International Journal of Clinical and Experimental Neurology
ISSN (Print): 2379-7789 ISSN (Online): 2379-7797 Website: https://www.sciepub.com/journal/ijcen Editor-in-chief: Zhiyou Cai, MD
Open Access
Journal Browser
Go
International Journal of Clinical and Experimental Neurology. 2017, 5(1), 1-4
DOI: 10.12691/ijcen-5-1-1
Open AccessArticle

Correlation between Levels of Transforming Growth Factor Beta 1 (TGF-β1) serum with Clinical Outcome on Acute Anterior Circulation Ischemic Strokes

Vivien Puspitasari1, , Syarifuddin Wahid2, Amiruddin Aliah3 and Budhianto Suhadi4

1Department of Neurology, Faculty of Medicine Pelita Harapan University, Tangerang, Indonesia

2Department of Anatomical Pathology, Faculty of Medicine Hassanuddin University, Makassar, Indonesia

3Department of Neurology, Faculty of Medicine Hassanuddin University, Makassar, Indonesia

4Department of Clinical Pathology, Faculty of Medicine Pelita Harapan University, Tangerang, Indonesia

Pub. Date: January 11, 2017

Cite this paper:
Vivien Puspitasari, Syarifuddin Wahid, Amiruddin Aliah and Budhianto Suhadi. Correlation between Levels of Transforming Growth Factor Beta 1 (TGF-β1) serum with Clinical Outcome on Acute Anterior Circulation Ischemic Strokes. International Journal of Clinical and Experimental Neurology. 2017; 5(1):1-4. doi: 10.12691/ijcen-5-1-1

Abstract

Transforming Growth Factor Beta (TGFβ) was a major regulatory molecule to suppress the immune response in the inflammatory process. TGFβ was also a growth factor that affects growth, homeostasis, angiogenesis and tissue repair. In the acute phase of stroke, astrocytes were activated and the cells were able to produce anti-inflammatory cytokines such as TGFβ. The purpose of this study was to determine whether there is a correlation between serum levels of TGFβ at acute phase of ischemic stroke and patients’ clinical outcomes. The study was conducted in patients with acute anterior system ischemic stroke who came to Siloam Hospital in Tangerang, Indonesia. Blood samples were taken to measure the levels of TGFβ-1serum at ≤ 72 hours and the 3rd day of onset. Clinical severity of stroke assessed using the National Institute of Health (NIH) Stroke Scale at 72 hours, 7th days and 30th days after stroke. The mean serum levels of TGFβ-1 at ≤ 72 hours in the group of subjects with mild NIH Stroke Scale degree was higher than in the group of subjects with moderate/severe NIH Stroke Scale degree (p = 0.046). The subjects with elevated levels of TGF-β1 in the acute phase of stroke had better clinical degrees at the 30th day after the stroke, although statistically was not significant (p = 0.241). Result of this study showed that TGFβ-1 may act as a neuroprotector against brain tissue damage after ischemic stroke.

Keywords:
ischemic stroke TGF-β1 stroke outcome National Institute of Health Stroke Scale

Creative CommonsThis work is licensed under a Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

References:

[1]  World Health Organization [Internet]. Global burden of stroke. [Cited 2014 Aug 10]. Available from: http://www.who.int/cardiovascular_diseases/en/cvd_atlas_15_burden stroke.pdf.
 
[2]  Go AS, Mozaffarian D, Roger VL. (2013). Heart Disease and Stroke Statistics-2013 Update: A Report from the American Heart Association. Circulation. 127:e6-e245.
 
[3]  Kusuma Y, Venketasubramanian, Kiemas LS, Misbach J. (2009). Burden of stroke in Indonesia. Int J Stroke, 4(5): 379-80.
 
[4]  Truelsen T., Bonita R. (2003). Advances in Ischemic Stroke Epidemiology. In: Barnett HJM, Bogousslavsky, Meldnun H. Advances in Neurology Ischemic Stroke. Lipincott Williams and Wilkin pp. 1-11.
 
[5]  Brea D, Sobrino T, Ramos-Cabrer P, et al. (2009). Inflammatory and neuroimmunomodulatory changes in acute cerebral ischemia. Cerebrovasc Dis , 27, pp. 48-64.
 
[6]  Iadecola C, Anrather J. (2012). The immunology of stroke: from mechanism to translation. Nat Med, 17(7): 796-808.
 
[7]  Ceuleman A, Zgvac T, Koojman R. (2010). The dual role of the neuroinflammatory response after ischemic stroke: modulatory effects of hypothermia. Journal of Neuroinflammation, 7(74): 1-18.
 
[8]  Ma M, Ma Y, Yi X. (2008). Intranasal delivery of transforming growth factor-beta 1 in mice after stroke reduces infarct volume and increases neurogenesis in the subventriculat zone. BMC Neuroscience, 9: 117.
 
[9]  Dobolyi A, Vincze C, Pal G, et al. (2012). The Neuroprotective Functions of Trasnforming Growth Factor Beta Proteins. Int J Mol Sci, 13, pp. 8219-8258.
 
[10]  Boche D, Cunningham C, Gauldie J, Perry VH. (2003). Transforming Growth Factor- β1 -Mediated Neuroprotection Against Excitotoxic Injury in Vivo. J Cereb Blood Flow Metab, 23 (10): 1174-1182.
 
[11]  Beck H, Plate KH. (2009). Angiogenesis after cerebral ischemia. Acta Neuropathol, 117: 481-496 .
 
[12]  Hamby ME, Sofroniew MV. (2010) Reactive Astrocytes as Therapeutic Targets for CNS disorders. Neurotherapeutics, 7(4): 494-506.
 
[13]  Yudiarto F, Machfoed M, Darwin A, Ong A, et all. 2014. Indonesia Stroke Registry. Neurology, 82(10) supplement S12.003.
 
[14]  Doyle KP, Cekanaviciute E. Maner L, Buckwater MS. (2010). TGFβ signaling in the brain increases with aging and signals to astrocytes and innate immune cells in the weeks after stroke. Journal of Neuroinflammation, 7(62): 1-13.