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    Thermo Fisher cerebral microvessels
    Cerebral microvascular structural changes in rTg-DI rats. A and B: Brain sections from wild-type ( A ) and rTg-DI ( B ) rats at 12 months of age were immunolabeled with an antibody to collagen IV to identify cerebral <t>microvessels.</t> Images shown are from the thalamic region of the rats. Numerous fragmented and string vessels ( arrows ) were identified in the rTg-DI rats. C: The tortuosity of the cerebral capillaries was measured in the cortex, hippocampus, and thalamic region of wild-type and rTg-DI rats. D: The capillary area was measured in the cortex, hippocampus, and thalamic region of wild-type and rTg-DI rats. The data show that cerebral capillaries in rTg-DI rats exhibit structural abnormalities, increased tortuosity, and, in the thalamic region, increased vascularization. Data are expressed as means ± SD. n = 5 to 6 rats per group ( C and D ). ∗∗∗ P ÂÂ
    Cerebral Microvessels, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    86
    Agilent technologies microvessels
    Photomicrographs of esophageal tissue sections immunostained for Factor VIII-related antigen. A : ulcer base of vehicle-treated rat 6 days after ulcer induction. B : ulcer base of misoprostol-treated rat 6 days after ulcer induction. Specific staining (red color) is present in endothelial cells. Misoprostol treatment resulted in numerous <t>microvessels</t> with well-formed lumina in granulation tissue of esophageal ulcer base (bars = 100 μm).
    Microvessels, supplied by Agilent technologies, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 86 stars, based on 1 article reviews
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    microvessels - by Bioz Stars, 2021-03
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    86
    Abcam microvessels
    VWF structure is influenced by shear stress, flow acceleration and vessel curvature. In this figure, all of the vessels shown were activated with phorbol myristate acetate (PMA) before being perfused with buffer. ( a ) VWF deposition in a vessel segment one-fourth of the diameter of the segment that immediately precedes it. The calculated shear stress in the narrower segment was ∼3 dyn cm −2 . ( b ) VWF clumps formed in stenosed <t>microvessels</t> of small internal diameter with flow acceleration. Green: VWF and blue: nuclei. ( c , d ) z-projection of confocal images of a stimulated ‘UW' vessel. Red: CD31, green: VWF and blue: nuclei. ( d ) zoomed image of VWF structure near the narrowest region in ( c ), showing that the VWF clump blocks > 50% of the vessel cross-sectional area. ( e ) (i) Wall shear rate in the U-shaped segment of the vessel, simulated with COMSOL. White lines: streamlines; colour: shear rate; and (ii) Schematic of VWF structures along the vessels when flow converges and diverges in the region of the curve. N > 3 for each condition.
    Microvessels, supplied by Abcam, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    86
    Becton Dickinson microvessels
    Expression of PRX protein in human brain vessel fractions. Fractions of human brain from autopsy were analyzed for presence of indicated proteins. Lane 1: 293 cells transfected with L-PRX full length cDNA (encoding Genbank Protein ID AAH67266.1; purchased from OriGene); Lane 2: Human whole brain (Hwb) lysate; Lane 3: Partially purified <t>microvessel</t> proteins from human brain. Lane 1 was underloaded to avoid overloading PRX. ( A ) Western blotting of brain vessels showed expression of a protein band corresponding to the larger form of PRX (L-PRX), as seen in transfected 293 cells. As controls, the same protein lysates were probed for ( B ) vWF, ( C ) CD31, and ( D ) tubulin. Quantification of the degree of enrichment of vascular proteins in vascular fractions was computed by first calculating the ratio of the protein of interest to tubulin ( D ) and then normalizing this ratio in vessels to the ratio in human whole brain. ( E ) shows overall levels of protein enrichment in vessel fractions of multiple individuals (n = 3 for PRX and vWF and n = 2 for CD31; *indicates p
    Microvessels, supplied by Becton Dickinson, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    Cerebral microvascular structural changes in rTg-DI rats. A and B: Brain sections from wild-type ( A ) and rTg-DI ( B ) rats at 12 months of age were immunolabeled with an antibody to collagen IV to identify cerebral microvessels. Images shown are from the thalamic region of the rats. Numerous fragmented and string vessels ( arrows ) were identified in the rTg-DI rats. C: The tortuosity of the cerebral capillaries was measured in the cortex, hippocampus, and thalamic region of wild-type and rTg-DI rats. D: The capillary area was measured in the cortex, hippocampus, and thalamic region of wild-type and rTg-DI rats. The data show that cerebral capillaries in rTg-DI rats exhibit structural abnormalities, increased tortuosity, and, in the thalamic region, increased vascularization. Data are expressed as means ± SD. n = 5 to 6 rats per group ( C and D ). ∗∗∗ P ÂÂ

