M Siedlecka, S Szlufik, W Grajkowska, M Roszkowski, J Jóźwiak1. 1. Jarosław Jóźwiak, Department of Histology and Embryology, Center for Biostructure Research, Medical University of Warsaw, ul. Chalubinskiego 5, 02-004 Warsaw, Poland, fax: +48 22 629 52 82, e-mail: jaroslaw.jozwiak@gmail.com.
Abstract
INTRODUCTION: Subependymal nodule (SEN) and subependymal giant cell astrocytoma (SEGA) are brain lesions frequently found in tuberous sclerosis (TS). As about 10-15% of SENs enlarge and transform into SEGAs, we examined here the possible mechanism of the phenomenon. MATERIAL AND METHODS: Using Western blot we studied 1 SEN and 3 SEGA samples; SEN and 1 SEGA came from the same TS patient. We evaluated e.g. the activation of the phosphorylated forms of proteins belonging to Akt, Erk and mTOR pathways. RESULTS: Differences in Erk pathway activation between SEN and SEGA were found. There was no upregulation of p-Erk, p-Mek or p-RSK1 in the SEN specimen, whilst we found these proteins to be significantly uptriggered in SEGA samples. Also, for the first time, we found p-Akt, p-GSK3 and p-PDK1 upregulated in both SEN and SEGA from the same TS patient. CONCLUSIONS: Our current study shows for the first time the possible mechanism of SEN/SEGA transformation, where Erk pathway hyperactivation seems to be significant. We hypothesize that SEN/SEGA transformation may depend on Erk potentiation.
INTRODUCTION:Subependymal nodule (SEN) and subependymal giant cell astrocytoma (SEGA) are brain lesions frequently found in tuberous sclerosis (TS). As about 10-15% of SENs enlarge and transform into SEGAs, we examined here the possible mechanism of the phenomenon. MATERIAL AND METHODS: Using Western blot we studied 1 SEN and 3 SEGA samples; SEN and 1 SEGA came from the same TS patient. We evaluated e.g. the activation of the phosphorylated forms of proteins belonging to Akt, Erk and mTOR pathways. RESULTS: Differences in Erk pathway activation between SEN and SEGA were found. There was no upregulation of p-Erk, p-Mek or p-RSK1 in the SEN specimen, whilst we found these proteins to be significantly uptriggered in SEGA samples. Also, for the first time, we found p-Akt, p-GSK3 and p-PDK1 upregulated in both SEN and SEGA from the same TS patient. CONCLUSIONS: Our current study shows for the first time the possible mechanism of SEN/SEGA transformation, where Erk pathway hyperactivation seems to be significant. We hypothesize that SEN/SEGA transformation may depend on Erk potentiation.
Authors: David Kapfhamer; James McKenna; Caroline J Yoon; Tracy Murray-Stewart; Robert A Casero; Michael J Gambello Journal: Hum Mol Genet Date: 2020-08-11 Impact factor: 6.150
Authors: Ann-Sofie De Meulemeester; Lise Heylen; Aleksandra Siekierska; James D Mills; Alessia Romagnolo; Nicole N Van Der Wel; Eleonora Aronica; Peter A M de Witte Journal: Front Cell Dev Biol Date: 2022-09-27