal demise. Accordingly, considerable cellular resources are expended in maintaining low resting cytosolic levels of Ca 2+ . These include contributions by a host of proteins involved in the sequestration and transport of Ca 2+ , many of which are expressed within intracellular organelles, including lysosomes, mitochondria as well as the endoplasmic reticulum (ER homeostasis is an important trigger of pathological processes. Here we review a growing body of evidence suggesting that ER dysfunction is an important factor contributing to neuronal injury and loss post-ischemia. Specifically, the contribution of the ER to cytosolic Ca 2+ elevations during ischemia will be considered, as will the signalling cascades recruited as a consequence of disrupting ER homeostasis and function.

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Appearance of Nuclear-sorted Caspase-12 Fragments in Cerebral Cortical and Hippocampal Neurons in Rats Damaged by Autologous Blood Clot Embolic Brain Infarctions

Cited by 10 publications

References 32 publications

Melatonin modulates nmda-receptor 2b/calpain-1/caspase-12 pathways in rat brain after long time exposure to gsm radiation

Melatonin modulates nmda-receptor 2b/calpain-1/caspase-12 pathways in rat brain after long time exposure to gsm radiation

Inhibiting Caspase-12 Mediated Inflammasome Activation protects against Oxygen-Glucose Deprivation Injury in Primary Astrocytes

Loss of endoplasmic reticulum Ca2+ homeostasis: contribution to neuronal cell death during cerebral ischemia

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