    Journal: The American Journal of Pathology

    Article Title: A Novel Transgenic Rat Model of Robust Cerebral Microvascular Amyloid with Prominent Vasculopathy

    doi: 10.1016/j.ajpath.2018.07.030

    Figure Lengend Snippet: Cerebral microvascular structural changes in rTg-DI rats. A and B: Brain sections from wild-type ( A ) and rTg-DI ( B ) rats at 12 months of age were immunolabeled with an antibody to collagen IV to identify cerebral microvessels. Images shown are from the thalamic region of the rats. Numerous fragmented and string vessels ( arrows ) were identified in the rTg-DI rats. C: The tortuosity of the cerebral capillaries was measured in the cortex, hippocampus, and thalamic region of wild-type and rTg-DI rats. D: The capillary area was measured in the cortex, hippocampus, and thalamic region of wild-type and rTg-DI rats. The data show that cerebral capillaries in rTg-DI rats exhibit structural abnormalities, increased tortuosity, and, in the thalamic region, increased vascularization. Data are expressed as means ± SD. n = 5 to 6 rats per group ( C and D ). ∗∗∗ P ÂÂ

    Article Snippet: Staining for fibrillar amyloid was performed using either Amylo-Glo, as described by the manufacturer (Biosensis Inc., Thebarton, SA, Australia), or thioflavin S. The following antibodies were used for immunohistochemical analysis: mAb 66.1 (1:250), which recognizes residues 1 to 5 of human Aβ ; mAb 2B4 to detect Aβ42 (1:1000) and rabbit polyclonal antibody to detect Aβ40 (1:200; Biosource, Camarillo, CA); rabbit polyclonal antibody to collagen type IV to visualize cerebral microvessels (1:100; ThermoFisher, Rockford, IL); and rabbit polyclonal antibodies to glial fibrillary acidic protein (GFAP; 1:200; Dako, Santa Clara, CA) and ionized calcium-binding adapter molecule 1 (Iba-1; 1:200; Fujifilm Wako Pure Chemical, Osaka, Japan) for detection of astrocytes and microglia, respectively.

    Techniques: Immunolabeling

    Detection of microhemorrhage by magnetic resonance imaging (MRI) in rTg-DI rats. A and B: Two-dimensional T2*-weighted MRI (echo time = 7 milliseconds; A ) matched to the corresponding Perl-stained histologic slice ( B ). A: The dense dark areas in the thalamus shown on the T2*-weighted MRI correspond to microvessels characterized by Perl stain–positive microbleeds and occluded vessels. D: Perl-stained histologic slice was overlaid on the T2*-weighted images under conditions where the histologic slice has been rendered transparent to highlight the low signal intensity susceptibility features on the T2*-weighted MRI observed bilaterally in the thalamus, which is caused by presence of hemosiderin. C and E: Higher magnifications of the boxed areas in B and D , respectively. F and G: Three-dimensional volume-rendered MRIs of the same rat showing the brain outlined in light yellow; and the Perl stain–positive associated low signal intensity area in the thalamus has been volume rendered (green) to illustrate the near-perfect symmetry of the microhemorrhage/occluded microvessel areas. Scale bars: 100 μm ( C and E ); 500 μm ( A , B , and D ); 3.5 mm ( F and G ).

    Journal: The American Journal of Pathology

    Article Title: A Novel Transgenic Rat Model of Robust Cerebral Microvascular Amyloid with Prominent Vasculopathy

    doi: 10.1016/j.ajpath.2018.07.030

    Figure Lengend Snippet: Detection of microhemorrhage by magnetic resonance imaging (MRI) in rTg-DI rats. A and B: Two-dimensional T2*-weighted MRI (echo time = 7 milliseconds; A ) matched to the corresponding Perl-stained histologic slice ( B ). A: The dense dark areas in the thalamus shown on the T2*-weighted MRI correspond to microvessels characterized by Perl stain–positive microbleeds and occluded vessels. D: Perl-stained histologic slice was overlaid on the T2*-weighted images under conditions where the histologic slice has been rendered transparent to highlight the low signal intensity susceptibility features on the T2*-weighted MRI observed bilaterally in the thalamus, which is caused by presence of hemosiderin. C and E: Higher magnifications of the boxed areas in B and D , respectively. F and G: Three-dimensional volume-rendered MRIs of the same rat showing the brain outlined in light yellow; and the Perl stain–positive associated low signal intensity area in the thalamus has been volume rendered (green) to illustrate the near-perfect symmetry of the microhemorrhage/occluded microvessel areas. Scale bars: 100 μm ( C and E ); 500 μm ( A , B , and D ); 3.5 mm ( F and G ).

    Article Snippet: Staining for fibrillar amyloid was performed using either Amylo-Glo, as described by the manufacturer (Biosensis Inc., Thebarton, SA, Australia), or thioflavin S. The following antibodies were used for immunohistochemical analysis: mAb 66.1 (1:250), which recognizes residues 1 to 5 of human Aβ ; mAb 2B4 to detect Aβ42 (1:1000) and rabbit polyclonal antibody to detect Aβ40 (1:200; Biosource, Camarillo, CA); rabbit polyclonal antibody to collagen type IV to visualize cerebral microvessels (1:100; ThermoFisher, Rockford, IL); and rabbit polyclonal antibodies to glial fibrillary acidic protein (GFAP; 1:200; Dako, Santa Clara, CA) and ionized calcium-binding adapter molecule 1 (Iba-1; 1:200; Fujifilm Wako Pure Chemical, Osaka, Japan) for detection of astrocytes and microglia, respectively.

