Neonatal hypoxic ischemic encephalopathy-related biomarkers in serum and cerebrospinal fluid

Lv, Haiyan; Wang, Qiuli; Wu, Sujing; Yang, Lihong; Ren, Pengshun; Yang, Yihui; Gao, Jie; Li, Lianxiang

doi:10.1016/j.cca.2015.08.021

Cited by 109 publications

(137 citation statements)

References 63 publications

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“…Although S100B is glial specific and expressed primarily by astrocytes and Schwann cells, it is also found in several non-nervous system cells such as adipocytes, chondrocytes, skin, glioblastoma, and melanoma cells (Zimmer et al, 1995). S100B has a serum half-life of only 2 h, (GuingabCagmat et al, 2013) but is stable in blood and not affected by hemolysis (Lv et al, 2015). Since S100B is produced outside the CNS, general trauma without brain injury can increase its levels (Rothoerl and Woertgen, 2001).…”

Section: Neuron-specific Enolase (Nse)mentioning

confidence: 99%

“…This small (25 kDa) enzyme comprises about 2% of the total soluble protein in the brain and hydrolyzes the C-terminal bond of ubiquitin or unfolded polypeptides (Setsuie and Wada, 2007). Because of its high and specific expression in brain tissue, increased levels of UCHL1 have been suggested as a marker of CNS injury such as acute cerebral ischemic disease and early stage severe traumatic brain injury (Lv et al, 2015). Serum UCHL1 is a useful biomarker of severe traumatic brain injury both in the acute phase and in the 1st week after injury (Mondello et al, 2012b).…”

Section: Ubiquitin Carboxy-terminal Hydrolase L1 Protein (Uchl1)mentioning

confidence: 99%

“…It is one of the most abundant proteins in white matter, representing 30% of the protein content of myelin (Yokobori et al, 2013). Under normal conditions only a small amount is released into the blood stream, but in white matter brain injury the concentration of MBP in blood and CSF increases rapidly reflecting the severity of myelin damage which allows MBP to be used as a specific biomarker of white matter lesions or nerve fiber demyelination (Lv et al, 2015). MBP diminishes significantly in the contused rat cortex as early as 2 h after traumatic brain injury reaching its lowest level at 48 h (Ottens et al, 2008).…”

Section: Myelin Basic Protein (Mbp)mentioning

confidence: 99%

“…Ideally, serum biomarkers should provide information on the pathophysiology of injury, improve stratification of patients by injury severity, assist in the monitoring of secondary insults and injury progression, monitor response to treatment and predict functional outcome (Papa et al, 2008). Circulating brain injury biomarker levels in neonatal HIE could indicate brain injury and reflect the extent of damage, solving a clinical dilemma in the discrimination of mild vs. moderate-severe injury (Lv et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

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Blood biomarkers for evaluation of perinatal encephalopathy: state of the art

Graham

Everett

Delpech

et al. 2018

Current Opinion in Pediatrics

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Recent research in identification of brain injury after trauma shows many possible blood biomarkers that may help identify the fetus and neonate with encephalopathy. Traumatic brain injury shares many common features with perinatal hypoxic-ischemic encephalopathy. Trauma has a hypoxic component, and one of the 1st physiologic consequences of moderate-severe traumatic brain injury is apnea. Trauma and hypoxia-ischemia initiate an excitotoxic cascade and free radical injury followed by the inflammatory cascade, producing injury in neurons, glial cells and white matter. Increased excitatory amino acids, lipid peroxidation products, and alteration in microRNAs and inflammatory markers are common to both traumatic brain injury and perinatal encephalopathy. The blood-brain barrier is disrupted in both leading to egress of substances normally only found in the central nervous system. Brain exosomes may represent ideal biomarker containers, as RNA and protein transported within the vesicles are protected from enzymatic degradation. Evaluation of fetal or neonatal brain derived exosomes that cross the blood-brain barrier and circulate peripherally has been referred to as the "liquid brain biopsy." A multiplex of serum biomarkers could improve upon the current imprecise methods of identifying fetal and neonatal brain injury such as fetal heart rate abnormalities, meconium, cord gases at delivery, and Apgar scores. Quantitative biomarker measurements of perinatal brain injury and recovery could lead to operative delivery only in the presence of significant fetal risk, triage to appropriate therapy after birth and measure the effectiveness of treatment.

