Journal: The European journal of neuroscience

Article Title: VEGF-E Attenuates Injury After Ischemic Stroke by Promoting Reparative Revascularization.

doi: 10.1111/ejn.70114

Figure Lengend Snippet: FIGURE 3 | Revascularization is stabilized by VEGF-E associated with attenuation of neuronal degeneration. (a) Representative fluorescence images of CD31 and PDGFRβ immunolabeling at the injury site in vehicle (VEH)- and VEGF-E-treated mice 4 days after stroke. (b) Analysis of the density of perivascular PDGFRβ+ cells at the injury site 4 days after stroke. (c) Analysis of CD31 and PDGFRβ colocalization at the injury site. (d) Analysis of the number of CD31+ microvascular stalls at the injury site. (e) Representative fluorescence images of CD13 and CD105 immunolabeling at the injury site in VEH- and VEGF-E-treated mice. (f) Analysis of the density of CD105+ microvessels at the injury site. (g) Analysis of CD105 and CD13 colocalization at the injury site. (h) Representative fluorescence images of FJB+ degenerating neurons in the ipsilateral cortex and ipsilateral striatum. Stereological analysis of the density of FJB+ degenerating neurons in the (i) ipsilateral cortex and (j) ipsilateral striatum. Data are boxplot with min/max or stacked histogram (n = 6–7 animals/group). *p < 0.05, **p < 0.01, ***p < 0.001 compared to control (b, d, f, i, unpaired two-tailed t- test). Abbreviations: IF, immunofluorescence; VEGF, vascular endothelial growth factor; VEH, vehicle.

Article Snippet: The following primary antibodies were used: rat anti- mouse cluster of differentiation (CD31) (1/500; BD Biosciences, ON, Canada; 550274), goat anti- mouse aminopeptidase N (CD13) (1/250; R&D systems), rat anti- mouse glial fibrillary acidic protein (GFAP) (1/500; Invitrogen, MA, USA; 13- 0300), rabbit anti- mouse ionized calcium binding adaptor molecule (IBA1) (1/500; WAKO, ON, Canada; 019- 19741), goat anti- rat CD45 (1/500; BD Biosciences; 553076), rabbit anti- mouse PDGFRβ (1/250; Abcam, ON, Canada; ab32570), rat anti- mouse endoglin (CD105) (1/250; Novus Biologicals, ON, Canada; NB100- 77666), and rabbit anti- mouse aquaporine- 4 (AQP4) (1/500; Cell Signaling Technology, MA, USA; 59678S).

Techniques: Fluorescence, Immunolabeling, Control, Two Tailed Test, Immunofluorescence

Journal: The Journal of cell biology

Article Title: Anisotropic expansion of hepatocyte lumina enforced by apical bulkheads.

doi: 10.1083/jcb.202103003

Figure Lengend Snippet: Figure 1. Lumen morphogenesis in hepatocytes is accompanied by specific actin structures that interconnect the two lumen-forming cells. (a) Schematic overview of primary Dlk1+ hepatoblasts in culture differentiating into hepatocytes and recapitulating BC formation. (b) Differentiated hep- atocytes form branched interconnected BC lumina. Immunofluorescence microscopy images of differentiated hepatocytes (Protocol 2, Materials and methods) stained for F-actin with phalloidin–Alexa 488, and for apical markers CD13 and ZO-1. Scale bar: 10 µm. (c) In vitro differentiated (Diff.) hepatocytes express

Article Snippet: The primary antibodies rat monoclonal anti-CD13 (Novus; NB100-64843; RRID:AB_959651; 1:500) and rabbit monoclonal anti-Sox9 (clone EPR14335-78; Abcam; cat. no. ab185966; RRID:AB_2728660; 1: 500) were diluted in Tx buffer (0.2% gelatin, 300 mMNaCl, and 0.3% Triton X-100 in PBS) and incubated for 2 d at RT.

