TY - JOUR
T1 - Identification of Plasma Biomarkers of Human Intracerebral Hemorrhage Subtypes through Microarray Technology
AU - Merino-Zamorano, Cristina
AU - Delgado, Pilar
AU - De Retana, Sofía Fernández
AU - Fernández-Cadenas, Israel
AU - Rodríguez-Luna, David
AU - Montaner, Joan
AU - Hernández-Guillamon, Mar
N1 - Funding Information:
Source of funding: The Neurovascular Research Laboratory takes part in the INVICTUS network (RD12/0014/0005). This work was supported by grants from the Fondo de Investigaciones Sanitarias INTRASALUD PI 11/0176, financed by the Institute of Health Carlos III , Spain. C.M.-Z. is supported by the fellowship grant FI12/00089 , and M.H.-G., P.D., and I.F.-C. by the Miguel Servet programme ( CP12/03259 , CP09/136 , and CP12/03298 , respectively) from the Institute of Health Carlos III, Spain.
Publisher Copyright:
© 2016 National Stroke Association. All rights reserved.
PY - 2016/3/1
Y1 - 2016/3/1
N2 - Background Intracerebral hemorrhage (ICH) is a devastating form of stroke and depending on the underlying cause, primary ICH is mainly caused by hypertension (HTN-ICH) or cerebral amyloid angiopathy (CAA-ICH). Currently, neuroimaging markers are required to identify the pattern for each etiology. The discovery of new biomarkers to improve the management of this pathology is therefore needed. Methods A microarray analysis was carried out to analyze gene expression differences in blood samples from patients (>1.5 months since the last ICH event) who suffered a CAA-ICH and HTN-ICH, and controls. The results were replicated by quantitative polymerase chain reaction and the plasma protein level of the best candidate was measured with enzyme-linked immunosorbent assay. Results The microarray analysis and the validation study revealed an increase in Golgin A8 Family, Member A (GOLGA8A) mRNA and protein levels in ICH cases compared to controls (P < .01), although no differences were found between specific ICH etiologies. GOLGA8A plasma levels were also associated with the presence of multiple hemorrhages (P < .05). Conclusions The GOLGA8A level was increased in the blood of patients who suffered a primary ICH. We did not, however, find any candidate biomarker that distinguished CAA-ICH from HTN-ICH. The role of GOLGA8A in this fatal disorder has yet to be determined.
AB - Background Intracerebral hemorrhage (ICH) is a devastating form of stroke and depending on the underlying cause, primary ICH is mainly caused by hypertension (HTN-ICH) or cerebral amyloid angiopathy (CAA-ICH). Currently, neuroimaging markers are required to identify the pattern for each etiology. The discovery of new biomarkers to improve the management of this pathology is therefore needed. Methods A microarray analysis was carried out to analyze gene expression differences in blood samples from patients (>1.5 months since the last ICH event) who suffered a CAA-ICH and HTN-ICH, and controls. The results were replicated by quantitative polymerase chain reaction and the plasma protein level of the best candidate was measured with enzyme-linked immunosorbent assay. Results The microarray analysis and the validation study revealed an increase in Golgin A8 Family, Member A (GOLGA8A) mRNA and protein levels in ICH cases compared to controls (P < .01), although no differences were found between specific ICH etiologies. GOLGA8A plasma levels were also associated with the presence of multiple hemorrhages (P < .05). Conclusions The GOLGA8A level was increased in the blood of patients who suffered a primary ICH. We did not, however, find any candidate biomarker that distinguished CAA-ICH from HTN-ICH. The role of GOLGA8A in this fatal disorder has yet to be determined.
KW - Intracerebral hemorrhage
KW - biomarker
KW - cerebral amyloid angiopathy
KW - hypertensive-related hemorrhage
KW - microarray analysis
KW - stroke
UR - http://www.scopus.com/inward/record.url?scp=84959569667&partnerID=8YFLogxK
U2 - 10.1016/j.jstrokecerebrovasdis.2015.11.032
DO - 10.1016/j.jstrokecerebrovasdis.2015.11.032
M3 - Article
C2 - 26738811
AN - SCOPUS:84959569667
SN - 1052-3057
VL - 25
SP - 665
EP - 671
JO - Journal of Stroke and Cerebrovascular Diseases
JF - Journal of Stroke and Cerebrovascular Diseases
IS - 3
ER -