Journal: Biology of reproduction

Article Title: Distribution of immune cells in the epididymis of the aging Brown Norway rat is segment-specific and related to the luminal content.

doi: 10.1095/biolreprod61.3.705

Figure Lengend Snippet: FIG. 1. Light micrographs showing sec- tions of the epididymis of the Brown Nor- way rat stained with an antibody for monocytes-macrophages (ED1). A–C) Cor- pus, D–F) distal cauda. A, D) 3 mo, B, E) 18 mo with numerous spermatozoa in the lumen, C, F) 18 mo with occasional sper- matozoa in the lumen. lu, Lumen; it, inter- tubular space; p, principal cells; b, basal cells; c, clear cells; bm, basement mem- brane. Arrows, ED1-positive cells; aster- isks, halo cells. Scale bar, A–F 5 64 mm.

Article Snippet: Mouse anti-rat ED1 (Serotec USA, Washington, DC) was used at a dilution 1/100; this antibody recognizes a cytoplasmic antigen in monocytes and most macrophages.

Techniques: Staining

Journal: Biology of reproduction

Article Title: Distribution of immune cells in the epididymis of the aging Brown Norway rat is segment-specific and related to the luminal content.

doi: 10.1095/biolreprod61.3.705

Figure Lengend Snippet: FIG. 5. Light micrographs showing sec- tions of the corpus of the epididymis of Brown Norway rats. A, C) Three mo; B, D) 18 mo. Section stained with an antibody for A and B GST Yf and C and D ED1. Clear arrows, basal cells; dark arrows, ED1-positive cells; other labels as in Fig- ure 1. Scale bar, A–D 5 64 mm.

Article Snippet: Mouse anti-rat ED1 (Serotec USA, Washington, DC) was used at a dilution 1/100; this antibody recognizes a cytoplasmic antigen in monocytes and most macrophages.

Techniques: Staining

Journal: Brain Sciences

Article Title: Potential for Cell-Mediated Immune Responses in Mouse Models of Pelizaeus-Merzbacher Disease

doi: 10.3390/brainsci3041417

Figure Lengend Snippet: White matter microglia/macrophages are activated in the dorsal funiculi of male Plp1 mutant mice. Cervical spinal cord sections from ( A ) mildly-affected P16 rsh ( B ) severely-affected P16 msd ( C ) subclinical P25 Plp1 #66 heterozygous ( D ) moderately-affected P25 Plp1 #66 homozygous mice labeled with antibodies against Iba-1 (red) and CD68 (green). Many Iba-1 positive microglia/macrophages with swollen cell bodies and short processes are labeled with anti-CD68 antibodies in rsh and msd mice, which is indicative of activated cells. The insets in these panels show the canonical activated morphology revealed with anti-Iba-1 antibodies and strong CD68 staining. In contrast, there is little evidence for broad CD68 labeling in Plp1 #66 heterozygous mice in panel C, which is consistent with previous data that immune cells are rarely activated . Activation of microglia/macrophages is apparent for Plp1 #66 homozygous mice in panel D, which exhibit an intermediate level of CD68 labeling. Scale bar: 95 μm, insets 15 μm.

Article Snippet: Antibodies used were: mouse anti-MBP (1:1000, SMI99, Sternberger Monoclonal Inc., Baltimore, MD, USA); rabbit anti-Iba-1; monoclonal anti-human CD68 antibody (clone 514H12, AbD Serotec, Oxford, UK).

Techniques: Mutagenesis, Labeling, Staining, Activation Assay

Journal: Brain Sciences

Article Title: Potential for Cell-Mediated Immune Responses in Mouse Models of Pelizaeus-Merzbacher Disease

doi: 10.3390/brainsci3041417

Figure Lengend Snippet: Proportion of cervical spinal cord Iba-1 + microglia/macrophages in dorsal column, ventral column and lateral funiculus that are activated (CD68 + ).

Article Snippet: Antibodies used were: mouse anti-MBP (1:1000, SMI99, Sternberger Monoclonal Inc., Baltimore, MD, USA); rabbit anti-Iba-1; monoclonal anti-human CD68 antibody (clone 514H12, AbD Serotec, Oxford, UK).