Techniques: Immunofluorescence, Microscopy, Staining, In Vitro

Journal: The European Journal of Neuroscience

Article Title: VEGF‐E Attenuates Injury After Ischemic Stroke by Promoting Reparative Revascularization

doi: 10.1111/ejn.70114

Figure Lengend Snippet: VEGF‐E potently improves vascular density while preserving functionality. (a) Representative fluorescence images of CD31 and CD13 immunolabeling at the injury site in vehicle (VEH)‐, VEGF‐E‐, and VEGF‐A‐treated mice 4 days after stroke. (b) Analysis of the density of CD31 + microvessels at the injury site. (c) Analysis of the density of perivascular CD13 + cells at the injury site. (d) Analysis of CD31 and CD13 colocalization at the injury site. (e) Representative laser Speckle contrast imaging (LSCI) in VEH‐, VEGF‐E‐, and VEGF‐A‐treated mice at Day 4 after stroke presented as ipsilateral/contralateral ratio of blood flow at Day 4 over 5 min after stroke. Data are boxplot with min/max or stacked histogram ( n = 5–7 animals/group). **** p < 0.0001 compared to control (b, c, one‐way ANOVA). Abbreviations: ANOVA, analysis of variance; IF, immunofluorescence; VEGF, vascular endothelial growth factor; VEH, vehicle.

Article Snippet: The following primary antibodies were used: rat anti‐mouse cluster of differentiation (CD31) (1/500; BD Biosciences, ON, Canada; 550274), goat anti‐mouse aminopeptidase N (CD13) (1/250; R&D systems), rat anti‐mouse glial fibrillary acidic protein (GFAP) (1/500; Invitrogen, MA, USA; 13‐0300), rabbit anti‐mouse ionized calcium binding adaptor molecule (IBA1) (1/500; WAKO, ON, Canada; 019‐19741), goat anti‐rat CD45 (1/500; BD Biosciences; 553076), rabbit anti‐mouse PDGFRβ (1/250; Abcam, ON, Canada; ab32570), rat anti‐mouse endoglin (CD105) (1/250; Novus Biologicals, ON, Canada; NB100‐77666), and rabbit anti‐mouse aquaporine‐4 (AQP4) (1/500; Cell Signaling Technology, MA, USA; 59678S).

Techniques: Preserving, Fluorescence, Immunolabeling, Imaging, Control, Immunofluorescence

Journal: The European Journal of Neuroscience

Article Title: VEGF‐E Attenuates Injury After Ischemic Stroke by Promoting Reparative Revascularization

doi: 10.1111/ejn.70114

Figure Lengend Snippet: Revascularization is stabilized by VEGF‐E associated with attenuation of neuronal degeneration. (a) Representative fluorescence images of CD31 and PDGFRβ immunolabeling at the injury site in vehicle (VEH)‐ and VEGF‐E‐treated mice 4 days after stroke. (b) Analysis of the density of perivascular PDGFRβ + cells at the injury site 4 days after stroke. (c) Analysis of CD31 and PDGFRβ colocalization at the injury site. (d) Analysis of the number of CD31 + microvascular stalls at the injury site. (e) Representative fluorescence images of CD13 and CD105 immunolabeling at the injury site in VEH‐ and VEGF‐E‐treated mice. (f) Analysis of the density of CD105 + microvessels at the injury site. (g) Analysis of CD105 and CD13 colocalization at the injury site. (h) Representative fluorescence images of FJB + degenerating neurons in the ipsilateral cortex and ipsilateral striatum. Stereological analysis of the density of FJB + degenerating neurons in the (i) ipsilateral cortex and (j) ipsilateral striatum. Data are boxplot with min/max or stacked histogram ( n = 6–7 animals/group). * p < 0.05, ** p < 0.01, *** p < 0.001 compared to control (b, d, f, i, unpaired two‐tailed t ‐test). Abbreviations: IF, immunofluorescence; VEGF, vascular endothelial growth factor; VEH, vehicle.

Article Snippet: The following primary antibodies were used: rat anti‐mouse cluster of differentiation (CD31) (1/500; BD Biosciences, ON, Canada; 550274), goat anti‐mouse aminopeptidase N (CD13) (1/250; R&D systems), rat anti‐mouse glial fibrillary acidic protein (GFAP) (1/500; Invitrogen, MA, USA; 13‐0300), rabbit anti‐mouse ionized calcium binding adaptor molecule (IBA1) (1/500; WAKO, ON, Canada; 019‐19741), goat anti‐rat CD45 (1/500; BD Biosciences; 553076), rabbit anti‐mouse PDGFRβ (1/250; Abcam, ON, Canada; ab32570), rat anti‐mouse endoglin (CD105) (1/250; Novus Biologicals, ON, Canada; NB100‐77666), and rabbit anti‐mouse aquaporine‐4 (AQP4) (1/500; Cell Signaling Technology, MA, USA; 59678S).

Techniques: Fluorescence, Immunolabeling, Control, Two Tailed Test, Immunofluorescence