FIBROBLAST GROWTH FACTOR 2 HYPEREXPRESSION IN TEMPORAL LOBE EPILEPSY PATIENTS
Abstract number :
1.014
Submission category :
1. Translational Research: 1A. Mechanisms
Year :
2013
Submission ID :
1749648
Source :
www.aesnet.org
Presentation date :
12/7/2013 12:00:00 AM
Published date :
Dec 5, 2013, 06:00 AM
Authors :
L. D'Souza-Li, A. E. Ferreira, M. Teocchi, E. Oliveira, H. Tedeschi
Rationale: Temporal lobe epilepsy (TLE) is the most common focal epilepsy in adults. Seizures are linked to structural and functions changes in hippocampus, such as synapse reorganization in the dentate gyrus, involving dispersion of granule cells, neurogenesis, growth of axon and mossy fibers sprouting and changes in the excitatory circuits. Fibroblast growth factor 2 (FGF2) is a protein with a multifunctional role involved in fetal development and in synapse reorganization, angiogenesis, proliferation, cellular differentiation and tumor growth in adult organisms. In addition, FGF2 is also involved in neurogenesis, excitability and plasticity, regulating the survival, migration, proliferation and differentiation of neural cells. Although the role of FGF2 and epilepsy is reported in animal model, there is no study of FGF2 in TLE patients. The objective of this study was to investigate the FGF2 expression in hippocampus of TLE patients. Methods: Reverse Transcription-quantitative PCR (RT-qPCR) was performed in resected hippocampal tissue samples from 10 TLE patients and four post mortem controls. GAPDH, HPRT1, ENO2 and TPB were used as reference genes. The FGF2 protein expression pattern was analyzed by immunofluorescence. Results: FGF2 was upregulated in TLE patients when compared to post mortem controls regardless the reference gene used (Mann-Whitney test, GAPDH: P = 0.002, HPRT1: P = 0.002 and ENO2: P = 0.018, TBP: P=0,004). Immunofluorescence confirmed FGF2 was expressed in neurons and glial cells. Conclusions: Our results showed that FGF2 is upregulated in TLE patients compared to controls. Similar to animal model, FGF2 may be involved in neurogenesis, excitatory synapses and mossy fibers sprouting in TLE patients. This finding impels us to further investigate the FGF2 signaling pathway in TLE patients.
Translational Research