Reduced Ischemic Brain Injury in Interleukin-1β Converting Enzyme—Deficient Mice

Schielke, Gerald P.; Yang, Guo‐Yuan; Shivers, Brenda D.; Betz, A. Lorris

doi:10.1097/00004647-199802000-00009

Cited by 297 publications

(165 citation statements)

References 42 publications

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“…Published data have shown a linear relationship between CBF reduction and MCAO as measured by simultaneous LDF or 14C-IMP. 47,48 We expressed the changes of CBF as a percentage by setting the baseline value as reference group for consistent measurement comparison at different time points. We found that AAVH9-VEGF improved CBF recovery in the perifocal cortex starting at 1 week of tMCAO, and that further recovery extended to the core area 2 weeks of tMCAO.…”

Section: Aavh9-vegf Promotes Angiogenesismentioning

confidence: 99%

Adeno-associated viral vector-mediated hypoxia-regulated VEGF gene transfer promotes angiogenesis following focal cerebral ischemia in mice

Shen

Fan

et al. 2007

Gene Ther

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Section: Aavh9-vegf Promotes Angiogenesismentioning

confidence: 99%

Adeno-associated viral vector-mediated hypoxia-regulated VEGF gene transfer promotes angiogenesis following focal cerebral ischemia in mice

Shen

Fan

et al. 2007

Gene Ther

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“…Early evidence that caspase-1 plays a role in neuronal cell death came from the findings that caspase-1-deficient neurons showed prolonged survival following trophic factor withdrawal-induced apoptosis. 69,70 Similarly, neuronal overexpression of a dominant negative and catalytically inactive (C 285 G) caspase-1 in mice resulted in an increase in resistance to neurotoxicity. 71 So far, there does not appear to be a common event responsible for inducing caspase-1 activation in neurodegenerative diseases.…”

Section: 12mentioning

confidence: 99%

The inflammatory caspases: guardians against infections and sepsis

2006

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Innate immunity is the primary host defense against invading microorganisms. Pathogen recognition, mediated through an elaborate 'microbial sensing' system comprising the Toll-like and Nod-like receptor families results in the activation of caspase-1, which is a prerequisite for pathogen clearance. Tight regulation of caspase-1 is necessary to control the magnitude of the innate immune response and protect the organism from possible damaging effects such as sepsis. Recent findings from population studies and animal models of infectious diseases and sepsis have uncovered a role for full-length caspase-12 in blocking the inflammatory response initiated by caspase-1, thus predisposing the organism to severe sepsis and sepsis-related lethality. In this review, we re-examine the relationship among the Group I caspases, their known substrates and their proposed role in apoptosis. We further discuss their function in inflammation and bacterial clearance, with an emphasis on their regulatory mechanisms during the innate immune response.

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“…Indeed, Caspase-3 activation contributes to brain tissue loss and downstream biochemical events leading to programmed cell death after traumatic brain injury (3,4). Both genetic disruption and pharmacological inhibition of caspases after stroke can reduce ischemic neuronal injury inducing a neuroprotective effect (5)(6)(7)(8). It has been suggested that silencing of apoptotic genes using in vivo RNA interference (RNAi) could be potentially an effective treatment for stroke (5,9) .…”

mentioning

confidence: 99%

Functional motor recovery from brain ischemic insult by carbon nanotube-mediated siRNA silencing

Al‐Jamal

Gherardini

Bardi

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

213

122

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Stroke is the second cause of death worldwide with ischemic stroke accounting for 80% of all stroke insults. Caspase-3 activation contributes to brain tissue loss and downstream biochemical events that lead to programmed cell death after traumatic brain injury. Alleviation of symptoms following ischemic neuronal injury can be potentially achieved by either genetic disruption or pharmacological inhibition of caspases. Here, we studied whether silencing of Caspase-3 using carbon nanotube-mediated in vivo RNA interference (RNAi) could offer a therapeutic opportunity against stroke. Effective delivery of siRNA directly to the CNS has been shown to normalize phenotypes in animal models of several neurological diseases. It is shown here that peri-lesional stereotactic administration of a Caspase-3 siRNA (siCas 3) delivered by functionalized carbon nanotubes (f-CNT) reduced neurodegeneration and promoted functional preservation before and after focal ischemic damage of the rodent motor cortex using an endothelin-1 induced stroke model. These observations illustrate the opportunity offered by carbon nanotube-mediated siRNA delivery and gene silencing of neuronal tissue applicable to a variety of different neuropathological conditions where intervention at well localized brain foci may offer therapeutic and functional benefits.nanomedicine | neurodegenerative | neuroprotection | neurosciences | gene therapy

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Reduced Ischemic Brain Injury in Interleukin-1β Converting Enzyme—Deficient Mice

Abstract: Both of these markers of brain injury were significantly re-

Cited by 297 publications

References 42 publications

Adeno-associated viral vector-mediated hypoxia-regulated VEGF gene transfer promotes angiogenesis following focal cerebral ischemia in mice

Adeno-associated viral vector-mediated hypoxia-regulated VEGF gene transfer promotes angiogenesis following focal cerebral ischemia in mice

The inflammatory caspases: guardians against infections and sepsis

Functional motor recovery from brain ischemic insult by carbon nanotube-mediated siRNA silencing

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