Techniques:

Journal: Brain Sciences

Article Title: Potential for Cell-Mediated Immune Responses in Mouse Models of Pelizaeus-Merzbacher Disease

doi: 10.3390/brainsci3041417

Figure Lengend Snippet: Oligodendrocytes in gray matter from P16 rsh and msd mice do not undergo a UPR and microglia/macrophages exhibit resting morphology. ( A – C ) Iba1 (red) and CD68 (green) antibody labeling in dorsal spinal cord white matter tracts of P16 wild type ( A ) rsh ( B ) and msd ( C ) mice. Although the morphology and CD68 staining is characteristic of resting microglia/macrophages in wild type mice (white arrowheads), these cells are activated in the Plp1 mutants. ( D – F ) In contrast to white matter regions, microglia/macrophages have a resting state phenotype in the adjacent substantia gelatinosa (gray matter) from wild type and mutant mice (black arrowheads). ( G – I ) A major difference between these regions in rsh and msd mice is the relative abundance of oligodendrocytes undergoing an unfolded protein response (UPR), which is evident by the large number of CHOP + cells (green) in white matter (above the dotted line) compared to gray matter (below). We have previously shown that 100% of CHOP + cells in these mutants are oligodendrocytes . Dotted lines mark the white/gray matter boundary. Scale bar in I: 100 μm.

Article Snippet: Antibodies used were: mouse anti-MBP (1:1000, SMI99, Sternberger Monoclonal Inc., Baltimore, MD, USA); rabbit anti-Iba-1; monoclonal anti-human CD68 antibody (clone 514H12, AbD Serotec, Oxford, UK).

Techniques: Antibody Labeling, Staining, Mutagenesis

Journal: Brain Sciences

Article Title: Potential for Cell-Mediated Immune Responses in Mouse Models of Pelizaeus-Merzbacher Disease

doi: 10.3390/brainsci3041417

Figure Lengend Snippet: Activation of rsh and msd microglia/macrophages in optic nerve at P16. ( A ) Longitudinal section from wild type mouse reveals Iba-1 + microglia/macrophages (red) with non-activated morphology (arrowheads). Most of these cells do not express CD68 or express the protein at low levels (green). ( B ) DAPI staining showing the nuclei of the microglia/macrophages in ( A ). ( C , E ) Iba-1 + microglia/macrophages from rsh ( C ) and msd ( E ) mice exhibit an activated morphology with enlarged cell bodies and thickened processes. Most of these cells express CD68 at high levels, which is localized to perinuclear regions. ( D , F ) DAPI staining of the fields in ( C , E ). Scale bar in F: 30 μm.

Article Snippet: Antibodies used were: mouse anti-MBP (1:1000, SMI99, Sternberger Monoclonal Inc., Baltimore, MD, USA); rabbit anti-Iba-1; monoclonal anti-human CD68 antibody (clone 514H12, AbD Serotec, Oxford, UK).

Techniques: Activation Assay, Staining

Journal: Brain Sciences

Article Title: Potential for Cell-Mediated Immune Responses in Mouse Models of Pelizaeus-Merzbacher Disease

doi: 10.3390/brainsci3041417

Figure Lengend Snippet: Expression fold changes of other non-chromosome 17 interferon-induced genes in microarray data for rsh and msd mice.

Article Snippet: Antibodies used were: mouse anti-MBP (1:1000, SMI99, Sternberger Monoclonal Inc., Baltimore, MD, USA); rabbit anti-Iba-1; monoclonal anti-human CD68 antibody (clone 514H12, AbD Serotec, Oxford, UK).

Techniques: Expressing, Microarray

Journal: Biologics: Targets and Therapy

Article Title: Globular domain of adiponectin: promising target molecule for detection of atherosclerotic lesions

doi: 10.2147/btt.s22863

Figure Lengend Snippet: Figure 3 Globular adiponectin is localized in the fibrous cap of atherosclerotic plaques. (A) For double-staining experiments, aortic sections of apoprotein E-deficient mice were coincubated with globular adiponectin-Atto655 20 µg/mL and AlexaFluor488-labeled rat antimouse CD31 antibody. The nuclei were stained with Hoechst (blue). Single Z-plane fluorescence images were taken at a depth of 4 µm from the top of an atherosclerotic plaque showing the localization of globular adiponectin-Atto655 in the endothelial layer. The aortic surface is shown in the small inserts. (B) Aortic sections of apoprotein E-deficient mice were coincubated with globular adiponectin-Atto655 and AlexaFluor488-labeled rabbit antihuman collagen type I antibody. Single Z-plane fluorescence images were taken at a depth of 7 µm from the top of an atherosclerotic plaque, showing colocalization of globular adiponectin and collagen type I. (C) For negative control experiments, aortic sections were preincubated with a high amount of native globular adiponectin. A stack of optical sections from an atherosclerotic plaque projected into one plane showed only a weak globular adiponectin-Atto655 signal, compared with the plaque image in the left panel in B. (D) Single Z-plane fluorescence light images from a globular adiponectin-Atto655 and an interleukin 10-Atto655-stained plaque at a depth of 10 µm from top of the plaque. Images show the different staining patterns between globular adiponectin and interleukin 10. Notes: Scale bars: A and C, 50 µm; B, 20 µm.

