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Human umbilical cord-derived mesenchymal stem cells promote repair of neonatal brain injury caused by hypoxia/ischemia in rats

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Neural Regeneration Research 2022年第11期17卷 2518-2525页

作者： Yang Jiao Yue-Tong Sun Nai-Fei Chen Li-Na Zhou Xin Guan Jia-Yi Wang Wen-Juan Wei Chao Han Xiao-Lei Jiang Ya-Chen Wang Wei Zou Jing Liu Stem Cell Clinical Research Center National Joint Engineering LaboratoryRegenerative Medicine CenterThe First Affiliated Hospital of Dalian Medical UniversityDalianLiaoning ProvinceChina Dalian Innovation Institute of Stem Cells and Precision Medicine DalianLiaoning ProvinceChina Department of Neurology The First Affiliated Hospital of Dalian Medical UniversityDalianLiaoning ProvinceChina College of Life Science Liaoning Normal UniversityDalianLiaoning ProvinceChina

Administration of human umbilical cord-derived mesenchymal stem cells(hUC-MSCs)is believed to be an effective method for treating neurodevelopmental disorde rs.In this study,we investigated the possibility of hUC-MSCs treatment of neonatal hypoxic/ischemic brain injury associated with maternal immune activation and the underlying mechanism.We established neonatal rat models of hypoxic/ischemic brain injury by exposing pregnant rats to lipopolysaccharide on day 16 or 17 of pregnancy.Rat offspring were intranasally administe red hUC-MSCs on postnatal day 14.We found that polypyrimidine tract-binding protein-1(PTBP-1)participated in the regulation of lipopolysaccharide-induced maternal immune activation,which led to neonatal hypoxic/ischemic brain injury.Intranasal delive ry of hUC-MSCs inhibited PTBP-1 expression,alleviated neonatal brain injury-related inflammation,and regulated the number and function of glial fibrillary acidic protein-positive astrocytes,there by promoting plastic regeneration of neurons and im p roving brain function.These findings suggest that hUC-MSCs can effectively promote the repair of neonatal hypoxic/ischemic brain injury related to maternal immune activation through inhibition of PTBP-1 expression and astrocyte activation.

关键词： developmental brain disease model disease-associated astrocytes intranasal administration lipopolysaccharide maternal immune activation neonatal brain injury neuroplasticity repair polypyrimidine tract-binding protein-1 stem cell therapy umbilical cord-derived mesenchymal stem cells

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Vulnerability of premyelinating oligodendrocytes to white-matter damage in neonatal brain injury

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Neuroscience Bulletin 2013年第2期29卷 229-238页

作者： Xiao-Bo Liu Yan Shen Jennifer M.Plane Wenbin Deng Department of Biochemistry and Molecular Medicine Institute for Pediatric Regenerative MedicineSchool of MedicineUniversity of California at Davis

Premature birth is a significant economic and public health burden, and its incidence is rising. Periventricular leukomalacia （PVL） is the predominant form of brain injury in premature infants and the leading cause of cerebral palsy. PVL is characterized by selective white-matter damage with prominent oligodendroglial injury. The maturation-dependent vulnerability of developing and premyelinating oligodendrocytes to excitotoxic, oxidative, and inflammatory forms of injury is a major factor in the pathogenesis of PVL. Recent studies using mouse models of PVL reveal that synapses between axons and developing oligodendrocytes are quickly and profoundly damaged in immature white matter. Axon-glia synapses are highly vulnerable to white-matter injury in the developing brain, and the loss of synapses between axons and premyelinating oligodendrocytes occurs before any cellular loss in the immature white matter. Microglial activation and astrogliosis play important roles in triggering white-matter injury. Impairment of white-matter development and function in the neonatal period contributes critically to functional and behavioral deficits. Preservation of the integrity of the white matter is likely key in the treatment of PVL and subsequent neurological consequences and disabilities.

