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Nikon differential interference contrast (dic) microscopy
The CSPG4 and perlecan interaction is involved in cell adhesion and spreading. (A) MM200 cell adhesion on fibronectin coated surface was used as a positive control (i). MM200 cell adhesion on HCAEC perlecan coated surfaces, in the absence of antibody (ii), in the presence of antibodies against α2β1 integrin clone BHA2.1 (iii), against perlecan clone A74 (iv) and against CSPG4 clones B5 (v) and clone 9.2.27 (vi). Cells were stained for actin filaments with Rhodamine-phalloidin (i–vi) and imaged using confocal <t>microscopy.</t> White arrows point out the polymerized actin filaments. Scale bar represents 10 µm. (B) Live cell images using <t>DIC</t> were also taken after MM200 cell adhesion on HCAEC perlecan coated surfaces in the absence of antibody (i), in the presence of antibody against CSPG4 clones B5 (ii) and clone 9.2.27 (iii) for 1 h. Scale bar represents 50 µm. (C) Analysis of the perimeter of cells exposed to the perlecan coating for 1 h in the absence or presence of antibodies from (B). A minimum of 10 cells were analysed from three confocal images taken at random for each condition. Individual data points are indicated as well as mean ± standard deviation. (D) The number of cells adhered to the perlecan coating after 1 h in the absence or presence of anti-CSPG4 antibodies determined from the live cell DIC images in (C). Individual data points were indicated as well as mean ± standard deviation. ‘*’ denoted significant differences compared to cells plated on perlecan in the absence of antibodies (P < 0.05) analysed by one-way ANOVA. Data shown are representative of three independent experiments.
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Nikon inverted nikon eclipse tie
The CSPG4 and perlecan interaction is involved in cell adhesion and spreading. (A) MM200 cell adhesion on fibronectin coated surface was used as a positive control (i). MM200 cell adhesion on HCAEC perlecan coated surfaces, in the absence of antibody (ii), in the presence of antibodies against α2β1 integrin clone BHA2.1 (iii), against perlecan clone A74 (iv) and against CSPG4 clones B5 (v) and clone 9.2.27 (vi). Cells were stained for actin filaments with Rhodamine-phalloidin (i–vi) and imaged using confocal <t>microscopy.</t> White arrows point out the polymerized actin filaments. Scale bar represents 10 µm. (B) Live cell images using <t>DIC</t> were also taken after MM200 cell adhesion on HCAEC perlecan coated surfaces in the absence of antibody (i), in the presence of antibody against CSPG4 clones B5 (ii) and clone 9.2.27 (iii) for 1 h. Scale bar represents 50 µm. (C) Analysis of the perimeter of cells exposed to the perlecan coating for 1 h in the absence or presence of antibodies from (B). A minimum of 10 cells were analysed from three confocal images taken at random for each condition. Individual data points are indicated as well as mean ± standard deviation. (D) The number of cells adhered to the perlecan coating after 1 h in the absence or presence of anti-CSPG4 antibodies determined from the live cell DIC images in (C). Individual data points were indicated as well as mean ± standard deviation. ‘*’ denoted significant differences compared to cells plated on perlecan in the absence of antibodies (P < 0.05) analysed by one-way ANOVA. Data shown are representative of three independent experiments.
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Nikon phase contrast nikon eclipse ti-e inverted microscope
The CSPG4 and perlecan interaction is involved in cell adhesion and spreading. (A) MM200 cell adhesion on fibronectin coated surface was used as a positive control (i). MM200 cell adhesion on HCAEC perlecan coated surfaces, in the absence of antibody (ii), in the presence of antibodies against α2β1 integrin clone BHA2.1 (iii), against perlecan clone A74 (iv) and against CSPG4 clones B5 (v) and clone 9.2.27 (vi). Cells were stained for actin filaments with Rhodamine-phalloidin (i–vi) and imaged using confocal <t>microscopy.</t> White arrows point out the polymerized actin filaments. Scale bar represents 10 µm. (B) Live cell images using <t>DIC</t> were also taken after MM200 cell adhesion on HCAEC perlecan coated surfaces in the absence of antibody (i), in the presence of antibody against CSPG4 clones B5 (ii) and clone 9.2.27 (iii) for 1 h. Scale bar represents 50 µm. (C) Analysis of the perimeter of cells exposed to the perlecan coating for 1 h in the absence or presence of antibodies from (B). A minimum of 10 cells were analysed from three confocal images taken at random for each condition. Individual data points are indicated as well as mean ± standard deviation. (D) The number of cells adhered to the perlecan coating after 1 h in the absence or presence of anti-CSPG4 antibodies determined from the live cell DIC images in (C). Individual data points were indicated as well as mean ± standard deviation. ‘*’ denoted significant differences compared to cells plated on perlecan in the absence of antibodies (P < 0.05) analysed by one-way ANOVA. Data shown are representative of three independent experiments.
Phase Contrast Nikon Eclipse Ti E Inverted Microscope, supplied by Nikon, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


