hs 819  (ATCC)


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    Structured Review

    ATCC hs 819
    Nuclear YAP1 is required for the growth of CHS cells. A  IHC analysis of YAP1 expression in tissue arrays of CHS of different grades. Representative images are shown. Scale bar: 50 μm. Well (well-differentiated,  N  = 43), moderate (moderately differentiated, = 17), poor (poorly differentiated,  N  = 20).  B  Quantification of YAP1 expression scores in ( A ).  C  The expression scores of YAP1 in the cytoplasm and nucleus in poorly differentiated CHS (Poor) were quantified.  D  The percentage of YAP1 expression in the cytoplasm and nucleus in the chondrocytic cell line (CHON-001) and CHS cell lines (SW 1353 and Hs 819.T). C: cytoplasm, N: nucleus.  E  Representative IF image of YAP1 localization (green) in SW 1353 cells. DAPI (blue) indicates the nucleus, while F-actin (red) defines the cytoskeleton. Scale bar: 10 μm.  F  IB analysis of YAP1 and HA-tagged expression in primary chondrocytes infected with lentivirus-delivered HA-vector (Vector), HA-YAP1 (YAP1), or HA-YAP1-5SA (5SA). Red arrows indicated both the endogenous and exogenous YAP1 expression. The elastic modulus and adhesion properties of the indicated cells were analyzed by AFM for at least three individual cells; representative images are shown below.  G  SW 1353 cells stably expressing control shRNA or YAP1-specific shRNAs (shYAP#1, #2, #3, #4) were established, and the knockdown efficiency was confirmed using an antibody against YAP1 for IB (above). The cell viabilities of each construct at varying time points were determined by a CCK-8 assay (below).  H  Colony formation ability (number of colonies) of the indicated stable cells is shown (above). Representative images are shown below. Data are presented as the mean ± SD of at least three independent experiments in panel ( B – D ,  F – H ). One-way ANOVA followed by Dunnett’s test was applied for ( B ,  F ,  H ). Student’s  t -test for ( C ,  D ). Two-way ANOVA followed by Tukey’s test for ( G ). n.s. nonsignificant, * P
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    Images

    1) Product Images from "Sequential targeting of YAP1 and p21 enhances the elimination of senescent cells induced by the BET inhibitor JQ1"

    Article Title: Sequential targeting of YAP1 and p21 enhances the elimination of senescent cells induced by the BET inhibitor JQ1

