کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
3058490 1580293 2016 5 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Changes in differential gene expression during a fatal stroke
ترجمه فارسی عنوان
تغییر در بیان دیفرانسیلی ژن در طول یک سکته مغزی منجر به مرگ
کلمات کلیدی
بیان ژن؛ گرانزیم B؛ سکته مغزی
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی عصب شناسی
چکیده انگلیسی


• Early activators of the inflammatory response in acute stroke may be unrecognized.
• A woman had sampling for gene expression during the evolution of her fatal stroke.
• This was compared to her twin and healthy controls.
• Granzyme B demonstrated the most marked upregulation.
• This may assist with differentiating patients with stroke from stroke mimics.

We present a young woman (with an identical twin sister) who arrived at the Emergency Department (ED) within 1 hour of her initial stroke symptoms. Previous microarray studies have demonstrated differential expression of multiple genes between stroke patients and healthy controls. However, for many of these studies there is a significant delay between the initial symptoms and collection of blood samples, potentially leaving the important early activators/regulators of the inflammatory response unrecognised. Blood samples were collected from the patient for an analysis of differential gene expression over time during the evolution of a fatal stroke. The time points for blood collection were ED arrival (T0) and 1, 3 and 24 hours post ED arrival (T1, T3 and T24). This was compared to her identical twin and an additional two age and sex-matched healthy controls. When compared to the controls, the patient had 12 mRNA that were significantly upregulated at T0, and no downregulated mRNA (with a cut off fold change value ±1.5). Of the 12 upregulated mRNA at T0, granzyme B demonstrated the most marked upregulation on arrival, with expression steadily declining over time, whereas S100 calcium-binding protein A12 (S100A12) gene expression increased from T0 to T24, remaining >two-fold above that in the healthy controls at T24. Other genes, such as matrix metalloproteinase 9, high mobility group box 2 and interleukin-18 receptor I were not upregulated at T0, but they demonstrated clear upregulation from T1–T3, with gene expression declining by T24. A greater understanding of the underlying immunopathological mechanisms that are involved during the evolution of ischaemic stroke may help to distinguish between patients with stroke and stroke mimics.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Clinical Neuroscience - Volume 23, January 2016, Pages 130–134
نویسندگان
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