    Techniques: Magnetic Resonance Imaging, Staining

    Analysis of cerebral microvascular Aβ deposition in rTg-DI rats. A–C: Brain sections from rTg-DI rats at 12 months of age were immunolabeled with an antibody specific for Aβ40 (red; A ) and an antibody specific for Aβ42 (green; B ) and merged ( C ). D: Cerebral microvessels were isolated from 12-month–old rTg-DI rats, stained with thioflavin S to visualize fibrillar amyloid deposits (green), and immunolabeled with an antibody to collagen IV to view the cerebral microvessels (red). E: Cerebral microvascular amyloid deposits after digestion and removal of the capillaries and stained for fibrillar amyloid using thioflavin S (green). F: Enzyme-linked immunosorbent assay measurements were performed to determine the amounts of Aβ40 and Aβ42 in the microvessels isolated from rTg-DI rat brain. G: Fourier transform infrared (FTIR) spectra in the region of the amide I vibration of vascular amyloid isolated from vessels of rTg-DI rat brain. H: Thioflavin T fluorescence of fibril formation from seeds obtained from isolated vascular amyloid. Thioflavin fluorescence increases rapidly on the addition of 100 μmol/L Aβ40–wild-type (WT) monomer to sonicated vascular amyloid (black). Monomeric Aβ40-WT peptide exhibits a much slower increase in fluorescence in the absence of fibril seeds (blue). I: FTIR spectra in the region of the amide I vibration of Aβ40-WT fibrils produced from seeds of the rat vascular amyloid. The amide I vibration at 1632/cm corresponds to β-sheet. The vibration at 1607/cm corresponds to the amide vibration shifted as a result of 13 C=O labels at the backbone carbonyls of Leu17, Ala21, Gly33, and Gly37. The large intensity of the 1607/cm band relative to the β-sheet vibration at 1632/cm is characteristic of antiparallel β-sheet structure. The spectra were obtained after incubation for 48 hours at 37°C. Data are expressed as means ± SD ( F ). n = 5 rTg-DI rats ( F ). Scale bars = 50 μm ( A–E ). AU, arbitrary unit.

    Journal: The American Journal of Pathology

    Article Title: A Novel Transgenic Rat Model of Robust Cerebral Microvascular Amyloid with Prominent Vasculopathy

    doi: 10.1016/j.ajpath.2018.07.030

    Figure Lengend Snippet: Analysis of cerebral microvascular Aβ deposition in rTg-DI rats. A–C: Brain sections from rTg-DI rats at 12 months of age were immunolabeled with an antibody specific for Aβ40 (red; A ) and an antibody specific for Aβ42 (green; B ) and merged ( C ). D: Cerebral microvessels were isolated from 12-month–old rTg-DI rats, stained with thioflavin S to visualize fibrillar amyloid deposits (green), and immunolabeled with an antibody to collagen IV to view the cerebral microvessels (red). E: Cerebral microvascular amyloid deposits after digestion and removal of the capillaries and stained for fibrillar amyloid using thioflavin S (green). F: Enzyme-linked immunosorbent assay measurements were performed to determine the amounts of Aβ40 and Aβ42 in the microvessels isolated from rTg-DI rat brain. G: Fourier transform infrared (FTIR) spectra in the region of the amide I vibration of vascular amyloid isolated from vessels of rTg-DI rat brain. H: Thioflavin T fluorescence of fibril formation from seeds obtained from isolated vascular amyloid. Thioflavin fluorescence increases rapidly on the addition of 100 μmol/L Aβ40–wild-type (WT) monomer to sonicated vascular amyloid (black). Monomeric Aβ40-WT peptide exhibits a much slower increase in fluorescence in the absence of fibril seeds (blue). I: FTIR spectra in the region of the amide I vibration of Aβ40-WT fibrils produced from seeds of the rat vascular amyloid. The amide I vibration at 1632/cm corresponds to β-sheet. The vibration at 1607/cm corresponds to the amide vibration shifted as a result of 13 C=O labels at the backbone carbonyls of Leu17, Ala21, Gly33, and Gly37. The large intensity of the 1607/cm band relative to the β-sheet vibration at 1632/cm is characteristic of antiparallel β-sheet structure. The spectra were obtained after incubation for 48 hours at 37°C. Data are expressed as means ± SD ( F ). n = 5 rTg-DI rats ( F ). Scale bars = 50 μm ( A–E ). AU, arbitrary unit.

    Article Snippet: Staining for fibrillar amyloid was performed using either Amylo-Glo, as described by the manufacturer (Biosensis Inc., Thebarton, SA, Australia), or thioflavin S. The following antibodies were used for immunohistochemical analysis: mAb 66.1 (1:250), which recognizes residues 1 to 5 of human Aβ ; mAb 2B4 to detect Aβ42 (1:1000) and rabbit polyclonal antibody to detect Aβ40 (1:200; Biosource, Camarillo, CA); rabbit polyclonal antibody to collagen type IV to visualize cerebral microvessels (1:100; ThermoFisher, Rockford, IL); and rabbit polyclonal antibodies to glial fibrillary acidic protein (GFAP; 1:200; Dako, Santa Clara, CA) and ionized calcium-binding adapter molecule 1 (Iba-1; 1:200; Fujifilm Wako Pure Chemical, Osaka, Japan) for detection of astrocytes and microglia, respectively.