    Journal: Cell Death & Disease

    doi: 10.1038/s41419-021-03416-1

    Nuclear YAP1 is required for the growth of CHS cells. A  IHC analysis of YAP1 expression in tissue arrays of CHS of different grades. Representative images are shown. Scale bar: 50 μm. Well (well-differentiated,  N  = 43), moderate (moderately differentiated, = 17), poor (poorly differentiated,  N  = 20).  B  Quantification of YAP1 expression scores in ( A ).  C  The expression scores of YAP1 in the cytoplasm and nucleus in poorly differentiated CHS (Poor) were quantified.  D  The percentage of YAP1 expression in the cytoplasm and nucleus in the chondrocytic cell line (CHON-001) and CHS cell lines (SW 1353 and Hs 819.T). C: cytoplasm, N: nucleus.  E  Representative IF image of YAP1 localization (green) in SW 1353 cells. DAPI (blue) indicates the nucleus, while F-actin (red) defines the cytoskeleton. Scale bar: 10 μm.  F  IB analysis of YAP1 and HA-tagged expression in primary chondrocytes infected with lentivirus-delivered HA-vector (Vector), HA-YAP1 (YAP1), or HA-YAP1-5SA (5SA). Red arrows indicated both the endogenous and exogenous YAP1 expression. The elastic modulus and adhesion properties of the indicated cells were analyzed by AFM for at least three individual cells; representative images are shown below.  G  SW 1353 cells stably expressing control shRNA or YAP1-specific shRNAs (shYAP#1, #2, #3, #4) were established, and the knockdown efficiency was confirmed using an antibody against YAP1 for IB (above). The cell viabilities of each construct at varying time points were determined by a CCK-8 assay (below).  H  Colony formation ability (number of colonies) of the indicated stable cells is shown (above). Representative images are shown below. Data are presented as the mean ± SD of at least three independent experiments in panel ( B – D ,  F – H ). One-way ANOVA followed by Dunnett’s test was applied for ( B ,  F ,  H ). Student’s  t -test for ( C ,  D ). Two-way ANOVA followed by Tukey’s test for ( G ). n.s. nonsignificant, * P
    Figure Legend Snippet: Nuclear YAP1 is required for the growth of CHS cells. A IHC analysis of YAP1 expression in tissue arrays of CHS of different grades. Representative images are shown. Scale bar: 50 μm. Well (well-differentiated, N  = 43), moderate (moderately differentiated, = 17), poor (poorly differentiated, N  = 20). B Quantification of YAP1 expression scores in ( A ). C The expression scores of YAP1 in the cytoplasm and nucleus in poorly differentiated CHS (Poor) were quantified. D The percentage of YAP1 expression in the cytoplasm and nucleus in the chondrocytic cell line (CHON-001) and CHS cell lines (SW 1353 and Hs 819.T). C: cytoplasm, N: nucleus. E Representative IF image of YAP1 localization (green) in SW 1353 cells. DAPI (blue) indicates the nucleus, while F-actin (red) defines the cytoskeleton. Scale bar: 10 μm. F IB analysis of YAP1 and HA-tagged expression in primary chondrocytes infected with lentivirus-delivered HA-vector (Vector), HA-YAP1 (YAP1), or HA-YAP1-5SA (5SA). Red arrows indicated both the endogenous and exogenous YAP1 expression. The elastic modulus and adhesion properties of the indicated cells were analyzed by AFM for at least three individual cells; representative images are shown below. G SW 1353 cells stably expressing control shRNA or YAP1-specific shRNAs (shYAP#1, #2, #3, #4) were established, and the knockdown efficiency was confirmed using an antibody against YAP1 for IB (above). The cell viabilities of each construct at varying time points were determined by a CCK-8 assay (below). H Colony formation ability (number of colonies) of the indicated stable cells is shown (above). Representative images are shown below. Data are presented as the mean ± SD of at least three independent experiments in panel ( B – D , F – H ). One-way ANOVA followed by Dunnett’s test was applied for ( B , F , H ). Student’s t -test for ( C , D ). Two-way ANOVA followed by Tukey’s test for ( G ). n.s. nonsignificant, * P

    Techniques Used: Immunohistochemistry, Expressing, Infection, Plasmid Preparation, Stable Transfection, shRNA, Construct, CCK-8 Assay