The CSPG4 and perlecan interaction is involved in cell adhesion and spreading. (A) MM200 cell adhesion on fibronectin coated surface was used as a positive control (i). MM200 cell adhesion on HCAEC perlecan coated surfaces, in the absence of antibody (ii), in the presence of antibodies against α2β1 integrin clone BHA2.1 (iii), against perlecan clone A74 (iv) and against CSPG4 clones B5 (v) and clone 9.2.27 (vi). Cells were stained for actin filaments with Rhodamine-phalloidin (i–vi) and imaged using confocal microscopy. White arrows point out the polymerized actin filaments. Scale bar represents 10 µm. (B) Live cell images using DIC were also taken after MM200 cell adhesion on HCAEC perlecan coated surfaces in the absence of antibody (i), in the presence of antibody against CSPG4 clones B5 (ii) and clone 9.2.27 (iii) for 1 h. Scale bar represents 50 µm. (C) Analysis of the perimeter of cells exposed to the perlecan coating for 1 h in the absence or presence of antibodies from (B). A minimum of 10 cells were analysed from three confocal images taken at random for each condition. Individual data points are indicated as well as mean ± standard deviation. (D) The number of cells adhered to the perlecan coating after 1 h in the absence or presence of anti-CSPG4 antibodies determined from the live cell DIC images in (C). Individual data points were indicated as well as mean ± standard deviation. ‘*’ denoted significant differences compared to cells plated on perlecan in the absence of antibodies (P < 0.05) analysed by one-way ANOVA. Data shown are representative of three independent experiments.

Journal: Journal of Biochemistry

Article Title: Cell surface chondroitin sulphate proteoglycan 4 (CSPG4) binds to the basement membrane heparan sulphate proteoglycan, perlecan, and is involved in cell adhesion

doi: 10.1093/jb/mvy008

Figure Lengend Snippet: The CSPG4 and perlecan interaction is involved in cell adhesion and spreading. (A) MM200 cell adhesion on fibronectin coated surface was used as a positive control (i). MM200 cell adhesion on HCAEC perlecan coated surfaces, in the absence of antibody (ii), in the presence of antibodies against α2β1 integrin clone BHA2.1 (iii), against perlecan clone A74 (iv) and against CSPG4 clones B5 (v) and clone 9.2.27 (vi). Cells were stained for actin filaments with Rhodamine-phalloidin (i–vi) and imaged using confocal microscopy. White arrows point out the polymerized actin filaments. Scale bar represents 10 µm. (B) Live cell images using DIC were also taken after MM200 cell adhesion on HCAEC perlecan coated surfaces in the absence of antibody (i), in the presence of antibody against CSPG4 clones B5 (ii) and clone 9.2.27 (iii) for 1 h. Scale bar represents 50 µm. (C) Analysis of the perimeter of cells exposed to the perlecan coating for 1 h in the absence or presence of antibodies from (B). A minimum of 10 cells were analysed from three confocal images taken at random for each condition. Individual data points are indicated as well as mean ± standard deviation. (D) The number of cells adhered to the perlecan coating after 1 h in the absence or presence of anti-CSPG4 antibodies determined from the live cell DIC images in (C). Individual data points were indicated as well as mean ± standard deviation. ‘*’ denoted significant differences compared to cells plated on perlecan in the absence of antibodies (P < 0.05) analysed by one-way ANOVA. Data shown are representative of three independent experiments.

Article Snippet: Images were taken with differential interference contrast (DIC) microscopy (Nikon Eclipse TiE).

Techniques: Positive Control, Clone Assay, Staining, Confocal Microscopy, Standard Deviation