J Korean Soc Neonatol.
2007 Nov;14(2):162-169.
Expression of Fibroblast Growth Factor Receptor mRNAs according to Administration of Geneticin in Hypoxic Neuron Cell Culture
- Affiliations
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- 1Department of Ophthalmology, School of Medicine, DongGuk University, Kyeong-Ju, S. Korea.
- 2Department of Pediatrics, School of Medicine, Catholic University of Daegu, Daegu, S. Korea. wootykim@cu.ac.kr
Abstract
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PURPOSE: Recently, Geneticin (G418) were known to exert neuroprotective effects in the hypoxic-ischemic (H-I) brain injury, but the mechanism is still unclear. The roles of fibroblast growth factor (FGF) and FGF receptor (FGFR) ware not well known in the H-I brain injury. We investigated the neuroprotective effects of systemically administrated Geneticin through the regulation of FGFR following the H-I brain injury
METHODS
The cortical neuron cell culture of Spague-Dawley (SD) rat embryo brain (E18) was done in a hypoxic incubator. The cultured cells were divided three groups: a normoxia group, a hypoxia group, and an Geneticin-treated group. After verifying the desired amount of cellular injury in the hypoxia group, the Geneticin-treated group (after an H-I insult) was further divided into two groups. This produced four final groups: normoxia, hypoxia, and Geneticin-treated groups before H-I insult and a Geneticin-treated group after HI insult. The expression of FGFR-2 and FGFR-3 mRNA was measured using Northern blotting.
RESULTS
The expression of FGFR-2 and FGFR-3 mRNA was notably increased in the hypoxic group compared to the normoxic group. In both Geneticin-treated groups before and after a hypoxic insult, the expression of FGFR-2 and FGFR-3 mRNA was decreased.
CONCLUSION
It suggests that FGFR has an important role in hypoxic brain injury. Geneticin appears to exert a protective effect through down regulation of the expression of FGFR mRNA. However, more experiments are needed in order to demonstrate the usefulness of Geneticin as a preventative and rescue treatment for H-I brain injuries of neonatal brain.