    YAP1/TEAD controls cell cycle exit and induces cellular senescence. A  Cell cycle distribution analysis in the groups of control shRNA and YAP1-specific shRNAs (shYAP#2, #3, #4).  B ,  C  Control shRNA or YAP1-depleted SW 1353 cells were stained with SA-β-gal, and the representative images are shown in ( B ); the percentage of SA-β-gal-positive cells was quantified and shown in ( C ), scale bars: 10 μm.  D  Hs 819.T cells were infected with lentivirus of control shRNA or YAP1-specific shRNAs (shYAP#3, #4), and then the percentage of SA-β-gal-positive cells was quantified.  E ,  F  YAP1 depletion inhibits cell proliferation. Cell proliferation was determined by the EdU incorporation assay ( E ), scale bar: 10 μm. DAPI was used as a nuclear counterstain. The percentage of cells that incorporated EdU was quantified ( F ).  G  Knockdown of YAP1 induces the increase of p21 expression, independent of cell density. Expression of the indicated proteins was determined by IB.  H – J  YAP1-TEAD plays a role in regulating CHS cell senescence. control shRNA or YAP1-depleted SW 1353 cells were transiently transfected with HA-vector (Vector), HA-YAP1-5SA (YAP1-5SA), or HA-YAP1-5SA/S94A (YAP1-5SA/S94A) for 72 h, and then the protein levels of HA, Cyr61, and p21 were determined by IB ( H ). The percentage of SA-β-gal-positive cells was quantified ( I ), and representative images are shown in ( J ); scale bars: 10 μm. Data are presented as the mean ± SD of at least three independent experiments in ( A ,  C ,  D ,  F ,  I ). One-way ANOVA followed by Dunnett’s test was applied for ( A ,  C ,  D ,  F ). Two-way ANOVA followed by Tukey’s test for ( I ). n.s. nonsignificant, * P
    Figure Legend Snippet: YAP1/TEAD controls cell cycle exit and induces cellular senescence. A Cell cycle distribution analysis in the groups of control shRNA and YAP1-specific shRNAs (shYAP#2, #3, #4). B , C Control shRNA or YAP1-depleted SW 1353 cells were stained with SA-β-gal, and the representative images are shown in ( B ); the percentage of SA-β-gal-positive cells was quantified and shown in ( C ), scale bars: 10 μm. D Hs 819.T cells were infected with lentivirus of control shRNA or YAP1-specific shRNAs (shYAP#3, #4), and then the percentage of SA-β-gal-positive cells was quantified. E , F YAP1 depletion inhibits cell proliferation. Cell proliferation was determined by the EdU incorporation assay ( E ), scale bar: 10 μm. DAPI was used as a nuclear counterstain. The percentage of cells that incorporated EdU was quantified ( F ). G Knockdown of YAP1 induces the increase of p21 expression, independent of cell density. Expression of the indicated proteins was determined by IB. H – J YAP1-TEAD plays a role in regulating CHS cell senescence. control shRNA or YAP1-depleted SW 1353 cells were transiently transfected with HA-vector (Vector), HA-YAP1-5SA (YAP1-5SA), or HA-YAP1-5SA/S94A (YAP1-5SA/S94A) for 72 h, and then the protein levels of HA, Cyr61, and p21 were determined by IB ( H ). The percentage of SA-β-gal-positive cells was quantified ( I ), and representative images are shown in ( J ); scale bars: 10 μm. Data are presented as the mean ± SD of at least three independent experiments in ( A , C , D , F , I ). One-way ANOVA followed by Dunnett’s test was applied for ( A , C , D , F ). Two-way ANOVA followed by Tukey’s test for ( I ). n.s. nonsignificant, * P

    Techniques Used: shRNA, Staining, Infection, Expressing, Transfection, Plasmid Preparation

    2) Product Images from "Sequential targeting of YAP1 and p21 enhances the elimination of senescent cells induced by the BET inhibitor JQ1"

    Article Title: Sequential targeting of YAP1 and p21 enhances the elimination of senescent cells induced by the BET inhibitor JQ1

