A5069204640- Neonatal and fetal brain pathology
- Neonatal Respiratory Health Research
- Neuroscience of respiration and sleep
- Neuroinflammation and Neurodegeneration Mechanisms
- Anesthesia and Neurotoxicity Research
- Neurogenesis and neuroplasticity mechanisms
- Neuroscience and Neuropharmacology Research
- Neonatal Health and Biochemistry
- Traumatic Brain Injury and Neurovascular Disturbances
- Cancer, Hypoxia, and Metabolism
- Preterm Birth and Chorioamnionitis
- Congenital Diaphragmatic Hernia Studies
- Pharmacological Effects and Toxicity Studies
- S100 Proteins and Annexins
- Stress Responses and Cortisol
- Congenital limb and hand anomalies
- Developmental Biology and Gene Regulation
- Neurological Disease Mechanisms and Treatments
- RNA regulation and disease
- Drug-Induced Hepatotoxicity and Protection
- Genomics and Chromatin Dynamics
- Retinopathy of Prematurity Studies
- Infant Development and Preterm Care
- Immune cells in cancer
- Cancer-related molecular mechanisms research
Charité - Universitätsmedizin Berlin
2013-2024
Humboldt-Universität zu Berlin
2022-2024
Freie Universität Berlin
2022-2024
Technische Universität Berlin
2015
Berlin-Brandenburger Centrum für Regenerative Therapien
2013
Max Planck Institute for Molecular Genetics
2013
Sequelae of prematurity triggered by oxidative stress and free radical-mediated tissue damage have coined the term "oxygen radical disease prematurity". Caffeine, a potent scavenger adenosine receptor antagonist, reduces rates brain in preterm infants. In present study, we investigated effects caffeine on markers, anti-oxidative response, inflammation, redox-sensitive transcription factors, apoptosis, extracellular matrix following induction hyperoxia neonatal rats. The rat pups at postnatal...
While additional oxygen supply is often required for the survival of very premature infants in intensive care, this also brings an increasing risk progressive lung diseases and poor long-term outcomes. Caffeine administered to neonates neonatal care prevention treatment apneas has been shown reduce BPD incidence need mechanical ventilation, although it still unclear whether due a direct pulmonary action via antagonism adenosine receptors and/or indirect action. This experimental study aims...
Neonatal brain injury is often caused by preterm birth. Brain development vulnerable to increased environmental stress, including oxidative stress challenges. Due a premature change of the fetal living environment from low oxygen in utero into postnatal high-oxygen room air conditions ex utero, immature exposed relative hyperoxia, which can induce and impair neuronal cell development. To simulate drastic increase exposure brain, 5-day-old C57BL/6 mice were hyperoxia (80% oxygen) for 48 hours...
Abstract Preterm infants often show pathologies of the cerebellum, which are associated with impaired motor performance, lower IQ and poor language skills at school ages. Using a mouse model inflammation‐induced encephalopathy prematurity driven by systemic administration pro‐inflammatory IL‐1β, we sought to uncover causes cerebellar damage. In this model, IL‐1β is administered between postnatal day (P) 1 5, timing equivalent last trimester for brain development in humans. Structural MRI...
Gene regulation by transcription factors (TFs) determines developmental programs and cell identity. Consequently, mutations in TFs can lead to dramatic phenotypes humans disrupting gene regulation. To date, the molecular mechanisms that actually cause these have been difficult address experimentally. ChIP-seq, which couples chromatin immunoprecipitation with high-throughput sequencing, allows TF function be investigated on a genome-wide scale, enabling new approaches for investigation of...
According to recent research, brain injury after premature birth often includes impaired growth of the cerebellum. However, causes cerebellar in this population are poorly understood. In study, we analyzed whether postnatal hyperoxia perturbs white matter development cerebellum, and glial damage can be prevented by minocycline. We used a model neonatal rats providing 24 h exposure fourfold increased oxygen concentration (80% O2) from P6 P7, followed recovery room air until P9, P11, P15, P30....
The neurotransmitter GABA and its receptors assume essential functions during fetal postnatal brain development. last trimester of a human pregnancy early life involves vulnerable period In the second half gestation, there is developmental shift from depolarizing to hyperpolarizing in GABAergic system, which might be disturbed by preterm birth. Alterations are associated with several neurodevelopmental disorders. this vivo study, we investigated neurogenesis dentate gyrus (DG) response daily...
ABSTRACT The inhibitory GABAergic system in the brain is involved etiology of various psychiatric problems, including autism spectrum disorders (ASD), attention deficit hyperactivity disorder (ADHD) and others. These are influenced not only by genetic but also environmental factors, such as preterm birth, although underlying mechanisms known. In a translational hyperoxia model, exposing mice pups at P5 to 80% oxygen for 48 h mimic steep rise exposure caused birth from utero into room air, we...
