Published customer image: Effect of clustered ephrin-A1-Fc on vascular formation in the rat striatum. (A) Distribution of BrdU(+) endothelial cells. Brain of the unilaterally lesioned rats 6 weeks after infusion of clustered ephrin-A1-Fc were sectioned coronally and stained for BrdU and Rat Endothelial Cell Antigen-1 (RECA-1). Numbers of the BrdU(+) cells and BrdU(+)&RECA-1(+) cells were counted as describe in the Materials and Methods. Total numbers of BrdU(+) cells in 8 animals are shown on the top, and percentages of RECA-1(+) cells among BrdU(+) cells are shown on the bottom. Error bars represent SD. *p

Published customer image: ChABC and GF treatments attenuate the proliferation of microglia/macrophages and promote the generation of new endothelial cells after SCI. (A -D) Representative confocal images of BrdU+/NG2+ macrophages/microglia marked with Iba-1 in the injured spinal cord (arrows). (E -F) Under baseline SCI condition, macrophages/microglia comprised about 25% and 17% of BrdU+/NG2+ cells in rostral and caudal points to the injury center, respectively. After treatment with ChABC and/or GFs, we found a reduction in the number of BrdU+/NG2+/IbA-1+ cells that was statistically significant for ChABC and ChABC+GFs treatment groups relative to the vehicle group. (G -J) Representative confocal images show newly generated endothelial cells marked by Reca-1 and NG2 among BrdU+ cells. Reca-1 positive endothelial cells comprised a subpopulation of proliferating NG2+ cells after SCI (J). (K -L) Quantification of BrdU+/NG2+/Reca-1+ cells showed a significant number of newly generated endothelial cells after treatment with ChABC and/or GFs at both rostral and caudal points to the injury center compared to the vehicle group. *p

Published customer image:Morphology of microvessels stained with RECA-1 in Abeta 1-42-injected hippocampus. Panels show morphological features including fragments, looping microvessels, and vessels with knob-like and uneven diameters. The scale bar represents 40?um.From: Jantaratnotai N, Ryu JK, Schwab C, McGeer PL, McLarnon JG. Comparison of Vascular Perturbations in an Abeta-Injected Animal Model and in AD Brain. Int J Alzheimers Dis. 2011;2011:918280.

Published customer image:Representative patterns of RECA-1 staining in rat hippocampus. (a) Microvessels in control (PBS) injected rat hippocampus (left panel) and microvessels in Abeta1-42-injected hippocampus (right panel). Scale bar is for 70um. (b) Bar graph for the number of microvessels/mm2 (n = 5 each). (c) Bar graph for microvessel length (n = 5 each). *P = 0.05 for Abeta1-42 versus PBS.From: Jantaratnotai N, Ryu JK, Schwab C, McGeer PL, McLarnon JG. Comparison of Vascular Perturbations in an Abeta-Injected Animal Model and in AD Brain. Int J Alzheimers Dis. 2011;2011:918280.

Published customer image: AdV-ZFP-VEGF results in increased vessel counts and angiogenesis. (A) Left panel: Illustration of the area of spinal cord areas used for RECA-1 counting (2 grey matter areas, 2 white matter areas). (B) Representative sections taken 2 mm rostral to the epicenter from a AdV-ZFP-VEGF treated and AdV-eGFP control animal respectively immunostained with RECA-1 at 10 days after SCI; scale 100 um. An increased number of vessels were observed in the AdV-ZFP-VEGF treated group. (C) Bar graph illustrating the RECA-1 positive cell counts 10 days after SCI. AdV-ZFP-VEGF administration resulted in a significant increase in vascular counts (2 mm and 4 mm away from the epicenter) as compared with the control group. (D) Representative confocal image from an ADV-ZFP-VEGF treated animal at 5 days post-injury. Image was taken at 2 mm rostral from the epicenter, and shows double-labeled cells. Cells were stained for endothelial cells (RECA-1, green) and proliferation (Ki67, red). Scale bar = 50 um (30 um for magnified panel). (E) Angiogenesis was assessed by quantifying Ki67/RECA-1 co-labeled vessels. Data is presented at the percentage of RECA-1+ vessels that were also Ki67+, with an overall average increase of 10% vascular proliferation observed in the animals receiving AdV-ZFP-VEGF administration. All data are presented as mean +/- SEM, and was analyzed by Two-way ANOVA (Holm-Sidak post-hoc). Angiogenesis data were analyzed by performing an arcsine transformation of the values, prior to Two-way ANOVA and post-hoc testing. *p