    Techniques: Immunolabeling, Isolation, Staining, Enzyme-linked Immunosorbent Assay, Fluorescence, Sonication, Produced, Incubation

    Progressive cerebral microvascular occlusions in rTg-DI rats. A: Twelve-month–old brain sections from rTg-DI rats were stained for hemosiderin to identify microhemorrhages (blue) and counterstained with pararosaniline (pink) in the thalamus. B: Adjacent tissue sections were stained for calcium (black) and counterstained with pararosaniline (pink) in the thalamus. C: Lower magnification revealed that the occluded, calcified microvessels were restricted to the thalamic region. D: The number of thalamic microvessel occlusions was counted in progressively aged rTg-DI rats. Numerous occluded capillaries/microvessels were observed around microbleeds specifically in the thalamic region of rTg-DI rats. Data are expressed as means ± SD. n = 5 to 6 rTg-DI rats per group ( D ). Scale bars: 50 μm ( A and B ); 200 μm ( C ).

    Journal: The American Journal of Pathology

    Article Title: A Novel Transgenic Rat Model of Robust Cerebral Microvascular Amyloid with Prominent Vasculopathy

    doi: 10.1016/j.ajpath.2018.07.030

    Figure Lengend Snippet: Progressive cerebral microvascular occlusions in rTg-DI rats. A: Twelve-month–old brain sections from rTg-DI rats were stained for hemosiderin to identify microhemorrhages (blue) and counterstained with pararosaniline (pink) in the thalamus. B: Adjacent tissue sections were stained for calcium (black) and counterstained with pararosaniline (pink) in the thalamus. C: Lower magnification revealed that the occluded, calcified microvessels were restricted to the thalamic region. D: The number of thalamic microvessel occlusions was counted in progressively aged rTg-DI rats. Numerous occluded capillaries/microvessels were observed around microbleeds specifically in the thalamic region of rTg-DI rats. Data are expressed as means ± SD. n = 5 to 6 rTg-DI rats per group ( D ). Scale bars: 50 μm ( A and B ); 200 μm ( C ).

    Article Snippet: Staining for fibrillar amyloid was performed using either Amylo-Glo, as described by the manufacturer (Biosensis Inc., Thebarton, SA, Australia), or thioflavin S. The following antibodies were used for immunohistochemical analysis: mAb 66.1 (1:250), which recognizes residues 1 to 5 of human Aβ ; mAb 2B4 to detect Aβ42 (1:1000) and rabbit polyclonal antibody to detect Aβ40 (1:200; Biosource, Camarillo, CA); rabbit polyclonal antibody to collagen type IV to visualize cerebral microvessels (1:100; ThermoFisher, Rockford, IL); and rabbit polyclonal antibodies to glial fibrillary acidic protein (GFAP; 1:200; Dako, Santa Clara, CA) and ionized calcium-binding adapter molecule 1 (Iba-1; 1:200; Fujifilm Wako Pure Chemical, Osaka, Japan) for detection of astrocytes and microglia, respectively.

    Techniques: Staining

    Progressive accumulation of microvascular cerebral amyloid angiopathy in rTg-DI rats. A–I: Brain sections from rTg-DI rats at 3 months ( A–C ), 6 months ( D–F ), and 12 months ( G–I ) of age were stained for fibrillar amyloid using thioflavin S (green) and immunolabeled for collagen type IV (coll IV) to identify cerebral microvessels (red). The rTg-DI rats develop early-onset and progressive cerebral microvascular fibrillar amyloid in the cortical, hippocampal, and thalamic regions. J: Quantitation of microvascular thioflavin S–positive amyloid load in different brain regions of 3-month–old (blue bars), 6-month–old (gray bars), and 12-month–old (red bars) rTg-DI rats. K: rTg-DI rats show consistently fewer return approaches within a session to four novel objects placed in an open field arena compared with wild-type rats at 3 and 12 months of age. Data are expressed as means ± SD. n = 6 to 7 rTg-DI rats per group ( J and K ). ∗ P ÂÂ

    Journal: The American Journal of Pathology

    Article Title: A Novel Transgenic Rat Model of Robust Cerebral Microvascular Amyloid with Prominent Vasculopathy

    doi: 10.1016/j.ajpath.2018.07.030

    Figure Lengend Snippet: Progressive accumulation of microvascular cerebral amyloid angiopathy in rTg-DI rats. A–I: Brain sections from rTg-DI rats at 3 months ( A–C ), 6 months ( D–F ), and 12 months ( G–I ) of age were stained for fibrillar amyloid using thioflavin S (green) and immunolabeled for collagen type IV (coll IV) to identify cerebral microvessels (red). The rTg-DI rats develop early-onset and progressive cerebral microvascular fibrillar amyloid in the cortical, hippocampal, and thalamic regions. J: Quantitation of microvascular thioflavin S–positive amyloid load in different brain regions of 3-month–old (blue bars), 6-month–old (gray bars), and 12-month–old (red bars) rTg-DI rats. K: rTg-DI rats show consistently fewer return approaches within a session to four novel objects placed in an open field arena compared with wild-type rats at 3 and 12 months of age. Data are expressed as means ± SD. n = 6 to 7 rTg-DI rats per group ( J and K ). ∗ P ÂÂ

