کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10768099 | 1050803 | 2005 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Lib, transcriptionally induced in senile plaque-associated astrocytes, promotes glial migration through extracellular matrix
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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![عکس صفحه اول مقاله: Lib, transcriptionally induced in senile plaque-associated astrocytes, promotes glial migration through extracellular matrix Lib, transcriptionally induced in senile plaque-associated astrocytes, promotes glial migration through extracellular matrix](/preview/png/10768099.png)
چکیده انگلیسی
In an effort to identify astrocyte-derived molecules that may be intimately associated with progression of Alzheimer's disease (AD), Lib, a type I transmembrane protein belonging to leucine-rich repeat superfamily, has been identified as a distinctly inducible gene, responsive to β-amyloid as well as pro-inflammatory cytokines in astrocytes. To evaluate the roles of Lib in AD, we investigated Lib expression in AD brain. In non-AD brain, Lib mRNA has been detected in neurons but not in quiescent astrocytes. On the contrary, in AD brain, Lib mRNA is expressed in activated astrocytes associated with senile plaques, but not expressed in neurons around lesions. Lib-expressing glioma cells displayed promotion of migration ability through reconstituted extracellular matrix and recombinant Lib protein bound to constituents of extracellular matrix. These observations suggest that Lib may contribute to regulation of cell-matrix adhesion interactions with respect to astrocyte recruitment around senile plaques in AD brain.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 335, Issue 2, 23 September 2005, Pages 631-636
Journal: Biochemical and Biophysical Research Communications - Volume 335, Issue 2, 23 September 2005, Pages 631-636
نویسندگان
Kazuki Satoh, Mitsumi Hata, Tomoko Shimizu, Hiroshi Yokota, Hiroyasu Akatsu, Takayuki Yamamoto, Kenji Kosaka, Tatsuo Yamada,