Published customer image: Pyruvate reduces R/M hypoglycemia-induced cortical blood vessel loss. (A) Bright field photomicrographs from coronal sections of cortex demonstrate loss of blood vessels at three days after R/M hypoglycemia by RECA-1 (rat endothelial cell antigen 1) staining. Panels show the progression of blood vessel changes in the parietal (PT Ctx) and perirhinal (PRh Ctx) cortex. After R/M hypoglycemia, blood vessels showed decreased density compared to sham-operated rats. Intraperitoneal injection of pyruvate as an adjuvant to glucose at ten minutes after R/M hypoglycemia reduced blood vessel disappearance. Scale bar = 100 um. (B) Graph represents the % area of RECA-1 immunoreactivity in the parietal and perirhinal cortex. Data are means +/- s.e.m., n=5-6 from each group, *P

Published customer image:Endothelial cell number and capillary length post radiation. (A) Representative images of sections from the corpus callosum immunostained for rat endothelial cell antigen (RECA) at various time points post radiation. RECA expression declines immediately post radiation but is restored and maintained through 15 months. Stereological estimates of the number of capillary segments in the cortex (B) and corpus callosum (C) and of capillary length in both regions (D, E). (*** p

Published customer image: Transduction of AdV-eGFP/AdV-ZFP-VEGF into the spinal cord. (A) Photomicrographs showing a transverse section of rat spinal cord obtained adjacent to the injury site 10 days after spinal cord injury and AdV-eGFP injection. eGFP signal was detected in both the gray matter and white matter. (B) High-power (63X) confocal images show that the AdV-eGFP vector (green) transfected neurons (NeuN), astrocytes (GFAP), oligodendrocytes (CC1) and endothelial cells (RECA-1). Cells have been counter-stained with DAPI (blue) as nuclear marker. (C) Bar graph displays quantification of transduced cell types +/- SEM, as identified by the cell-specific markers NeuN, GFAP, RECA-1 and CC1. (D) Evaluation of AdV-ZFP-VEGF gene transfer. Western blot showed that the NF?B p65 rabbit polyclonal antibody recognizes the p65 activation domain in the AdV-ZFP-VEGF treated animals. The higher molecular weight bands are endogenous NF?Bp65 fragments, which are also recognized by the antibody; however, these bands are present in both the control and treatment groups. The lower band (arrow) corresponds to the AdV-ZFP-VEGF and was only present in the treated animals. Lower panel shows actin expression as a protein control. Scale bar: 1000 um for A; 100 um for B.From: Figley SA, Liu Y, Karadimas SK, Satkunendrarajah K, Fettes P, et al. (2014) Delayed Administration of a Bio-Engineered Zinc-Finger VEGF-A Gene Therapy Is Neuroprotective and Attenuates Allodynia Following Traumatic Spinal Cord Injury. PLoS ONE 9(5): e96137.

Published customer image: Effect of clustered ephrin-A1-Fc on vascular formation in the rat striatum. Clustered ephrin-A1-Fc was injected into the lesioned side of the lateral ventricle in the unilaterally lesioned rats. Brains taken 6 weeks after injection were sectioned coronally and stained for GFAP (green) and RECA-1 (red) and with DAPI (nuclei; blue). The rectangular insets are shown in Fig. 8B. Scale bar: 100 um.From: Jing X, Miwa H, Sawada T, Nakanishi I, Kondo T, et al. (2012) Ephrin-A1-Mediated Dopaminergic Neurogenesis and Angiogenesis in a Rat Model of Parkinson's Disease. PLoS ONE 7(2): e32019.