    Article Snippet: Staining for fibrillar amyloid was performed using either Amylo-Glo, as described by the manufacturer (Biosensis Inc., Thebarton, SA, Australia), or thioflavin S. The following antibodies were used for immunohistochemical analysis: mAb 66.1 (1:250), which recognizes residues 1 to 5 of human Aβ ; mAb 2B4 to detect Aβ42 (1:1000) and rabbit polyclonal antibody to detect Aβ40 (1:200; Biosource, Camarillo, CA); rabbit polyclonal antibody to collagen type IV to visualize cerebral microvessels (1:100; ThermoFisher, Rockford, IL); and rabbit polyclonal antibodies to glial fibrillary acidic protein (GFAP; 1:200; Dako, Santa Clara, CA) and ionized calcium-binding adapter molecule 1 (Iba-1; 1:200; Fujifilm Wako Pure Chemical, Osaka, Japan) for detection of astrocytes and microglia, respectively.

    Techniques: Staining, Immunolabeling, Quantitation Assay

    Perivascular glial activation in rTg-DI rats. Twelve-month–old brain sections from wild-type ( A and C ) and rTg-DI ( B and D ) rats were stained for fibrillar amyloid (blue), immunolabeled with an antibody to collagen IV (coll IV) to identify cerebral microvessels (red), and immunolabeled with an antibody to glial fibrillary acidic protein (GFAP) to identify astrocytes (green; A and B ) or immunolabeled with an antibody to Iba-1 to identify microglia (green; C and D ). rTg-DI rats exhibit strong increases in perivascular reactive astrocytes and activated microglia in response to the prominent cerebral microvascular amyloid. Scale bars = 50 μm ( A–D ).

    Journal: The American Journal of Pathology

    Article Title: A Novel Transgenic Rat Model of Robust Cerebral Microvascular Amyloid with Prominent Vasculopathy

    doi: 10.1016/j.ajpath.2018.07.030

    Figure Lengend Snippet: Perivascular glial activation in rTg-DI rats. Twelve-month–old brain sections from wild-type ( A and C ) and rTg-DI ( B and D ) rats were stained for fibrillar amyloid (blue), immunolabeled with an antibody to collagen IV (coll IV) to identify cerebral microvessels (red), and immunolabeled with an antibody to glial fibrillary acidic protein (GFAP) to identify astrocytes (green; A and B ) or immunolabeled with an antibody to Iba-1 to identify microglia (green; C and D ). rTg-DI rats exhibit strong increases in perivascular reactive astrocytes and activated microglia in response to the prominent cerebral microvascular amyloid. Scale bars = 50 μm ( A–D ).

    Article Snippet: Staining for fibrillar amyloid was performed using either Amylo-Glo, as described by the manufacturer (Biosensis Inc., Thebarton, SA, Australia), or thioflavin S. The following antibodies were used for immunohistochemical analysis: mAb 66.1 (1:250), which recognizes residues 1 to 5 of human Aβ ; mAb 2B4 to detect Aβ42 (1:1000) and rabbit polyclonal antibody to detect Aβ40 (1:200; Biosource, Camarillo, CA); rabbit polyclonal antibody to collagen type IV to visualize cerebral microvessels (1:100; ThermoFisher, Rockford, IL); and rabbit polyclonal antibodies to glial fibrillary acidic protein (GFAP; 1:200; Dako, Santa Clara, CA) and ionized calcium-binding adapter molecule 1 (Iba-1; 1:200; Fujifilm Wako Pure Chemical, Osaka, Japan) for detection of astrocytes and microglia, respectively.

    Techniques: Activation Assay, Staining, Immunolabeling

    Photomicrographs of esophageal tissue sections immunostained for Factor VIII-related antigen. A : ulcer base of vehicle-treated rat 6 days after ulcer induction. B : ulcer base of misoprostol-treated rat 6 days after ulcer induction. Specific staining (red color) is present in endothelial cells. Misoprostol treatment resulted in numerous microvessels with well-formed lumina in granulation tissue of esophageal ulcer base (bars = 100 μm).

    Journal: American Journal of Physiology - Gastrointestinal and Liver Physiology

    Article Title: Novel mechanisms and signaling pathways of esophageal ulcer healing: the role of prostaglandin EP2 receptors, cAMP, and pCREB

    doi: 10.1152/ajpgi.00177.2014

    Figure Lengend Snippet: Photomicrographs of esophageal tissue sections immunostained for Factor VIII-related antigen. A : ulcer base of vehicle-treated rat 6 days after ulcer induction. B : ulcer base of misoprostol-treated rat 6 days after ulcer induction. Specific staining (red color) is present in endothelial cells. Misoprostol treatment resulted in numerous microvessels with well-formed lumina in granulation tissue of esophageal ulcer base (bars = 100 μm).

    Article Snippet: To identify microvessels, enhanced polymer one-step staining ( ) with mouse monoclonal anti-factor VIII-related antigen (Factor VIII RA) antibody (Dako, Carpenteria, CA), which specifically detects endothelial cells, was employed.

