Short-, Mid-, and Long-Term Effect of Granulocyte Colony-Stimulating Factor/Stem Cell Factor and Fms-Related Tyrosine Kinase 3 Ligand Evaluated in an In Vivo Model of Hypoxic-Hyperoxic Ischemic Neonatal Brain Injury

Posod, Anna; Wegleiter, K; Neubauer, Vera; Urbanek, M; Huber, E.; Kiechl‐Kohlendorfer, Ursula; Keller, Matthias; Griesmaier, Elke

doi:10.1155/2019/5935279

Cited by 3 publications

(1 citation statement)

References 50 publications

(78 reference statements)

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“…Hence, both G-CSF and SCF may work synergistically in improving the overall outcome of neonatal HI brain damage. Caspase-3 activation is reduced when G-CSF and SCF treatment are combined resulting in decreased apoptotic cell death, though other studies further reported that G-CSF/SCF and FL treatment did not affect apoptosis-inducing factor-dependent apoptosis or cell proliferation, and thus does not convey neuroprotection in neonatal HIE [ 112 , 113 ]. Indeed, there are mixed reports about the neuroprotective effect of combinational G-CSF and SCF treatment in neonatal HI-induced brain injury.…”

Section: Combinational Therapy With Other Agentsmentioning

confidence: 99%

The role of G-CSF neuroprotective effects in neonatal hypoxic-ischemic encephalopathy (HIE): current status

Dumbuya

Chen

et al. 2021

J Neuroinflammation

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Hypoxic-ischemic encephalopathy (HIE) is an important cause of permanent damage to central nervous system (CNS) that may result in neonatal death or manifest later as mental retardation, epilepsy, cerebral palsy, or developmental delay. The primary cause of this condition is systemic hypoxemia and/or reduced cerebral blood flow with long-lasting neurological disabilities and neurodevelopmental impairment in neonates. About 20 to 25% of infants with HIE die in the neonatal period, and 25-30% of survivors are left with permanent neurodevelopmental abnormalities. The mechanisms of hypoxia-ischemia (HI) include activation and/or stimulation of myriad of cascades such as increased excitotoxicity, oxidative stress, N-methyl-d-aspartic acid (NMDA) receptor hyperexcitability, mitochondrial collapse, inflammation, cell swelling, impaired maturation, and loss of trophic support. Different therapeutic modalities have been implicated in managing neonatal HIE, though translation of most of these regimens into clinical practices is still limited. Therapeutic hypothermia, for instance, is the most widely used standard treatment in neonates with HIE as studies have shown that it can inhibit many steps in the excito-oxidative cascade including secondary energy failure, increases in brain lactic acid, glutamate, and nitric oxide concentration. Granulocyte-colony stimulating factor (G-CSF) is a glycoprotein that has been implicated in stimulation of cell survival, proliferation, and function of neutrophil precursors and mature neutrophils. Extensive studies both in vivo and ex vivo have shown the neuroprotective effect of G-CSF in neurodegenerative diseases and neonatal brain damage via inhibition of apoptosis and inflammation. Yet, there are still few experimentation models of neonatal HIE and G-CSF’s effectiveness, and extrapolation of adult stroke models is challenging because of the evolving brain. Here, we review current studies and/or researches of G-CSF’s crucial role in regulating these cytokines and apoptotic mediators triggered following neonatal brain injury, as well as driving neurogenesis and angiogenesis post-HI insults.

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Section: Combinational Therapy With Other Agentsmentioning

confidence: 99%

The role of G-CSF neuroprotective effects in neonatal hypoxic-ischemic encephalopathy (HIE): current status

Dumbuya

Chen

et al. 2021

J Neuroinflammation

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Neuroprotection of Bone Marrow-Derived Mesenchymal Stem Cell-Derived Extracellular Vesicle-Enclosed miR-410 Correlates with HDAC4 Knockdown in Hypoxic-Ischemic Brain Damage

2022

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Assessment of fetal resistance to hypoxia using the Stange test as an adjunct to Apgar scale assessment of neonatal health status

Shabanov,

Urakov,

Urakova

2024

Medical academic journal

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It has been established that the cause of biological death of fetuses in stillbirths and the cause of neonatal encephalopathies in live births is hypoxic brain cell damage in fetuses. Timely cesarean section remains the most effective way to preserve fetal life and health in the face of lethal intrauterine hypoxia. However, there is no universally recognized methodology for assessing fetal adaptation reserves to hypoxia and no methodology for selecting the type of delivery in order to perform a timely cesarean section if necessary. The Apgar score, which has been used since 1952, allows assessment of neonatal health at 1 and 5 minutes after birth, but this assessment is made without taking into account the health of the fetus before delivery. In recent years, it has been established that the outcome of fetal hypoxia is determined not only by its duration, but also by the amount of adaptive reserves available in the fetus to hypoxia. It was found that the duration of fetal immobility during apnea of a pregnant woman is an indicator of fetal resistance to hypoxia. In 2011, a method of assessing fetal resistance to intrauterine hypoxia based on the Stange test was developed in Russia. It has been found that the maximum duration of fetal immobility during maternal apnea is normally more than 30 seconds, while in the presence of fetal signs of fetoplacental insufficiency it does not reach 30 seconds, and in the presence of signs of severe fetoplacental insufficiency it does not reach 10 seconds. Therefore, it was proposed to consider good fetal resistance to hypoxia as an indication for vaginal delivery, and poor fetal resistance to hypoxia as an indication for cesarean section. A technique for assessing fetal resistance to hypoxia is described that has been developed for independent use by every pregnant woman. It is shown that it is sufficient for her to have a stopwatch and to be able to record the maximum period of fetal immobility during voluntary apnea. It is hoped that a measure of fetal resistance to hypoxia could be a meaningful complement to the Apgar score of neonatal health. It is envisioned that the use of a modified Stange test could help physicians prevent stillbirths and neonatal encephalopathies.

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Short-, Mid-, and Long-Term Effect of Granulocyte Colony-Stimulating Factor/Stem Cell Factor and Fms-Related Tyrosine Kinase 3 Ligand Evaluated in an In Vivo Model of Hypoxic-Hyperoxic Ischemic Neonatal Brain Injury

Cited by 3 publications

References 50 publications

The role of G-CSF neuroprotective effects in neonatal hypoxic-ischemic encephalopathy (HIE): current status

The role of G-CSF neuroprotective effects in neonatal hypoxic-ischemic encephalopathy (HIE): current status

Neuroprotection of Bone Marrow-Derived Mesenchymal Stem Cell-Derived Extracellular Vesicle-Enclosed miR-410 Correlates with HDAC4 Knockdown in Hypoxic-Ischemic Brain Damage

Assessment of fetal resistance to hypoxia using the Stange test as an adjunct to Apgar scale assessment of neonatal health status

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