关键词： prematurity neonatal brain injury white matter oligodendrocyte myelin periventricular leukomalacia

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Biomarkers of hypoxic-ischemic encephalopathy:a systematic review

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World Journal of Pediatrics 2023年第6期19卷 505-548页

作者： Ines Caramelo Margarida Coelho Miguel Rosado Carla M.P.Cardoso Alexandra Dinis Carlos B.Duarte Mario Graos Bruno Manadas CNC-Center for Neuroscience and Cell Biology University of Coimbra3004‑504 CoimbraPortugal PhD Programme in Experimental Biology and Biomedicine Institute for Interdisciplinary Research(IIIUC)University of CoimbraCasa Costa Alemão3030‑789 CoimbraPortugal Chemistry Department Faculty of Sciences and TechnologyUniversity of Coimbra3004‑535 CoimbraPortugal Stemlab SA 3060‑197 CantanhedePortugal Pediatric Intensive Care Unit Hospital PediátricoCentro Hospitalar E Universitário de Coimbra3000‑075 CoimbraPortugal Department of Life Sciences University of Coimbra3001‑401 CoimbraPortugal Biocant Technology Transfer Association3060‑197 CantanhedePortugal Institute for Interdisciplinary Research University of Coimbra(IIIUC)3030‑789 CoimbraPortugal

Background Current diagnostic criteria for hypoxic–ischemic encephalopathy in the early hours lack objective measurement tools.Therefore,this systematic review aims to identify putative molecules that can be used in diagnosis in daily clinical practice(PROSPERO ID:CRD42021272610).Data sources Searches were performed in PubMed,Web of Science,and Science Direct databases until November 2020.English original papers analyzing samples from newborns>36 weeks that met at least two American College of Obstetricians and Gynecologists diagnostic criteria and/or imaging evidence of cerebral damage were included.Bias was assessed by the Newcastle–Ottawa Scale.The search and data extraction were verified by two authors separately.Results From 373 papers,30 met the inclusion criteria.Data from samples collected in the first 72 hours were extracted,and increased serum levels of neuron-specific enolase and S100-calcium-binding protein-B were associated with a worse prognosis in newborns that suffered an episode of perinatal asphyxia.In addition,the levels of glial fibrillary acidic protein,ubiquitin carboxyl terminal hydrolase isozyme-L1,glutamic pyruvic transaminase-2,lactate,and glucose were elevated in newborns diagnosed with hypoxic–ischemic encephalopathy.Moreover,pathway analysis revealed insulin-like growth factor signaling and alanine,aspartate and glutamate metabolism to be involved in the early molecular response to insult.Conclusions Neuron-specific enolase and S100-calcium-binding protein-B are potential biomarkers,since they are correlated with an unfavorable outcome of hypoxic-ischemic encephalopathy newborns.However,more studies are required to determine the sensitivity and specificity of this approach to be validated for clinical practice.

关键词： Biomarker Hypoxic-ischemic encephalopathy neonatal brain injury Newborn Neuron-specific enolase S100-calcium-binding protein-B

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Monocytes in neonatal stroke and hypoxic-ischemic encephalopathy:Pathophysiological mechanisms and therapeutic possibilities

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Neuroprotection 2023年第1期1卷 20-33页

作者： Pedro M.Pimentel-Coelho Carlos Chagas Filho Biophysics Institute Federal University of Rio de JaneiroRio de JaneiroBrazil

neonatal arterial ischemic stroke(NAIS)and neonatal hypoxic-ischemic encephalopathy(HIE)are common causes of neurological impairments in infants,for which treatment options are very limited.NAIS and HIE induce an innate immune response that involves the recruitment of peripheral immune cells,including monocytes,into the brain.Monocytes and monocyte-derived cells have the potential to contribute to both harmful and beneficial pathophysiological processes,such as neuroinflammation and brain repair,but their roles in NAIS and HIE remain poorly understood.Furthermore,recent evidence indicates that monocyte-derived macrophages can persist in the brain for several months following NAIS and HIE in mice,with possible long-lasting consequences that are still unknown.This review provides a comprehensive overview of the mechanisms of monocyte infiltration and their potential functions in the ischemic brain,focusing on HIE and NAIS.Therapeutic strategies targeting monocytes and the possibility of using monocytes for cell-based therapies are also discussed.

关键词： bone marrow cerebral ischemia microglia monocyte-derived macrophages monocytes neonatal brain injury neonatal hypoxia-ischemia perinatal stroke

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