Genetics of perinatal brain injury in the preterm infant

Baier, R J

doi:10.2741/1890

Cited by 56 publications

(54 citation statements)

References 129 publications

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“…Other potential mechanisms involved in eliciting a differential response/recovery from hypoxic insult may include differences in VEGF expression and induction, 61 differences in BDNF expression level, induction, 62 and polymorphism 63 and polymorphisms in several cytokines and extracellular matrix components. 64,65 Thus, in this report we have documented significant differences in HIF-1␣ translation and responsiveness to SDF-1 in C57 and CD-1 NSCs (shaded aspects of the signaling pathways are illustrated in Figure 7). 48,50 -52 Specifically, C57 NSCs exhibit blunted HIF-1␣ translation in response to a reduced O 2 culture environment.…”

Section: Discussionsupporting

confidence: 52%

Strain Differences in Behavioral and Cellular Responses to Perinatal Hypoxia and Relationships to Neural Stem Cell Survival and Self-Renewal

Liu

Michaud

et al. 2009

The American Journal of Pathology

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Premature infants have chronic hypoxia, resulting in cognitive and motor neurodevelopmental handicaps caused by suboptimal neural stem cell (NSC) repair/ recovery in neurogenic zones (including the subventricular and the subgranular zones). Understanding the variable central nervous system repair response is crucial to identifying "at risk" infants and to increasing survival and clinical improvement of affected infants. Using mouse strains found to span the range of responsiveness to chronic hypoxia, we correlated differential NSC survival and self-renewal with differences in behavior. We found that C57BL/6 (C57) pups displayed increased hyperactivity after hypoxic insult; CD-1 NSCs exhibited increased hypoxia-induced factor 1␣ (HIF-1␣) mRNA and protein, increased HIF-1␣, and decreased prolyl hydroxylase domain 2 in nuclear fractions, which denotes increased transcription/translation and decreased degradation of HIF-1␣. C57 NSCs exhibited blunted stromal-derived factor 1-induced migratory responsiveness, decreased matrix metalloproteinase-9 activity, and increased neuronal differentiation. Adult C57 mice exposed to hypoxia from P3 to P11 exhibited learning impairment and increased anxiety. These findings support the concept that behavioral differences between C57 and CD-1 mice are a consequence of differential responsiveness to hypoxic insult, leading to differences in HIF-1␣ signaling and resulting in lower NSC proliferative/migratory and higher apoptosis rates in C57 mice. Information gained from these studies will aid in design and effective use of preventive therapies in the very low birth weight infant population. Preterm birth is known to result in cognitive and motor disabilities and recent evidence suggests that there can be significant recovery over time in some patients.

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Section: Discussionsupporting

confidence: 52%

Strain Differences in Behavioral and Cellular Responses to Perinatal Hypoxia and Relationships to Neural Stem Cell Survival and Self-Renewal

Liu

Michaud

et al. 2009

The American Journal of Pathology

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“…4 A recent study by Ko et al 12 revealed that polymorphism of the eNOS allele led to a statistically significant increase in risk of vasospasm after subarachnoid hemorrhage, specifically the CC genotype of the eNOS -786 polymorphism. 2 We have shown that this C allele is also linked to an increased risk of specific conditions of prematurity.…”

Section: 11mentioning

confidence: 94%

“…Furthermore, the effects of IVH can be devastating, including periventricular scarring, white matter gliosis, and free radical and cytokine generation, all of which produce secondary damage to the early developing brain. [1][2][3][4][5]7 Studies have shown that infants who suffer large IVH are associated with an increased rate of developing major disabilities. As many as 60% of infants with Grade IV IVH will have severe motor and/or cognitive handicaps.…”

mentioning

confidence: 99%

Is an endothelial nitric oxide synthase gene mutation a risk factor in the origin of intraventricular hemorrhage?

Vannemreddy¹,

Notarianni²,

Yanamandra

et al. 2010

FOC

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Object Studies have shown decreased levels of nitric oxide (NO), the product of endothelial NO synthase (eNOS) gene activity, in infants with respiratory conditions and intraventricular hemorrhage (IVH). The authors evaluated the association of the eNOS gene promoter polymorphism T-786C with the cause of these conditions (respiratory conditions and IVH) in premature infants. Methods Blood samples from 124 African American premature infants were studied. The DNA was isolated and microplate polymerase chain reaction–restriction fragment length polymorphism assay was performed. Genotypes were scored as: TT homozygotes with 140 bp and 40 bp; CC homozygotes with 90 bp, 50 bp, and 40 bp; and TC heterozygotes with 140 bp, 90 bp, 50 bp, and 40 bp. Genotypes were stratified according to ethnicity, preterm status, and prematurity conditions. Results The mutant allele -786C was present in 15.3% of premature infants with respiratory distress syndrome, bronchopulmonary dysplasia, and IVH, compared with 7.25% in those premature infants without these conditions. A significant 2-fold increase of the mutant allele in patients compared with controls (p = 0.04, OR 2.3) reveals that the eNOS -786C allele could be a significant risk factor in the origin of respiratory conditions and IVH in premature infants. Conclusions These results suggest that the mutant eNOS -786C allele is a significant risk factor in the origin of respiratory and IVH diseases, probably mediating an insufficient supply of endogenous NO in premature infants.

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“…Sitokinler ile ilgili polimorfizmlerin pre ve perinatal beyin hasarını etkilediğine yönelik gün geçtikçe daha çok delil elde edilmektedir [31]. Bu polimorfizmler, proinflamatuar veya antiinflamatuar sitokinlerin salınımını etkileyen genetik farklılıklardır.…”

Section: Patofizyolojiunclassified

Hidden Danger for the Fetus: Chorioamnionitis

Berber¹,

Çekmez²,

Purtuloglu³

2014

Ann Clin Anal Med

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ÖzetKoryoamniyonit, tıptaki tüm gelişmelere rağmen halen tüm dünyada önemli bir morbidite ve mortaliteyi nedenidir. Koryoamniyonite neden olan en önem-li sebep intrauterin enfeksiyonlardır. Antenatal dönemde gelişen enfeksiyonlar doğrudan veya dolaylı olarak erken dönemde fetüsün kaybı, organ gelişi-minde anormalliklere ve preterm doğumlara yol açabilirken uzun dönemde ise değişik sistemlerde oluşturduğu hasara göre mental retardasyon, serebral palsi, prematüre retinopatisi, tiroid hormon eksikliği ve bronkopulmoner displazi gibi ciddi problemlere yol açabilmektedir. Koryoamniyonit tespit edilen bir gebelikte olası etkenlerin erken tedavisi, bebek ve anneye ait morbidite ve mortaliteyi azaltmak için en etkili tedavidir. Bu makalede koryoamniyonitin etiyolojisi, epidemiyolojisi, patofizyolojisi ve bebek açısından klinik öne-mi ile ilgili güncel bilgiler gözden geçirilmiştir. Anahtar Kelimeler

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Genetics of perinatal brain injury in the preterm infant

Cited by 56 publications

References 129 publications

Strain Differences in Behavioral and Cellular Responses to Perinatal Hypoxia and Relationships to Neural Stem Cell Survival and Self-Renewal

Strain Differences in Behavioral and Cellular Responses to Perinatal Hypoxia and Relationships to Neural Stem Cell Survival and Self-Renewal

Is an endothelial nitric oxide synthase gene mutation a risk factor in the origin of intraventricular hemorrhage?

Hidden Danger for the Fetus: Chorioamnionitis

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