Transplantation of Neural Stem Cells That Overexpress Sod1 Enhances Amelioration of Intracerebral Hemorrhage in Mice

Wakai, Takuma; Sakata, Hiroyuki; Narasimhan, Purnima; Yoshioka, Hideyuki; Kinouchi, Hiroyuki; Chan, Pak H.

doi:10.1038/jcbfm.2013.215

Cited by 36 publications

(33 citation statements)

References 42 publications

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“…The efficacy of free radical scavengers has provided direct evidence for a causal relationship between ROS and ICH injury. Specifically, overexpression of copper/zinc-superoxide dismutase (Wakai, et al, 2014) or treatment with deferoxamine (Cui, et al, 2015, Ni, et al, 2015, H. Wu, et al, 2011), a chelator of pro-oxidative iron, significantly reduced brain injury in animal models of ICH.…”

Section: Discussionmentioning

confidence: 99%

Progesterone exerts neuroprotective effects and improves long-term neurologic outcome after intracerebral hemorrhage in middle-aged mice

Jiang

Zuo

Wang

et al. 2016

Neurobiology of Aging

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In this study, we examined the effect of progesterone on histopathologic and functional outcomes of intracerebral hemorrhage (ICH) in 10–12-month-old mice. Progesterone or vehicle was administered by intraperitoneal injection 1 hour after collagenase-induced ICH and then by subcutaneous injections at 6, 24, and 48 hours. Oxidative and nitrosative stress were assayed at 12 hours post-ICH. Injury markers were examined on day 1, and lesion was examined on day 3. Neurologic deficits were examined for 28 days. Progesterone posttreatment reduced lesion volume, brain swelling, edema, and cell degeneration and improved long-term neurologic function. These protective effects were associated with reductions in protein carbonyl formation, protein nitrosylation, and MMP-9 activity and attenuated cellular and molecular inflammatory responses. Progesterone also reduced VEGF expression, increased neuronal-specific Na+/K+ ATPase α3 subunit expression, and reduced PKC-dependent Na+/K+ ATPase phosphorylation. Furthermore, progesterone reduced glial scar thickness, myelin loss, brain atrophy, and residual injury volume on day 28 after ICH. With multiple brain targets, progesterone warrants further investigation for its potential use in ICH therapy.

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Section: Discussionmentioning

confidence: 99%

Progesterone exerts neuroprotective effects and improves long-term neurologic outcome after intracerebral hemorrhage in middle-aged mice

Jiang

Zuo

Wang

et al. 2016

Neurobiology of Aging

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“…Other studies have used neural stem cell transplantation to treat SBI following cerebral hemorrhage, but the host reaction after transplantation led to graft failure and death, which may be related to elevated levels of oxidative stress after transplant. Therefore, Wakai and colleagues transplanted neural stem cells overexpressing SOD1 (copper/zinc-superoxide dismutase) to treat cerebral hemorrhage, which significantly reduced mortality and oxidative stress, speeding up recovery from neurological disorders after ICH [ 196 ].…”

Section: Antioxidant Therapy After Ichmentioning

confidence: 99%

Intracerebral Hemorrhage, Oxidative Stress, and Antioxidant Therapy

Duan

Wen

Shen

et al. 2016

Oxidative Medicine and Cellular Longevity

231

177

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Hemorrhagic stroke is a common and severe neurological disorder and is associated with high rates of mortality and morbidity, especially for intracerebral hemorrhage (ICH). Increasing evidence demonstrates that oxidative stress responses participate in the pathophysiological processes of secondary brain injury (SBI) following ICH. The mechanisms involved in interoperable systems include endoplasmic reticulum (ER) stress, neuronal apoptosis and necrosis, inflammation, and autophagy. In this review, we summarized some promising advances in the field of oxidative stress and ICH, including contained animal and human investigations. We also discussed the role of oxidative stress, systemic oxidative stress responses, and some research of potential therapeutic options aimed at reducing oxidative stress to protect the neuronal function after ICH, focusing on the challenges of translation between preclinical and clinical studies, and potential post-ICH antioxidative therapeutic approaches.

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“…SOD1 overexpression in transgenic rats was linked to reduced OS, BBB disruption, and neuronal apoptosis in a Hb-injection model [ 42 ]. A recent study on cell replacement therapy in ICH found that neural stem cells (NSCs) overexpressing SOD1 3 days after ICH could increase neuronal survival, indicating that SOD1 enhancement alone or combined with other treatments may be effective in ICH [ 91 ]. Moreover, SOD1 hyperexpression is also protective against the spontaneous occurrence of ICH in hypertensive mice by decreasing superoxide.…”

Section: Antioxidative System In Ichmentioning

confidence: 99%

Oxidative Stress in Intracerebral Hemorrhage: Sources, Mechanisms, and Therapeutic Targets

Tao

Gan

et al. 2015

Oxidative Medicine and Cellular Longevity

124

121

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Intracerebral hemorrhage (ICH) is associated with the highest mortality and morbidity despite only constituting approximately 10–15% of all strokes. Complex underlying mechanisms consisting of cytotoxic, excitotoxic, and inflammatory effects of intraparenchymal blood are responsible for its highly damaging effects. Oxidative stress (OS) also plays an important role in brain injury after ICH but attracts less attention than other factors. Increasing evidence has demonstrated that the metabolite axis of hemoglobin-heme-iron is the key contributor to oxidative brain damage after ICH, although other factors, such as neuroinflammation and prooxidases, are involved. This review will discuss the sources, possible molecular mechanisms, and potential therapeutic targets of OS in ICH.

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Transplantation of Neural Stem Cells That Overexpress Sod1 Enhances Amelioration of Intracerebral Hemorrhage in Mice

Cited by 36 publications

References 42 publications

Progesterone exerts neuroprotective effects and improves long-term neurologic outcome after intracerebral hemorrhage in middle-aged mice

Progesterone exerts neuroprotective effects and improves long-term neurologic outcome after intracerebral hemorrhage in middle-aged mice

Intracerebral Hemorrhage, Oxidative Stress, and Antioxidant Therapy

Oxidative Stress in Intracerebral Hemorrhage: Sources, Mechanisms, and Therapeutic Targets

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