scholarly journals Proteomic Analysis of Importin α-interacting Proteins in Adult Mouse Brain

2011 ◽  
Vol 36 (1) ◽  
pp. 57-67 ◽  
Author(s):  
Masahiro Fukumoto ◽  
Toshihiro Sekimoto ◽  
Yoshihiro Yoneda
Keyword(s):  
Mouse Brain ◽  
Proteomic Analysis ◽  
Adult Mouse ◽  
Interacting Proteins ◽  
Adult Mouse Brain ◽  
Importin Α

Importin-α and β expression in the neonatal and adult mouse brain

2007 ◽  
Vol 58 ◽  
pp. S41
Author(s):  
Koji Hosokawa ◽  
Mayumi Nishi ◽  
Mitsuhiro Kawata
Keyword(s):  
Mouse Brain ◽  
Adult Mouse ◽  
Adult Mouse Brain ◽  
Importin Α

Corrigendum to “Localization and fate of Fgf10-expressing cells in the adult mouse brain implicate Fgf10 in control of neurogenesis” [Mol. Cell. Neurosci. 37 (2008) 857–868]

2010 ◽  
Vol 43 (2) ◽  
pp. 259
Author(s):  
Mohammad K. Hajihosseini ◽  
Stijn De Langhe ◽  
Eva Lana-Elola ◽  
Harris Morrison ◽  
Neil Sparshott ◽  
...  
Keyword(s):  
Mouse Brain ◽  
Adult Mouse ◽  
Adult Mouse Brain

scholarly journals Comparative Analysis of the Frequency and Distribution of Stem and Progenitor Cells in the Adult Mouse Brain

Stem Cells ◽  
2008 ◽  
Vol 26 (4) ◽  
pp. 979-987 ◽  
Author(s):  
Mohammad G. Golmohammadi ◽  
Daniel G. Blackmore ◽  
Beatrice Large ◽  
Hassan Azari ◽  
Ebrahim Esfandiary ◽  
...  
Keyword(s):  
Comparative Analysis ◽  
Progenitor Cells ◽  
Mouse Brain ◽  
Adult Mouse ◽  
Adult Mouse Brain ◽  
Stem And Progenitor Cells

scholarly journals Embryonic Cerebrospinal Fluid Activates Neurogenesis of Neural Precursors within the Subventricular Zone of the Adult Mouse Brain

2013 ◽  
Vol 198 (5) ◽  
pp. 398-404 ◽  
Author(s):  
E. Carnicero ◽  
M.I. Alonso ◽  
R. Carretero ◽  
F. Lamus ◽  
J.A. Moro ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Mouse Brain ◽  
Subventricular Zone ◽  
Adult Mouse ◽  
Adult Mouse Brain ◽  
Neural Precursors

scholarly journals MicroRNA-210 overexpression induces angiogenesis and neurogenesis in the normal adult mouse brain

Gene Therapy ◽  
2013 ◽  
Vol 21 (1) ◽  
pp. 37-43 ◽  
Author(s):  
L Zeng ◽  
X He ◽  
Y Wang ◽  
Y Tang ◽  
C Zheng ◽  
...  
Keyword(s):  
Mouse Brain ◽  
Adult Mouse ◽  
Normal Adult ◽  
Adult Mouse Brain

Abstract 3153: Endoglin Deficiency in Bone Marrow is Sufficient to Cause Vascular Dysplasia in the Adult Mouse Brain After VEGF Stimulation

Stroke ◽  
2012 ◽  
Vol 43 (suppl_1) ◽  
Author(s):  
Eun-Jung Choi ◽  
Espen J. Walker ◽  
Kristine Jun ◽  
Robert Kuo ◽  
Hua Su ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Mouse Brain ◽  
Adult Mouse ◽  
Viral Vector ◽  
Vascular Density ◽  
Index Number ◽  
Adult Mouse Brain ◽  
Healthy Human ◽  
Angiogenic Response ◽  
The Mean

Background and Objective: We have previously demonstrated that VEGF overexpression in the brain of adult Eng+/- mice causes vascular abnormalities. We also found that bone marrow-derived cells (BMDCs) home to vascular endothelial growth factor (VEGF)-induced angiogenic foci in the adult mouse brain and contribute to angiogenesis. Impaired angiogenesis in infarcted myocardium of Eng+/- mice was rescued using treatment with healthy human BMDCs but not with BMDCs from Hereditary Hemorrhagic Telangiectasia (HHT1) patients carrying ENG mutations. We hypothesized that ENG-haploinsufficiency in BMDCs can cause cerebrovascular dysplasia in the adult mouse after VEGF stimulation. Methods: WT or Eng+/- BM (2×106 cells) were transplanted to lethally irradiated C57BL/6 recipient mice (8-10 weeks old) via tail vein injection. After 4 weeks of BM transplantation, adeno-associated viral vector expressing VEGF (AAV-VEGF, 2×109 genome copies) was stereotactically injected into the basal ganglia. Brain sections were collected at 4 weeks after virus injection. The vascular density (vessels per 20× objective field) and dysplasia index (number of vessels >15µm in diameter per 200 vessels) were quantified on lectin-stained brain sections. Results: To examine the angiogenic response to VEGF, the vascular density around the AAV-VEGF injection site was analyzed. The mean vascular density increased in all mice with VEGF stimulation. Mice transplanted with Eng+/- BM showed less vascular density compared to mice transplanted with WT BM. The mean vascular densities were167 ± 21 (Eng+/-BM, n=4) and 202 ± 15 (WT BM, n=5) (P<0.01). Further, mice with WT BM had angiogenesis with normal vascular morphology. In contrast, mice with Eng+/- BM had markedly enlarged and dysmorphic vessels. To assess the degree of the dysplastic response, dysplasia index was analyzed. Mice with Eng+/- BM had several fold-higher dysplasia index than mice with WT BM: 2.6 ± 1.4 (Eng+/- BM) versus 0.7 ± 0.4 (WT BM) (P<0.01). Conclusions: In the adult mouse after VEGF stimulation, ENG-deficiency in BM (1) caused a 17% reduction in brain angiogenic response, and (2) increased cerebrovascular dysplasia, compared to control animals. These data support the possibility that cerebrovascular malformations resulting from VEGF stimulation with ENG-haploinsufficiency is attributable to impaired cell-autonomous monocyte/macrophage function, in contrast to the view that ENG dysfunction is primarily an endothelial phenomenon.

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