    Techniques: Staining

    Misoprostol accelerates esophageal ulcer healing and stimulates angiogenesis. Rats were treated intragastrically twice daily with either 50 μg/kg misoprostol or its vehicle for 3 or 6 days starting 3 days after ulcer induction. A : ulcer healing dynamics. Ulcer area was measured by a computerized video analysis of the ulcer images. The results are expressed as a percentage of ulcer area at day 3 . Misoprostol treatment significantly reduced ulcer area, reflecting increased esophageal ulcer healing in rats. B : microvessel density in granulation tissue at the ulcer base. The results are expressed as the number of microvessels per square millimeter of granulation tissue section (n/mm 2 ). Misoprostol treatment significantly increased microvessel density (reflecting angiogenesis) in granulation tissue at the esophageal ulcer base. C : proliferating cell nuclear antigen (PCNA) labeling index (LI) in the epithelium at the ulcer margin. The results are expressed as the percentage of increase in the number of labeled cells in the epithelium of the ulcer margin over the number of labeled cells in the epithelium distant from the ulcer. Misoprostol treatment slightly increased epithelial cell proliferation at the esophageal ulcer margin. NS, not significant. Values are means ± SD. For each column ( n = 6).

    Journal: American Journal of Physiology - Gastrointestinal and Liver Physiology

    Article Title: Novel mechanisms and signaling pathways of esophageal ulcer healing: the role of prostaglandin EP2 receptors, cAMP, and pCREB

    doi: 10.1152/ajpgi.00177.2014

    Figure Lengend Snippet: Misoprostol accelerates esophageal ulcer healing and stimulates angiogenesis. Rats were treated intragastrically twice daily with either 50 μg/kg misoprostol or its vehicle for 3 or 6 days starting 3 days after ulcer induction. A : ulcer healing dynamics. Ulcer area was measured by a computerized video analysis of the ulcer images. The results are expressed as a percentage of ulcer area at day 3 . Misoprostol treatment significantly reduced ulcer area, reflecting increased esophageal ulcer healing in rats. B : microvessel density in granulation tissue at the ulcer base. The results are expressed as the number of microvessels per square millimeter of granulation tissue section (n/mm 2 ). Misoprostol treatment significantly increased microvessel density (reflecting angiogenesis) in granulation tissue at the esophageal ulcer base. C : proliferating cell nuclear antigen (PCNA) labeling index (LI) in the epithelium at the ulcer margin. The results are expressed as the percentage of increase in the number of labeled cells in the epithelium of the ulcer margin over the number of labeled cells in the epithelium distant from the ulcer. Misoprostol treatment slightly increased epithelial cell proliferation at the esophageal ulcer margin. NS, not significant. Values are means ± SD. For each column ( n = 6).

    Article Snippet: To identify microvessels, enhanced polymer one-step staining ( ) with mouse monoclonal anti-factor VIII-related antigen (Factor VIII RA) antibody (Dako, Carpenteria, CA), which specifically detects endothelial cells, was employed.

    Techniques: Labeling

    VWF structure is influenced by shear stress, flow acceleration and vessel curvature. In this figure, all of the vessels shown were activated with phorbol myristate acetate (PMA) before being perfused with buffer. ( a ) VWF deposition in a vessel segment one-fourth of the diameter of the segment that immediately precedes it. The calculated shear stress in the narrower segment was ∼3 dyn cm −2 . ( b ) VWF clumps formed in stenosed microvessels of small internal diameter with flow acceleration. Green: VWF and blue: nuclei. ( c , d ) z-projection of confocal images of a stimulated ‘UW' vessel. Red: CD31, green: VWF and blue: nuclei. ( d ) zoomed image of VWF structure near the narrowest region in ( c ), showing that the VWF clump blocks > 50% of the vessel cross-sectional area. ( e ) (i) Wall shear rate in the U-shaped segment of the vessel, simulated with COMSOL. White lines: streamlines; colour: shear rate; and (ii) Schematic of VWF structures along the vessels when flow converges and diverges in the region of the curve. N > 3 for each condition.

    Journal: Nature Communications

    Article Title: Flow-driven assembly of VWF fibres and webs in in vitro microvessels

    doi: 10.1038/ncomms8858

    Figure Lengend Snippet: VWF structure is influenced by shear stress, flow acceleration and vessel curvature. In this figure, all of the vessels shown were activated with phorbol myristate acetate (PMA) before being perfused with buffer. ( a ) VWF deposition in a vessel segment one-fourth of the diameter of the segment that immediately precedes it. The calculated shear stress in the narrower segment was ∼3 dyn cm −2 . ( b ) VWF clumps formed in stenosed microvessels of small internal diameter with flow acceleration. Green: VWF and blue: nuclei. ( c , d ) z-projection of confocal images of a stimulated ‘UW' vessel. Red: CD31, green: VWF and blue: nuclei. ( d ) zoomed image of VWF structure near the narrowest region in ( c ), showing that the VWF clump blocks > 50% of the vessel cross-sectional area. ( e ) (i) Wall shear rate in the U-shaped segment of the vessel, simulated with COMSOL. White lines: streamlines; colour: shear rate; and (ii) Schematic of VWF structures along the vessels when flow converges and diverges in the region of the curve. N > 3 for each condition.

    Article Snippet: After the live-imaging experiment, the microvessels were immediately washed with PBS then fixed and stained for an endothelial marker (CD31, 1:50 dilution, Abcam) for further imaging.