Proper astroglial functioning is essential for the development and survival of neurons oligodendroglia under physiologic pathological circumstances.Indeed, malfunctioning astrocytes represents an important factor contributing to brain injury.However, molecular pathways this dysfunction are poorly defined.In work we show that aging itself can drastically perturb astrocyte viability with increase inflammation, cell death astrogliosis.Moreover, demonstrate oxygen glucose deprivation (OGD) has a...
Abstract In the naturally hypoxic in utero fetal environment of preterm infants, oxygen and oxygen‐sensitive signaling pathways play an important role brain development, with hypoxia‐inducible factor‐1α (HIF1α) being regulator. Early exposure to nonphysiological high concentrations by birth room can induce HIF1α degradation may affect neuronal glial development. This involves dysregulation astroglial maturation function, which turn might contribute oxygen‐induced injury. this study, we...
Abstract The premature increase of oxygen tension may contribute to oligodendroglial precursor cell (OPC) damage in preterm infants. Fetal OPCs are exposed low tissue tensions not matched when cells cultured room air. Maturation (A2B5, O4, O1, MBP, CNP, arborization), oxidative stress (nitrotyrosine Western blot, NRF2 and SOD2 expression), apoptosis (TUNEL), proliferation (Ki67), expression transcription factors regulated by Hypoxia-Inducible-Factor-1-alpha (Hif-1α) expressed (Olig1, Olig2,...
Myelination of axons in the neonatal brain is a highly complex process primarily achieved by oligodendroglial cells (OLs). OLs express receptors for γ-aminobutyric acid (GABA) which released from cortical interneurons on basal level, while glial can be source GABA, too. We investigated GABA-induced maturation, proliferation, apoptosis, and myelin production after pharmacological inhibition GABAA GABAB rat brain. Daily injections reverse receptor agonist (DMCM) antagonist (CGP35348) were...
Abstract In preterm infants, the changes from fetal life to ex‐utero conditions often coincide with reduced growth and white matter damage of cerebellum. The premature increase in arterial oxygen tension caused by birth may dysregulate cerebellar development. a hyperoxia rat model mimic steep levels 24 h exposure 80% O 2 postnatal day 6 (P6) 7, we analyzed factor (GF) synthesis astrocytes. Determination GF production was performed astrocytes after Magnetic‐activated cell sorting (MACS)...
Brain injury of preterm infants has widely been ascribed to the cerebrum, but recent studies demonstrate that cerebellum occurs, too [1]. Causes cerebellar pathologies in and ways protection are underinvestigated. In general, perinatal infection/inflammation, hypocarbia, hyperoxia factors associated with brain damage [1, 2]. We investigate whether oxidative stress induced by postnatal impairs development white matter. We used a neonatal model rats 80% oxygen exposure for 24h from P6 P7,...
<h3></h3> Although brain injury of preterm infants has widely been ascribed to the cerebrum, recent studies demonstrate that cerebellum often occurs, too. However, mechanisms cerebellar are hardly understood. In general, hypoxia-ischemia, infection/inflammation, and hyperoxia supposed be toxic stimuli in immature brain. We used a model established rats by using 80% O<sub>2</sub> exposure for 24 h from P6 P7, determined development maturation oligodendroglial cells during recovery room air...
Background Neonatal hypoxia-ischemia (HI) is a common cause of morbidity and mortality in neonates. It can result persistent motor, sensory, cognitive impairments. Recent evidence suggests that the transcription factor hypoxia-inducible 1α (HIF-1α) plays key role neurological outcomes after HI. Microglia are brain resident macrophages respond rapidly to HI by producing proinflammatory mediators via HIF-1α-dependent mechanism. However, precise HIF-1α – dependent repair damage mechanisms on...
Die neuronale Entwicklung kann durch Veränderung der physiologischen Sauerstoffkonzentration beeinträchtigt werden. Speziell unreif geborene Kinder zeigen häufig eine Störung Gehirnentwicklung erhöhte Sauerstoffexposition. Dabei spielen sauerstoffsensitive Signalwege entscheidende Rolle. Eine wichtige Funktion hat hierbei Hypoxie-induzierte Faktor 1α (HIF1α). Bei niedrigen Sauerstoffkonzentrationen kommt es zu einer Aktivierung von HIF1α, höhere führen Degradation HIF1α.
Abstract Preterm infants often show pathologies of the cerebellum, which are associated with impaired motor performance, lower IQ and poor language skills at school ages. Because 1 in 10 babies is born preterm cerebellar injury a significant clinical problem. The causes damage yet to be fully explained. Herein, we tested hypothesis that perinatal inflammatory stimuli may play key role infants. We undertook our studies an established mouse model inflammation-induced encephalopathy prematurity...