Glial fibrillary acidic protein as a prognostic marker of acute ischemic stroke

Liu, G; Geng, Jia

doi:10.1177/0960327117751236

Cited by 34 publications

(32 citation statements)

References 25 publications

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“…Accordingly, a series of gainand loss-of-function assays in our study underscored the inhibitory action of overexpressed Smurf2 on auxo-action of TMAO on astrogliosis, migration, and activation, which was indicated by diminished expression of GFAP, Neurocan, and Phosphacan. Peculiarly, GFAP has been defined as a complementary biomarker for the prediction of functional outcome in patients suffering from acute ischemic stroke (Liu and Geng, 2018). However, reduced Neurocan level in reactive astrocytes has been demonstrated to enhance the axonal regeneration, thus playing a catalytic role in the neurorestorative action of bone marrow stromal cells (Shen et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

TMAO Aggregates Neurological Damage Following Ischemic Stroke by Promoting Reactive Astrocytosis and Glial Scar Formation via the Smurf2/ALK5 Axis

Fan

Zhang

et al. 2021

Front. Cell. Neurosci.

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Ischemic stroke has been reported to cause significant changes to memory, thinking, and behavior. Intriguingly, recently reported studies have indicated the association of Trimethylamine N-oxide (TMAO) with the acute phase of ischemic stroke. However, the comprehensive underlying mechanism remained unknown. The objective of the present study was to investigate the association between TMAO and recovery of neurological function after ischemic stroke. For this purpose, a middle cerebral artery occlusion/reperfusion (MCAO/R) rat model was established and treated with TMAO or/and sh-ALK5, followed by the neurological function evaluation. Behaviors of rats were observed through staircase and cylinder tests. Moreover, the expression of Smurf2 and ALK5 was detected by immunohistochemistry while expression of GFAP, Neurocan, and Phosphacan in brain tissues was determined by immunofluorescence. Thereafter, gain- and loss-of-function assays in astrocytes, the proliferation, viability, and migration were evaluated by the EdU, CCK-8, and Transwell assays. Besides, Smurf2 mRNA expression was determined by the RT-qPCR, whereas, Smurf2, ALK5, GFAP, Neurocan, and Phosphacan expression was evaluated by the Western blotting. Finally, the interaction of Smurf2 with ALK5 and ALK5 ubiquitination was assessed by the co-immunoprecipitation. Notably, our results showed that TMAO promoted the proliferation of reactive astrocyte and formation of glial scar in MCAO/R rats. However, this effect was abolished by the Smurf2 overexpression or ALK5 silencing. We further found that TMAO upregulated the ALK5 expression by inhibiting the ubiquitination role of Smurf2. Overexpression of ALK5 reversed the inhibitory effect of Smurf2 on astrocyte proliferation, migration, and viability. Collectively, our work identifies the evolutionarily TMAO/Smurf2/ALK5 signaling as a major genetic factor in the control of reactive astrocyte proliferation and glial scar formation in ischemic stroke, thus laying a theoretical foundation for the identification of ischemic stroke.

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Section: Discussionmentioning

confidence: 99%

TMAO Aggregates Neurological Damage Following Ischemic Stroke by Promoting Reactive Astrocytosis and Glial Scar Formation via the Smurf2/ALK5 Axis

Fan

Zhang

et al. 2021

Front. Cell. Neurosci.

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“…In the last years, the relation between CoQ 10 and inflammation and oxidative stress has been reported in cell and animal models. Glial fibrillary acidic protein (GFAP), MDA, and superoxide dismutase (SOD) activity are important biomarkers in oxidative stress and neuroinflammatory processes after stroke, and they can predict functional outcomes [134][135][136]. In a short RCT, 60 patients with acute ischemic stroke were randomly assigned to a placebo or CoQ 10 -supplemented group (300 mg/day) for 4 weeks.…”

