Serum S100B is a useful surrogate marker for long-term outcomes in photochemically-induced thrombotic stroke rat models

Tanaka, Yu; Koizumi, Chie; Marumo, Toshiyuki; Omura, Tomohiro; Yoshida, Shigeru

doi:10.1016/j.lfs.2007.06.031

Cited by 12 publications

(7 citation statements)

References 36 publications

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“…Serum S100B levels have also been reported as an informative surrogate biomarker for ischemia-related brain damage. 26, 27 Strikingly, ELISA-measured S100B level in the sera from the blood collected on postoperative day 7 showed a significant decrease in BM-B&V group compared to both BM-Vehicle and PBS blank controls, although it was still slightly higher than the sham control (Figure 4b). Hematoxylin & eosin (H&E) staining demonstrated the normal morphology and no damaged cells in hippocampal CA1 and temporal cortex areas in the brain from the sham control, but massive damaged cells with notable neural cell loss in the corresponding areas in the brains from both PBS blank and BM-Vehicle controls after CA-GCII.…”

Section: Resultsmentioning

confidence: 95%

Enhanced neuroprotective efficacy of bone marrow mesenchymal stem cells co-overexpressing BDNF and VEGF in a rat model of cardiac arrest-induced global cerebral ischemia

Zhou

Wang

et al. 2017

Cell Death Dis

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Cardiac arrest-induced global cerebral ischemia injury (CA-GCII) usually leads to a poor neurological outcome without an effective treatment. Bone marrow-derived mesenchymal stem cells (BMMSCs) may provide a potential cell-based therapy against neurologic disorders through induction of brain-derived neurotrophic factor (BDNF) and vascular endothelial growth factor (VEGF). To optimize the neuroprotective efficacy of BMMSCs further, in this study we have derived BMMSCs, which co-overexpress both BDNF and VEGF, and tested them for the treatment of CA-GCII in a rat model. Lentiviruses that express rat BDNF exon IV or VEGF-A were created using the bicistronic shuttle vectors of pLVX-IRES-ZsGreen1 and pLVX-IRES-tdTomato, respectively. BMMSCs that were co-transduced with the engineered lentiviruses with co-overexpression of both BDNF and VEGF along with corresponding fluorescent protein reporters were injected via jugular vein of rats that just recovered from a cardiac arrest. Animals were then scored for neurofunctional deficits and examined for brain pathology and gene expression relevant to the engraftment seven days after the treatments. We demonstrate that anchorage of lentiviral vector-transduced BMMSCs, which co-overexpressed both BDNF and VEGF in the hippocampus and temporal cortex along with significantly ameliorated brain pathology and improved neurofunctional performance in CA-GCII rats after transplantation. These findings provide a proof of concept for the further validation of engineered BMMSCs for the treatment of CA-GCII patients in clinical practice in the future.

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Section: Resultsmentioning

confidence: 95%

Enhanced neuroprotective efficacy of bone marrow mesenchymal stem cells co-overexpressing BDNF and VEGF in a rat model of cardiac arrest-induced global cerebral ischemia

Zhou

Wang

et al. 2017

Cell Death Dis

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“…It is well known that ischemic model because of middle cerebral artery (MCA) occlusion with photochemically induced thrombosis (PIT) is analogous to clinical condition (Tanaka et al . ). In this ischemic mouse model, there was a significant behavioral damage evaluated by clinical score (Fig.…”

Section: Resultsmentioning

confidence: 97%

“…Similar results of the recovery of cerebral ischemia-induced blood vessels damages by P 30 were observed in the striatum and hippocampus at 24 h after 1 h tMCAO (data are not shown). P 30 ameliorates the ischemic brain caused by photochemically induced thrombosis It is well known that ischemic model because of middle cerebral artery (MCA) occlusion with photochemically induced thrombosis (PIT) is analogous to clinical condition (Tanaka et al 2007). In this ischemic mouse model, there was a significant behavioral damage evaluated by clinical score (Fig.…”

Section: P 30 Inhibits the Cerebral Ischemia-induced Blood Vessel Dammentioning

confidence: 95%

Novel neuroprotective action of prothymosin alpha‐derived peptide against retinal and brain ischemic damages

