Effect of Rac1 haploinsufficiency on the gene expression profile of mouse endothelial cells

ABSTRACT: The therapeutic potential of neurotrophic factors has been hampered by their inability to achieve adequate tissue penetration. Brain blood vessels, however, could be an alternative target for neuro-salvage therapies by virtue of their close proximity to neurons. Here we show that hemizygous deletion of Rac1 in mouse endothelial cells (ECs) attenuates brain injury and edema following focal cerebral ischemia. To explore the mechanisms whereby decrease of Rac1 in ECs provide neuroprotection, ECs were derived from Rac1+/+ and Rac1+/- mice. Microarray analysis was performed to determine the differential gene expression between Rac1+/+ and Rac1+/- ECs. Rac1+/+ and Rac1+/- ECs were cultured to subconfluence. Total RNA was extracted and reverse transcribed. Rac1+/+ (n = 2) and Rac1+/- (n = 2) EC cDNAs were labeled with Cy3 and Cy5, respectively, and equimolar mixtures of labeled Rac1+/+ and Rac1+/- probes were hybridized to 2 slides (sample #21648, #21649). Additionally, Rac1+/+ (n = 2) and Rac1+/- (n=2) EC cDNAs labeled with Cy5 and Cy3 (dye-swapping) were hybridized to 2 slides (sample #21650, #21651). Comparison of signal intensities between Rac1+/+ (channel 2) and Rac1+/- (channel 1) was conducted on each slide (sample), and the ratio of intensities from 4 slides were statistically assessed for each gene feature to investigate differential gene expression.

ORGANISM(S): Mus musculus

SUBMITTER: Naoki Sawada 

PROVIDER: E-GEOD-15003 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress