期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 99, 期 24, 页码 15729-15734出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.232568799
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资金
- NHLBI NIH HHS [T32-HL07778, T32 HL007778] Funding Source: Medline
- NIDDK NIH HHS [DK38979] Funding Source: Medline
- NINDS NIH HHS [NS32578, P01 NS035476, NS 35476, NS 27116, NS42238, R01 NS027116] Funding Source: Medline
Infants born prematurely risk significant life-long cognitive disability, representing a major pediatric health crisis. The neuropathology of this cohort is accurately modeled in mice subjected to sublethal postnatal hypoxia. Massively parallel transcriptome analysis using cDNA microchips (9,262 genes), combined with immunohistochemical and protein assays, reveals that sublethal hypoxia accentuates genes subserving presynaptic function, and it suppresses genes involved with synaptic maturation, postsynaptic function, and neurotransmission. Other significantly affected pathways include those involved with glial maturation, vasculogenesis, and components of the cortical and microtubular cytoskeleton. These patterns reveal a global dysynchrony in the maturation programs of the hypoxic developing brain, and offer insights into the vulnerabilities of processes that guide early postnatal cerebral maturation.
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