    Techniques: Flow Cytometry

    Assembly of VWF strands depends on vessel diameter and turns. ( a , b ) Secreted VWF from the activated endothelium formed strands along the direction of flow on a single straight vessel with a diameter of 500 μm ( b . zoomed-in view of A, showing neighbouring parallel VWF fibres assembled to thicker strands). ( c , d ) Secreted VWF near the luminal wall of a vessel with diameter of 150 μm, ( c ) multiple strands from one or two cells converged to one thicker strand and ( d ) VWF strands follow the major direction of flow, but show some deviation due to surface irregularities. ( e ) VWF strands follow vessel turns, changing directions and remaining bound to the vessel wall in a 500-μm diameter vessel. ( f ) VWF strands remain bound to the vessel wall in a tortuous vessel with a diameter of 500 μm. Arrowheads: individual VWF strands self-associated into thicker strands in regions of high shear stress; asterisks: regions of low shear stress lack VWF strands; green: VWF, blue: nuclei. The upper left corner of the panel shows the COMSOL simulation of flow streamlines (white lines) and shear rate colour map at the cross-sectional plane with a distance to the bottom wall of 5% of the vessel diameter. ( g ) z-stack projection and cross-sectional view of confocal image of VWF transluminal bundles through microvessels of diameter

    Journal: Nature Communications

    Article Title: Flow-driven assembly of VWF fibres and webs in in vitro microvessels

    doi: 10.1038/ncomms8858

    Figure Lengend Snippet: Assembly of VWF strands depends on vessel diameter and turns. ( a , b ) Secreted VWF from the activated endothelium formed strands along the direction of flow on a single straight vessel with a diameter of 500 μm ( b . zoomed-in view of A, showing neighbouring parallel VWF fibres assembled to thicker strands). ( c , d ) Secreted VWF near the luminal wall of a vessel with diameter of 150 μm, ( c ) multiple strands from one or two cells converged to one thicker strand and ( d ) VWF strands follow the major direction of flow, but show some deviation due to surface irregularities. ( e ) VWF strands follow vessel turns, changing directions and remaining bound to the vessel wall in a 500-μm diameter vessel. ( f ) VWF strands remain bound to the vessel wall in a tortuous vessel with a diameter of 500 μm. Arrowheads: individual VWF strands self-associated into thicker strands in regions of high shear stress; asterisks: regions of low shear stress lack VWF strands; green: VWF, blue: nuclei. The upper left corner of the panel shows the COMSOL simulation of flow streamlines (white lines) and shear rate colour map at the cross-sectional plane with a distance to the bottom wall of 5% of the vessel diameter. ( g ) z-stack projection and cross-sectional view of confocal image of VWF transluminal bundles through microvessels of diameter

    Article Snippet: After the live-imaging experiment, the microvessels were immediately washed with PBS then fixed and stained for an endothelial marker (CD31, 1:50 dilution, Abcam) for further imaging.

    Techniques: Flow Cytometry

    Effect of ADAMTS13 on VWF strand structure and thrombus formation. ( a , b ) PMA-stimulated microvessels in the presence of normal human plasma ( a ) or plasma from a TTP patient with 5% ADAMTS13 activity ( b ). The left panels in a and b show accumulated vessel wall VWF, and the right panels show zoomed-in views with vessel-wall staining also shown. Green: VWF, red: CD31 and blue: nuclei. ( c ) Comparison of length range of VWF strands from PMA-stimulated vessels perfused with: PBS, recombinant ADAMTS13, normal plasma or TTP plasma. *** P

    Journal: Nature Communications

    Article Title: Flow-driven assembly of VWF fibres and webs in in vitro microvessels

    doi: 10.1038/ncomms8858

    Figure Lengend Snippet: Effect of ADAMTS13 on VWF strand structure and thrombus formation. ( a , b ) PMA-stimulated microvessels in the presence of normal human plasma ( a ) or plasma from a TTP patient with 5% ADAMTS13 activity ( b ). The left panels in a and b show accumulated vessel wall VWF, and the right panels show zoomed-in views with vessel-wall staining also shown. Green: VWF, red: CD31 and blue: nuclei. ( c ) Comparison of length range of VWF strands from PMA-stimulated vessels perfused with: PBS, recombinant ADAMTS13, normal plasma or TTP plasma. *** P

    Article Snippet: After the live-imaging experiment, the microvessels were immediately washed with PBS then fixed and stained for an endothelial marker (CD31, 1:50 dilution, Abcam) for further imaging.

    Techniques: Activity Assay, Staining, Recombinant

    Microvessel system. ( a ) Schematic of the microvessel system in collagen gels. ( b ) Schematics of the different microvessel geometries: straight vessel, grid network, tortuous vessels, stenosed vessels and geometries using fonts or symbols. ( c ) Endothelial cells from a vessel that forms a large straight channel. Note the abundant VWF in Weibel–Palade bodies. Red: CD31, green: VWF and blue: nuclei. ( d ) z-projection of confocal sections of endothelialized grid microvessel networks and its cross-sectional view (right panel). ( e ) z-projection of confocal sections of endothelialized tortuous microvessels and cross-sectional views (bottom). Red: CD31 and blue: nuclei. Number of replicates for each type of vessel > 10.

