Identification of Plasma Biomarkers of Human Intracerebral Hemorrhage Subtypes through Microarray Technology

详细信息    查看全文

• 作者：Cristina Merino-Zamorano ; MSc^* ; Pilar Delgado ; MD ; PhD^* ; Sofí ; a Ferná ; ndez de Retana ; MSc^* ; Israel Ferná ; ndez-Cadenas ; PhD^* ; David Rodrí ; guez-Luna ; MD ; PhD^&dagger ; ; Joan Montaner ; MD ; PhD^* ; ^&dagger ; ; Mar Herná ; ndez-Guillamon ; PhD^* ; ^{mar.hernandez.guillamon@vhir.org" class="auth_mail" title="E-mail the corresponding author}
• 关键词：Intracerebral hemorrhage ; stroke ; biomarker ; cerebral amyloid angiopathy ; hypertensive-related hemorrhage ; microarray analysis
• 刊名：Journal of Stroke and Cerebrovascular Diseases
• 出版年：2016
• 出版时间：March 2016
• 年：2016
• 卷：25
• 期：3
• 页码：665-671
• 全文大小：843 K

文摘

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.