Article Snippet: AlexaFluor488-prelabeled rat antimouse CD31 and rat antimouse CD68 antibodies were used as endothelial cell and macrophage markers, respectively (AbD Serotec, Dusseldorf, Germany).

Techniques: Double Staining, Labeling, Staining, Fluorescence, Negative Control

Journal: Biologics: Targets and Therapy

Article Title: Globular domain of adiponectin: promising target molecule for detection of atherosclerotic lesions

doi: 10.2147/btt.s22863

Figure Lengend Snippet: Figure 5 High binding efficiency of globular adiponectin to atherosclerotic plaques is independent of interactions with known adiponectin receptors. Aortic sections of apoprotein E-deficient mice were incubated with gAd-Atto655 20 µg/mL (left panel) or fluorescence-labeled rabbit antimouse adipoR1 and adipoR2 antibody (middle), or sheep antimouse calreticulin antibody (right). (A) Single horizontal Z-plane fluorescence images from atherosclerotic plaques. (B) Overlay of vertical fluorescence and transmitted light images. Yellow arrows indicate plaque surface globular adiponectin staining; white arrows indicate plaque interior adipoR2 staining; orange arrows indicate plaque interior calreticulin staining. Anti-adipoR1 showed no staining signal (data not shown). Note: Scale bars: A, 20 µm; B, 10 µm.

Article Snippet: AlexaFluor488-prelabeled rat antimouse CD31 and rat antimouse CD68 antibodies were used as endothelial cell and macrophage markers, respectively (AbD Serotec, Dusseldorf, Germany).

Techniques: Binding Assay, Incubation, Fluorescence, Labeling, Staining

Journal: Biologics: Targets and Therapy

Article Title: Globular domain of adiponectin: promising target molecule for detection of atherosclerotic lesions

doi: 10.2147/btt.s22863

Figure Lengend Snippet: Figure 4 Binding efficiency of the full-length adiponectin subfractions to atherosclerotic plaques is much lower than that of globular adiponectin. Aortic sections of apoprotein E-deficient mice were incubated with unspecific rat antihuman IgG2a labeled with Atto655 as negative control (left) or full-length adiponectin subfraction-Atto655 30 µg/mL (middle) or globular adiponectin-Atto655 3 µg/mL (right). The inserts shown in the left and middle panels on the left side are positive controls, staining atherosclerotic plaques with an AlexaFluor488-prelabeled antibody against the macrophage marker CD68. Note: Scale bars: 50 µm.

Article Snippet: AlexaFluor488-prelabeled rat antimouse CD31 and rat antimouse CD68 antibodies were used as endothelial cell and macrophage markers, respectively (AbD Serotec, Dusseldorf, Germany).

Techniques: Binding Assay, Incubation, Labeling, Negative Control, Staining, Marker

Journal: International Journal of Clinical and Experimental Pathology

Article Title: Fibrinogen-like protein 2 prothrombinase may contribute to the progression of inflammatory bowel disease by mediating immune coagulation

doi:

Figure Lengend Snippet: Immunohistochemical staining of various indicators. TNF-α in IBD mice and patients (B and F, ×400), and normal controls (A and E ×400). FGL2 in IBD mice and patients (C and J, ×400), and normal controls (D ×200 and I ×400). Fibrin in normal control and IBD patients (H ×200 and G ×400). CD68 in normal control and IBD patients (L and K, ×400).

Article Snippet: Immunoperoxidase staining of macrophages A CD68 Ab (ProteinTech, at a dilution of 1:100) was used to detect macrophages using the similar methodology described above.

Techniques: Immunohistochemical staining, Staining, Control