Halder

Matsunaga

Yamaguchi

et al. 2013

Journal of Neurochemistry

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Prothymosin alpha (ProTa), a nuclear protein, is implicated in the inhibition of ischemia-induced necrosis as well as apoptosis in the brain and retina. Although ProTa has multiple biological functions through distinct regions in its sequence, it has remained which region is involved in this neuroprotection. This study reported that the active core peptide sequence P 30 (amino acids 49-78) of ProTa exerts its full survival effect in cultured cortical neurons against ischemic stress. Our in vivo study revealed that intravitreous administration of P 30 at 24 h after retinal ischemia significantly blocks the ischemia-induced functional damages of retina at day 7. In addition, P 30 completely rescued the retinal ischemia-induced ganglion cell damages at day 7 after the ischemic stress, along with partial blockade of the loss of bipolar, amacrine, and photoreceptor cells. On the other hand, intracerebroventricular (3 nmol) or systemic (1 mg/kg; i.v.) injection of P 30 at 1 h after cerebral ischemia (1 h tMCAO) significantly blocked the ischemiainduced brain damages and disruption of blood vessels. Systemic P 30 delivery (1 mg/kg; i.v.) also significantly ameliorated the ischemic brain caused by photochemically induced thrombosis. Taken together, this study confers a precise demonstration about the novel protective activity of ProTaderived small peptide P 30 against the ischemic damages in vitro and in vivo. Keywords: blood vessel, brain ischemia, neuroprotective peptide, prothymosin alpha, retinal ischemia.

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“…The S100B level in the blood has been used as a marker for the extent of acute damage to the brain parenchyma and BBB disruption [57,58]. Evidence has shown that the serum level of S100B was significantly correlated with the infarct volume and the levels were higher in acute stroke patients at risk of malignant infarction or hemorrhagic transformation [59][60][61]. S100B appears to be highly correlated with the extent of acute damage to the brain parenchyma, and its correlation with sTREM-1 levels may actually reflect the correlation between infarct size and neuroinflammatory response.…”

Section: Discussionmentioning

confidence: 99%

Serum Levels of Soluble Triggering Receptor Expressed on Myeloid Cells-1 Associated with the Severity and Outcome of Acute Ischemic Stroke

Huang

Chen

et al. 2020

JCM

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Stroke is a neurological emergency, where the mechanism of the blood supply to the brain is impaired, resulting in brain cell ischemia and death. Neuroinflammation is a key component in the ischemic cascade that results in cell damage and death after cerebral ischemia. The triggering receptor expressed on myeloid cells-1 (TREM-1) modulates neuroinflammation after acute ischemic stroke. In the present study, 60 patients with acute ischemic stroke, who had been subjected to neurological examinations and National Institutes of Health Stroke Scale (NIHSS) and brain magnetic resonance imaging studies, were enrolled in the emergency room of Kaohsiung Chang Gung Memorial Hospital. Twenty-four healthy volunteers were recruited as controls. The serum levels of soluble TREM-1 (sTREM-1), human S100 calcium-binding protein B (S100B), and proinflammatory cytokines and chemokines, including tumor necrosis α (TNF-α), interleukin 1β, interleukin 6 (IL-6), interleukin 8, and interferon-γ were measured immediately after acute ischemic stroke. The serum levels of sTREM-1, TNFα, IL-6, and S100B were correlated with the stroke volume and NIHSS, after acute ischemic stroke. Additionally, the serum levels of sTREM-1 were significantly positively correlated with S100B. The functional outcomes were evaluated 6 months after ischemic stroke by the Barthel index, which was correlated with the age and levels of sTREM-1 and S100B. We suggest that acute ischemic stroke induces neuroinflammation by the activation of the TREM-1 signaling pathway and the downstream inflammatory machinery that modulates the inflammatory response and ischemic neuronal cell death. From a translational perspective, our results may allow for the development of a new therapeutic strategy for acute ischemic stroke by targeting the TREM-1 signaling pathway.

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Serum S100B is a useful surrogate marker for long-term outcomes in photochemically-induced thrombotic stroke rat models

Cited by 12 publications

References 36 publications

Enhanced neuroprotective efficacy of bone marrow mesenchymal stem cells co-overexpressing BDNF and VEGF in a rat model of cardiac arrest-induced global cerebral ischemia

Enhanced neuroprotective efficacy of bone marrow mesenchymal stem cells co-overexpressing BDNF and VEGF in a rat model of cardiac arrest-induced global cerebral ischemia

Novel neuroprotective action of prothymosin alpha‐derived peptide against retinal and brain ischemic damages

Serum Levels of Soluble Triggering Receptor Expressed on Myeloid Cells-1 Associated with the Severity and Outcome of Acute Ischemic Stroke

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