    Journal: Cell Death & Disease

    doi: 10.1038/s41419-021-03416-1

    YAP1/TEAD controls cell cycle exit and induces cellular senescence. A  Cell cycle distribution analysis in the groups of control shRNA and YAP1-specific shRNAs (shYAP#2, #3, #4).  B ,  C  Control shRNA or YAP1-depleted SW 1353 cells were stained with SA-β-gal, and the representative images are shown in ( B ); the percentage of SA-β-gal-positive cells was quantified and shown in ( C ), scale bars: 10 μm.  D  Hs 819.T cells were infected with lentivirus of control shRNA or YAP1-specific shRNAs (shYAP#3, #4), and then the percentage of SA-β-gal-positive cells was quantified.  E ,  F  YAP1 depletion inhibits cell proliferation. Cell proliferation was determined by the EdU incorporation assay ( E ), scale bar: 10 μm. DAPI was used as a nuclear counterstain. The percentage of cells that incorporated EdU was quantified ( F ).  G  Knockdown of YAP1 induces the increase of p21 expression, independent of cell density. Expression of the indicated proteins was determined by IB.  H – J  YAP1-TEAD plays a role in regulating CHS cell senescence. control shRNA or YAP1-depleted SW 1353 cells were transiently transfected with HA-vector (Vector), HA-YAP1-5SA (YAP1-5SA), or HA-YAP1-5SA/S94A (YAP1-5SA/S94A) for 72 h, and then the protein levels of HA, Cyr61, and p21 were determined by IB ( H ). The percentage of SA-β-gal-positive cells was quantified ( I ), and representative images are shown in ( J ); scale bars: 10 μm. Data are presented as the mean ± SD of at least three independent experiments in ( A ,  C ,  D ,  F ,  I ). One-way ANOVA followed by Dunnett’s test was applied for ( A ,  C ,  D ,  F ). Two-way ANOVA followed by Tukey’s test for ( I ). n.s. nonsignificant, * P
    Figure Legend Snippet: YAP1/TEAD controls cell cycle exit and induces cellular senescence. A Cell cycle distribution analysis in the groups of control shRNA and YAP1-specific shRNAs (shYAP#2, #3, #4). B , C Control shRNA or YAP1-depleted SW 1353 cells were stained with SA-β-gal, and the representative images are shown in ( B ); the percentage of SA-β-gal-positive cells was quantified and shown in ( C ), scale bars: 10 μm. D Hs 819.T cells were infected with lentivirus of control shRNA or YAP1-specific shRNAs (shYAP#3, #4), and then the percentage of SA-β-gal-positive cells was quantified. E , F YAP1 depletion inhibits cell proliferation. Cell proliferation was determined by the EdU incorporation assay ( E ), scale bar: 10 μm. DAPI was used as a nuclear counterstain. The percentage of cells that incorporated EdU was quantified ( F ). G Knockdown of YAP1 induces the increase of p21 expression, independent of cell density. Expression of the indicated proteins was determined by IB. H – J YAP1-TEAD plays a role in regulating CHS cell senescence. control shRNA or YAP1-depleted SW 1353 cells were transiently transfected with HA-vector (Vector), HA-YAP1-5SA (YAP1-5SA), or HA-YAP1-5SA/S94A (YAP1-5SA/S94A) for 72 h, and then the protein levels of HA, Cyr61, and p21 were determined by IB ( H ). The percentage of SA-β-gal-positive cells was quantified ( I ), and representative images are shown in ( J ); scale bars: 10 μm. Data are presented as the mean ± SD of at least three independent experiments in ( A , C , D , F , I ). One-way ANOVA followed by Dunnett’s test was applied for ( A , C , D , F ). Two-way ANOVA followed by Tukey’s test for ( I ). n.s. nonsignificant, * P

    Techniques Used: shRNA, Staining, Infection, Expressing, Transfection, Plasmid Preparation

    3) Product Images from "Collagen type II suppresses articular chondrocyte hypertrophy and osteoarthritis progression by promoting integrin β1−SMAD1 interaction"

    Article Title: Collagen type II suppresses articular chondrocyte hypertrophy and osteoarthritis progression by promoting integrin β1−SMAD1 interaction