    Journal: Nature Communications

    Article Title: Flow-driven assembly of VWF fibres and webs in in vitro microvessels

    doi: 10.1038/ncomms8858

    Figure Lengend Snippet: Microvessel system. ( a ) Schematic of the microvessel system in collagen gels. ( b ) Schematics of the different microvessel geometries: straight vessel, grid network, tortuous vessels, stenosed vessels and geometries using fonts or symbols. ( c ) Endothelial cells from a vessel that forms a large straight channel. Note the abundant VWF in Weibel–Palade bodies. Red: CD31, green: VWF and blue: nuclei. ( d ) z-projection of confocal sections of endothelialized grid microvessel networks and its cross-sectional view (right panel). ( e ) z-projection of confocal sections of endothelialized tortuous microvessels and cross-sectional views (bottom). Red: CD31 and blue: nuclei. Number of replicates for each type of vessel > 10.

    Article Snippet: After the live-imaging experiment, the microvessels were immediately washed with PBS then fixed and stained for an endothelial marker (CD31, 1:50 dilution, Abcam) for further imaging.

    Techniques:

    Effect of VWF antibody on platelet binding and thrombi formation. ( a ) VWF, when labelled with antibodies, resisted being cleaved by ADAMTS13 and trapped blood cells including platelets and leukocytes. ( b , c ) Zoomed images of microvessels in the dashed box in a , showing VWF fibres with bound platelet and leukocytes in the vessel lumen after 30 min of blood perfusion. (i) Bright-field images and (ii,iii) immunofluorescence projected z-stack images. In particular, (bii), (biii) and (cii) were z-stack projected images of planes from the centre plane to the wall, and (ciii) was z-stack projected image of centre planes of 20 μm thickness. Red: CD31, green: VWF, magenta: CD41a and blue: nuclei. N > 3.

    Journal: Nature Communications

    Article Title: Flow-driven assembly of VWF fibres and webs in in vitro microvessels

    doi: 10.1038/ncomms8858

    Figure Lengend Snippet: Effect of VWF antibody on platelet binding and thrombi formation. ( a ) VWF, when labelled with antibodies, resisted being cleaved by ADAMTS13 and trapped blood cells including platelets and leukocytes. ( b , c ) Zoomed images of microvessels in the dashed box in a , showing VWF fibres with bound platelet and leukocytes in the vessel lumen after 30 min of blood perfusion. (i) Bright-field images and (ii,iii) immunofluorescence projected z-stack images. In particular, (bii), (biii) and (cii) were z-stack projected images of planes from the centre plane to the wall, and (ciii) was z-stack projected image of centre planes of 20 μm thickness. Red: CD31, green: VWF, magenta: CD41a and blue: nuclei. N > 3.

    Article Snippet: After the live-imaging experiment, the microvessels were immediately washed with PBS then fixed and stained for an endothelial marker (CD31, 1:50 dilution, Abcam) for further imaging.

    Techniques: Binding Assay, Immunofluorescence

    Expression of PRX protein in human brain vessel fractions. Fractions of human brain from autopsy were analyzed for presence of indicated proteins. Lane 1: 293 cells transfected with L-PRX full length cDNA (encoding Genbank Protein ID AAH67266.1; purchased from OriGene); Lane 2: Human whole brain (Hwb) lysate; Lane 3: Partially purified microvessel proteins from human brain. Lane 1 was underloaded to avoid overloading PRX. ( A ) Western blotting of brain vessels showed expression of a protein band corresponding to the larger form of PRX (L-PRX), as seen in transfected 293 cells. As controls, the same protein lysates were probed for ( B ) vWF, ( C ) CD31, and ( D ) tubulin. Quantification of the degree of enrichment of vascular proteins in vascular fractions was computed by first calculating the ratio of the protein of interest to tubulin ( D ) and then normalizing this ratio in vessels to the ratio in human whole brain. ( E ) shows overall levels of protein enrichment in vessel fractions of multiple individuals (n = 3 for PRX and vWF and n = 2 for CD31; *indicates p

    Journal: Scientific Reports

    Article Title: Expression of periaxin (PRX) specifically in the human cerebrovascular system: PDZ domain-mediated strengthening of endothelial barrier function

    doi: 10.1038/s41598-018-28190-7

    Figure Lengend Snippet: Expression of PRX protein in human brain vessel fractions. Fractions of human brain from autopsy were analyzed for presence of indicated proteins. Lane 1: 293 cells transfected with L-PRX full length cDNA (encoding Genbank Protein ID AAH67266.1; purchased from OriGene); Lane 2: Human whole brain (Hwb) lysate; Lane 3: Partially purified microvessel proteins from human brain. Lane 1 was underloaded to avoid overloading PRX. ( A ) Western blotting of brain vessels showed expression of a protein band corresponding to the larger form of PRX (L-PRX), as seen in transfected 293 cells. As controls, the same protein lysates were probed for ( B ) vWF, ( C ) CD31, and ( D ) tubulin. Quantification of the degree of enrichment of vascular proteins in vascular fractions was computed by first calculating the ratio of the protein of interest to tubulin ( D ) and then normalizing this ratio in vessels to the ratio in human whole brain. ( E ) shows overall levels of protein enrichment in vessel fractions of multiple individuals (n = 3 for PRX and vWF and n = 2 for CD31; *indicates p

    Article Snippet: The microvessels were then passed through 70 μM nylon mesh cell strainers (BD Falcon).

    Techniques: Expressing, Transfection, Purification, Western Blot, Protein Enrichment