Transcriptomic Profiling of Medial Temporal Lobe Epilepsy
Abhilash K. Venugopal1,2,3,4, Ghantasala S. Sameer Kumar1,2, Anita Mahadevan5, Lakshmi Dhevi N. Selvan1,6, Arivusudar Marimuthu1,7,Jyoti Bajpai Dikshit8, Pramila Tata8, Ramachandra YL2, Raghothama Chaerkady1,2,3,4, Sanjib Sinha9, Chandramouli BA10, Arivazhagan A10, Parthasarathy Satishchandra9*, Shankar SK5 and Akhilesh Pandey3,4,11,12*
- *Corresponding Authors:
- Dr. Akhilesh Pandey, MD, Ph.D
McKusick-Nathans Institute of Genetic Medicine
733 N. Broadway, BRB 527, Johns Hopkins University, Baltimore, USA
E-mail: [email protected]
- Dr. Satishchandra P, MD, DM
Department of Neurology
National Institute of Mental Health and Neurosciences
Fax: 91- 080-26564830
E-mail: sa[email protected]
Received Date: December 21, 2011; Accepted Date: January 18, 2012; Published Date: January 30, 2012
Citation: Venugopal AK, Sameer Kumar GS, Mahadevan A, Selvan LDN, Marimuthu A, et al. (2012) Transcriptomic Profiling of Medial Temporal Lobe Epilepsy. J Proteomics Bioinform 5: 031-039. doi: 10.4172/jpb.1000210
Copyright: © 2012 Venugopal AK, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Epilepsy is one of the most prevalent neurological disorders affecting ~1% of the population. Medial temporal lobe epilepsy (MTLE) is the most frequent type of epilepsy observed in adults who do not respond to pharmacological treatment. The reason for intractability in these patients has not been systematically studied. Further, no markers are available that can predict the subset of patients who will not respond to pharmacotherapy. To identify potential biomarkers of epileptogenicity, we compared the mRNA profiles of surgically resected tissue from seizure zones with non-seizure zones from cases of intractable MTLE. We identified 413 genes that exhibited ≥ 2-fold change that were statistically significant across these two groups. Several of these differentially expressed genes have not been previously described in the context of MTLE including claudin 11 ( CLDN11 ) and bone morphogenetic protein receptor, type IB ( BMPR1B ). In addition, we found significant downregulation of a subset of gamma-aminobutyric acid (GABA) associated genes. We also identified molecules such as BACH2 and ADAMTS15 , which are already known to be associated with epilepsy. We validated one upregulated molecule, serine/threonine kinase 31 ( STK31 ) and one downregulated molecule, SMARCA4, by immunohistochemical labeling of tissue sections. These molecules need to be further confirmed in large-scale studies to determine their potential use as diagnostic as well as prognostic markers in intractable MTLE.