    Journal: Bone Research

    doi: 10.1038/s41413-019-0046-y

    COL2A1 phosphorylated SMAD1 S206 by activating ERK1/2, which negatively influenced BMP-SMAD1 activity. a , b Immunoblotting evaluation of p-SMAD1 S463/465 , p-SMAD1 S206 , and SMAD1 in chondrocytes from Col2a1 mutant mice ( a ) and SW1353 and Hs819.T cells treated with 100 μg·mL −1 COL2A1 or vehicle (0.05 mol·L −1 acetic acid) for 1 h ( b ). c , d Immunoblotting evaluation of p-ERK1/2, ERK1/2, p-MAPK14, MAPK14, p-JNK1/2, and JNK1/2 in chondrocytes from Col2a1 mutant mice ( c ), and SW1353 and Hs819.T cells treated with COL2A1 or vehicle ( d ). e − g The expression levels of p-ERK1/2, p-SMAD1 S463/465 , p-SMAD1 S206 , ERK1/2, and SMAD1 proteins were detected by immunoblotting ( e ), and the expression levels of ID1 , ID2 , DLX5 , RUNX2 , and COL10A1 were tested by qPCR in SW1353 ( f ) and Hs819.T cells ( g ) pretreated with 10 μmol·L −1 U0126 or vehicle 1 (dimethylsulfoxide) for 1 h and then treated with 100 μg·mL −1 COL2A1 or vehicle 2 (0.05 mol·L −1 acetic acid) for 1 h. h , i Immunoprecipitation was performed on 293T cells treated with COL2A1 or vehicle with anti-SMAD1 antibody ( h ) or anti-ERK1/2 antibody ( i ), followed by immunoblotting with anti-ERK1/2 and anti-SMAD1 antibodies. j Immunoblotting evaluation of SMAD1 in both nuclear (Nuc) and cytoplasmic (Cyto) extracts in SW1353 and Hs819.T cells pretreated with U0126 or vehicle 1 and then treated with COL2A1 or vehicle 2. k, l Immunoprecipitation was performed on 293T cells treated with COL2A1 or vehicle with anti-SMAD1 antibody ( k ) or anti-SMAD4 antibody ( l ), followed by immunoblotting with anti-SMAD4 antibody and anti-SMAD1 antibody. Data in ( f ) and ( g ) are presented as the mean ± SD ( n = 3). * P
    Figure Legend Snippet: COL2A1 phosphorylated SMAD1 S206 by activating ERK1/2, which negatively influenced BMP-SMAD1 activity. a , b Immunoblotting evaluation of p-SMAD1 S463/465 , p-SMAD1 S206 , and SMAD1 in chondrocytes from Col2a1 mutant mice ( a ) and SW1353 and Hs819.T cells treated with 100 μg·mL −1 COL2A1 or vehicle (0.05 mol·L −1 acetic acid) for 1 h ( b ). c , d Immunoblotting evaluation of p-ERK1/2, ERK1/2, p-MAPK14, MAPK14, p-JNK1/2, and JNK1/2 in chondrocytes from Col2a1 mutant mice ( c ), and SW1353 and Hs819.T cells treated with COL2A1 or vehicle ( d ). e − g The expression levels of p-ERK1/2, p-SMAD1 S463/465 , p-SMAD1 S206 , ERK1/2, and SMAD1 proteins were detected by immunoblotting ( e ), and the expression levels of ID1 , ID2 , DLX5 , RUNX2 , and COL10A1 were tested by qPCR in SW1353 ( f ) and Hs819.T cells ( g ) pretreated with 10 μmol·L −1 U0126 or vehicle 1 (dimethylsulfoxide) for 1 h and then treated with 100 μg·mL −1 COL2A1 or vehicle 2 (0.05 mol·L −1 acetic acid) for 1 h. h , i Immunoprecipitation was performed on 293T cells treated with COL2A1 or vehicle with anti-SMAD1 antibody ( h ) or anti-ERK1/2 antibody ( i ), followed by immunoblotting with anti-ERK1/2 and anti-SMAD1 antibodies. j Immunoblotting evaluation of SMAD1 in both nuclear (Nuc) and cytoplasmic (Cyto) extracts in SW1353 and Hs819.T cells pretreated with U0126 or vehicle 1 and then treated with COL2A1 or vehicle 2. k, l Immunoprecipitation was performed on 293T cells treated with COL2A1 or vehicle with anti-SMAD1 antibody ( k ) or anti-SMAD4 antibody ( l ), followed by immunoblotting with anti-SMAD4 antibody and anti-SMAD1 antibody. Data in ( f ) and ( g ) are presented as the mean ± SD ( n = 3). * P

    Techniques Used: Activity Assay, Mutagenesis, Mouse Assay, Expressing, Real-time Polymerase Chain Reaction, Immunoprecipitation

