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Neonatal bronchopulmonary dysplasia increases neuronal apoptosis in the hippocampus through the HIF-1alpha and p53 pathways.

Authors: Yin, R  Yuan, L  Ping, L  Hu, L 
Citation: Yin R, etal., Respir Physiol Neurobiol. 2016 Jan;220:81-7. doi: 10.1016/j.resp.2015.09.011. Epub 2015 Sep 30.
Pubmed: (View Article at PubMed) PMID:26431790
DOI: Full-text: DOI:10.1016/j.resp.2015.09.011

Neonatal bronchopulmonary dysplasia (BPD) might lead to an increased risk for brain injury. The present study aims to investigate the effects of neonatal BPD on neuronal apoptosis in the hippocampus and cognitive function and to explore the underlying mechanisms. The results revealed that BPD model rat pups exhibited more apoptotic cells in the hippocampus and longer escape latencies in the Morris maze test. Both the caspase-dependent and caspase-nondependent signal pathways were activated. Further examinations showed an elevated p53 level by BPD via HIF-1alpha induction, while the caspase-3 in the hippocampus was suppressed by both HIF-1alpha and p53 inhibitor. These findings suggested that neonatal BPD caused impaired cognitive function and neuron apoptosis in hippocampus via p53 and HIF-1alpha. Although the precise mechanism requires further investigation, this study provided new evidence for and an explanation of the impaired CNS developmental outcomes of BPD.

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RGD Object Information
RGD ID: 11537057
Created: 2016-09-28
Species: All species
Last Modified: 2016-09-28
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.