The induction of TGF-βs in relation to immediate early genes following middle cerebral artery occlusion in rats

Abstract

Event Abstract Back to Event The induction of TGF-βs in relation to immediate early genes following middle cerebral artery occlusion in rats G. Pál1, C. Vincze2, E. A. Wappler3, G. Lovas2 and Á. Dobolyi1* 1 Semmelweis University and the Hungarian Academy of Sciences, Department of Anatomy, Histology and Embryology, Hungary 2 Semmelweis University, Department of Neurology, Hungary 3 Semmelweis University, Department of Anesthesiology and Intensive Therapy, Hungary Transforming growth factor βs (TGF-β1-3) form a small group of related proteins involved in the regulation of proliferation, differentiation, and survival of various cell types. TGF-β was suggested to be is neuroprotective because injection of TGF-β decrease, while injection of antagonist increased the infarct size. Previously, we described the expression of TGF-βs in the intact rat brain. In the present study, we induced focal ischemia using middle cerebral artery occlusion (MCAO) and examined the changes in the expression of TGF-β1, 2, and 3 using in situ hybridization histochemistry. All three types of TGF-βs were induced in neurons outside the infarct area. TGF-β1 showed elevated expression level in the penumbra around the lesion. The expression of TGF-β2 and 3 was increased in layers II, III, and V of the ipsilateral cerebral cortex. Subsequently, combinations of in situ hybridization histochemistry and immunolabeling was used to compare the distribution of TGF-βs with that of immediate-early genes Fos and activating transcription factor-3 (ATF-3). We demonstrated that TGF-β1 is co-localized with ATF-3 while TGF-β2 appears in Fos-expressing cells. In turn, these neurons did not contain Fluoro Jade C, a marker of neurodegenration. These observations suggest that endogenous TGF-β1 and TGF-β2 and 3 all participate in neuroprotection, although they are induced by different mechanisms following an ischemic attack. Acknowledgements Support: OTKA NNF78219, Bolyai Fellowship. Keywords: disorders, Neuroscience Conference: 13th Conference of the Hungarian Neuroscience Society (MITT), Budapest, Hungary, 20 Jan - 22 Jan, 2011. Presentation Type: Abstract Topic: Disorders Citation: Pál G, Vincze C, Wappler EA, Lovas G and Dobolyi Á (2011). The induction of TGF-βs in relation to immediate early genes following middle cerebral artery occlusion in rats. Front. Neurosci. Conference Abstract: 13th Conference of the Hungarian Neuroscience Society (MITT). doi: 10.3389/conf.fnins.2011.84.00012 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 03 Mar 2011; Published Online: 23 Mar 2011. * Correspondence: Dr. Á. Dobolyi, Semmelweis University and the Hungarian Academy of Sciences, Department of Anatomy, Histology and Embryology, Budapest, Hungary, dobolyi@ana.sote.hu Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers G. Pál C. Vincze E. A Wappler G. Lovas Á. Dobolyi Google G. Pál C. Vincze E. A Wappler G. Lovas Á. Dobolyi Google Scholar G. Pál C. Vincze E. A Wappler G. Lovas Á. Dobolyi PubMed G. Pál C. Vincze E. A Wappler G. Lovas Á. Dobolyi Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.