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Section: Neuron-specific Enolase (Nse)mentioning

confidence: 99%

Section: Ubiquitin Carboxy-terminal Hydrolase L1 Protein (Uchl1)mentioning

confidence: 99%

Section: Myelin Basic Protein (Mbp)mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Blood biomarkers for evaluation of perinatal encephalopathy: state of the art

Graham

Everett

Delpech

et al. 2018

Current Opinion in Pediatrics

View full text Add to dashboard Cite

show abstract

“…В США (Флорида) в настоящее время проводится исследование, которое определяет прогностическую зна-чимость концентрации UCHL1 и GFAP в пуповинной крови новорожденных, перенесших ГИПП центральной нервной системы [74].…”

Section: обзор литературыunclassified

Recent Information on the Pathogenesis and Treatment of Hypoxic-Ischemic Brain Lesions in Newborns

Каркашадзе¹,

Аникин²,

Зимина³

et al. 2016

Pediatr. farmakol.

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ВВЕДЕНИЕ Общемировой научно-технический прогресс в отно-шении исследовательских технологий за последние де-сятилетия привел к качественному и количественно-му скачку нейронаук. Наиболее активно наполняется новыми данными поле фундаментальных представлений о развитии головного мозга, что обусловливает интересы ученых к таким областям медицины, как перинатальная неврология и неврология раннего возраста. Несмотря на расширение представлений о вкладе генетической составляющей, по-прежнему большое внимание уделяет-ся изучению прямых патофизиологических механизмов гипоксически-ишемических поражений (ГИП) головного мозга у новорожденных. К настоящему моменту накоплен массив новых данных в этой области, что подталкивает медицину к внедрению передовых лечебных технологий.Цель работы -провести литературный обзор совре-менных научных данных о механизмах гипоксически-ише-мических повреждений мозга у новорожденных и разра-батываемых на их основании новых методов лечения. ПАТОФИЗИОЛОГИЧЕСКИЕ МЕХАНИЗМЫ ГИПОКСИЧЕСКИ-ИШЕМИЧЕСКИХ ПОРАЖЕНИЙТрадиционно основные лечебные тактики в острый период гипоксически-ишемических перинатальных поражений головного мозга (ГИППГМ) предусма-тривают медикаментозное поддержание сердечно-легочных функций и противосудорожную защиту [1]. Послед ние достижения в раскрытии патофизиологи-ческих механизмов непосредственно ГИП дают опору для поиска и внедрения новых лечебных технологий. У доношенных детей основным прямым механизмом ГИП является внутриутробная асфиксия, вызванная проблемами кровообращения, в том числе в области плацентарных артерий, отслойкой плаценты или вос-палительным процессом. За этим следуют снижение объема кислорода и углекислого газа в крови и тяже-лый лактат-ацидоз. Выраженное снижение сердечного выброса в условиях гипоксии, называемое гипоксией-ишемией, в течение 12-36 ч приводит к поражению головного мозга [2].

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CREG mitigates neonatal HIE injury through survival promotion and apoptosis inhibition in hippocampal neurons via activating AKT signaling

Zhang

Chen

2022

Cell Biology International

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Neonatal hypoxic ischemic encephalopathy (Neonatal HIE) is a common but serious disease caused by perinatal asphyxia injury in newborns. Elevated neuronal apoptosis plays an important role in the injury process post hypoxia ischemia of the brain, which accurate mechanism is still worthy to be studied. Cellular repressor of E1Astimulated genes (CREG) possesses the protective effect in ischemia-reperfusion in multiple organs, including livers and hearts. The main purpose of this work was to investigate whether CREG was involved in alleviating neonatal HIE and explore the possible mechanisms. We found that CREG expression was downregulated in the hippocampus of neonatal HIE rats as well as oxygen-glucose deprivation/reperfusion (OGD/R)-treated hippocampal neurons. Besides, CREG overexpression promoted survival while inhibited apoptosis in OGD/R-induced hippocampal neurons accompanied by AKT signaling activation, which could be reversed by CREG silence. In addition, the protective effects of CREG overexpression could be antagonized by AKT deactivation, indicating the function of CREG was attributed by regulating AKT pathway. Collectedly, we demonstrated that CREG protected hippocampal neurons from hypoxic ischemia-induced injury through regulating survival and apoptosis via activating AKT signaling pathway.

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Neonatal hypoxic ischemic encephalopathy-related biomarkers in serum and cerebrospinal fluid

Cited by 109 publications

References 63 publications

Blood biomarkers for evaluation of perinatal encephalopathy: state of the art

Blood biomarkers for evaluation of perinatal encephalopathy: state of the art

Recent Information on the Pathogenesis and Treatment of Hypoxic-Ischemic Brain Lesions in Newborns

CREG mitigates neonatal HIE injury through survival promotion and apoptosis inhibition in hippocampal neurons via activating AKT signaling

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