Section: Coq 10 and Ischemic Strokementioning

confidence: 99%

Coenzyme Q10: Clinical Applications in Cardiovascular Diseases

et al. 2020

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Coenzyme Q10 (CoQ10) is a ubiquitous factor present in cell membranes and mitochondria, both in its reduced (ubiquinol) and oxidized (ubiquinone) forms. Its levels are high in organs with high metabolism such as the heart, kidneys, and liver because it acts as an energy transfer molecule but could be reduced by aging, genetic factors, drugs (e.g., statins), cardiovascular (CV) diseases, degenerative muscle disorders, and neurodegenerative diseases. As CoQ10 is endowed with significant antioxidant and anti-inflammatory features, useful to prevent free radical-induced damage and inflammatory signaling pathway activation, its depletion results in exacerbation of inflammatory processes. Therefore, exogenous CoQ10 supplementation might be useful as an adjuvant in the treatment of cardiovascular diseases such as heart failure, atrial fibrillation, and myocardial infarction and in associated risk factors such as hypertension, insulin resistance, dyslipidemias, and obesity. This review aims to summarize the current evidences on the use of CoQ10 supplementation as a therapeutic approach in cardiovascular diseases through the analysis of its clinical impact on patients’ health and quality of life. A substantial reduction of inflammatory and oxidative stress markers has been observed in several randomized clinical trials (RCTs) focused on several of the abovementioned diseases, even if more RCTs, involving a larger number of patients, will be necessary to strengthen these interesting findings.

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“…По данным литературы, через 1 год после перенесенного ИИ уровни ГФКБ у пациентов с хорошим функциональным исходом, оцененным по шкале Rankin, были значительно ниже, чем у пациентов с плохим исходом (р < 0,001), при этом нескорректированный риск плохого исхода увеличивался в 12 раз, а скорректированный -в 6 раз при уровне ГФКБ более 0,28 нг/мл (p < 0,001). Liu G. и соавторы выявили, что уровни ГФКБ в первые 24 часа у пациентов при ИИ, которые умерли в остром периоде, были более чем в 2 раза выше по сравнению с пациентами, которые выжили (0,18-0,43 нг/мл против 0,08-0,23 нг/мл; р < 0,001) [40].…”

Section: уровни нсе гфкб Nr2-антител как прогностический маркерunclassified

New diagnostic and prognostic biomarkers of the ischemic brain damage

Алексеева

Топузова

Чайковская

et al. 2020

Transl. med. (Print)

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Резюме Актуальность. Для определения оптимального подхода к ведению пациентов в остром периоде инсульта продолжается поиск биомаркеров, которые смогут повысить ценность уже существующих методов диагностики. Цель исследования: уточнить значение уровней нейрон-специфической енолазы (НСЕ), глиального фибриллярного кислого белка (ГФКБ), NR2-антител в сыворотке крови (СК) у пациентов в остром периоде ишемического инсульта (ИИ) в динамике, определить их взаимосвязь с тяжестью неврологических нарушений и краткосрочным исходом. Материалы и методы. Обследовано 40 пациентов в остром периоде ИИ, средний возраст 72,6 ± 1,9 лет. Уровни биомаркеров определяли в СК в первые 72 часа ИИ и на 10-14 день. Результаты. Концентрация НСЕ и ГФКБ у больных с ИИ в первые 72 часа превышала референсные значения и значимо уменьшалась к 10-14 дню (34,9 ± 5,9 → 17,7 ± 1,1; p = 0,007 и 0,4 ± 0,1 → 0,2 ± 0,005; р = 0,22 соответственно). Уровень NR2-антител референсных значений не превысил (1,01 ± 0,3), а в динамике к 10-14 дню было отмечено нарастание показателя (1,1 ± 0,3), p = 0,007. У пациентов, имевших более тяжелую симптоматику, концентрация НСЕ, ГФКБ и NR2-антител к 10-14 дню была выше. Пациенты, имевшие неблагоприятный краткосрочный исход, к 10-14 дню имели более высокий уровень НСЕ, ГФКБ и NR2-антител. Заключение. Исследованные вещества могут быть использованы в качестве биомаркеров при ИИ для контроля степени повреждения мозговой ткани, мониторинга усугубления патологического процесса, а также с прогностической целью. Ключевые слова: биомаркеры инсульта, глиальный фибриллярный кислый белок, инсульт, ишемический инсульт, краткосрочный исход, нейрон-специфическая енолаза, прогноз NR2-антитела, N-метил-D-аспартат рецепторы.

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Glial fibrillary acidic protein as a prognostic marker of acute ischemic stroke

Abstract: GFAP levels are a novel and complementary biomarker to predict functional outcome 1 year after AIS.

Cited by 34 publications

References 25 publications

TMAO Aggregates Neurological Damage Following Ischemic Stroke by Promoting Reactive Astrocytosis and Glial Scar Formation via the Smurf2/ALK5 Axis

TMAO Aggregates Neurological Damage Following Ischemic Stroke by Promoting Reactive Astrocytosis and Glial Scar Formation via the Smurf2/ALK5 Axis

Coenzyme Q10: Clinical Applications in Cardiovascular Diseases

New diagnostic and prognostic biomarkers of the ischemic brain damage

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