    COL2A1 exerted suppression on chondrocyte hypertrophy and on the production of matrix-degrading enzymes. a , b SW1353 and Hs819.T cells were treated with COL2A1 (100 μg·mL −1 ) or vehicle (0.05 mol·L −1 acetic acid) for 48 h, and the expression levels of RUNX2 and COL10A1 were detected by qPCR ( a ) and immunoblotting ( b ). c , d Human articular chondrocytes were transfected with COL2A1 siRNA or negative control siRNA, and the expression levels of RUNX2 and COL10A1 were detected by qPCR ( c ) and immunoblotting ( d ). e − g Pellet cultures of MSCs were induced to undergo chondrogenesis for 14 d and then induced for hypertrophic differentiation for another 14 d with purified COL2A1 or vehicle. In addition, pellet cultures of MSCs induced to undergo chondrogenesis for 28 d were used as chondrogenic controls. e Gross appearance, HE staining, safranin O staining, and Alcian blue staining were evaluated. Scale bars in the images of gross appearance: 1 mm; other scale bars in ( e ): 200 μm. The expression levels of COL10A1, RUNX2, and MMP13 were detected by qPCR ( f ) and immunoblotting ( g ). Data in ( a ), ( c ), and ( f ) are presented as the mean ± SD ( n = 3). * P
    Figure Legend Snippet: COL2A1 exerted suppression on chondrocyte hypertrophy and on the production of matrix-degrading enzymes. a , b SW1353 and Hs819.T cells were treated with COL2A1 (100 μg·mL −1 ) or vehicle (0.05 mol·L −1 acetic acid) for 48 h, and the expression levels of RUNX2 and COL10A1 were detected by qPCR ( a ) and immunoblotting ( b ). c , d Human articular chondrocytes were transfected with COL2A1 siRNA or negative control siRNA, and the expression levels of RUNX2 and COL10A1 were detected by qPCR ( c ) and immunoblotting ( d ). e − g Pellet cultures of MSCs were induced to undergo chondrogenesis for 14 d and then induced for hypertrophic differentiation for another 14 d with purified COL2A1 or vehicle. In addition, pellet cultures of MSCs induced to undergo chondrogenesis for 28 d were used as chondrogenic controls. e Gross appearance, HE staining, safranin O staining, and Alcian blue staining were evaluated. Scale bars in the images of gross appearance: 1 mm; other scale bars in ( e ): 200 μm. The expression levels of COL10A1, RUNX2, and MMP13 were detected by qPCR ( f ) and immunoblotting ( g ). Data in ( a ), ( c ), and ( f ) are presented as the mean ± SD ( n = 3). * P

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction, Transfection, Negative Control, Purification, Staining

    The ITGB1 receptor mediated the effect of COL2A1 on the BMP pathway and chondrocyte hypertrophy. a , b Immunoprecipitation with anti-BMPR1A ( a ) or anti-BMPR1B ( b ) antibody was performed in extracts of 293T cells treated with 100 μg·mL −1 COL2A1 or vehicle (0.05 mol·L −1 acetic acid) for 1 h, and then, immunoblotting was conducted with anti-phospho-serine/threonine and anti-BMPR1A/B antibodies. c − e Immunoblotting evaluation of p-ITGB1 and ITGB1 in chondrocytes of Col2a1 p.Gly1170Ser mutant mice ( c ), SW1353 and Hs819.T cells treated with COL2A1 or vehicle ( d ), and human articular chondrocytes transfected with COL2A1 siRNAs or negative control siRNA ( e ). f − h SW1353 and Hs819.T cells were pretreated with 10 μg·mL −1 ITGB1 blocking antibody or anti-human IgG antibody for 1 h and then treated with COL2A1 or vehicle for 1 h. Immunoblotting evaluation of p-ITGB1, p-SMAD1 S463/465 , ITGB1, and SMAD1 ( f ), and qPCR evaluation of ID1 , ID2 , DLX5 , RUNX2 , and COL10A1 ( g, h ) were performed. i Immunoblotting evaluation of SMAD1 in both nuclear (Nuc) and cytoplasmic (Cyto) extracts was performed in SW1353 and Hs819.T cells pretreated with ITGB1 blocking antibody or anti-human IgG and then treated with COL2A1 or vehicle. Data in ( g ) and ( h ) are presented as the mean ± SD ( n = 3). * P
    Figure Legend Snippet: The ITGB1 receptor mediated the effect of COL2A1 on the BMP pathway and chondrocyte hypertrophy. a , b Immunoprecipitation with anti-BMPR1A ( a ) or anti-BMPR1B ( b ) antibody was performed in extracts of 293T cells treated with 100 μg·mL −1 COL2A1 or vehicle (0.05 mol·L −1 acetic acid) for 1 h, and then, immunoblotting was conducted with anti-phospho-serine/threonine and anti-BMPR1A/B antibodies. c − e Immunoblotting evaluation of p-ITGB1 and ITGB1 in chondrocytes of Col2a1 p.Gly1170Ser mutant mice ( c ), SW1353 and Hs819.T cells treated with COL2A1 or vehicle ( d ), and human articular chondrocytes transfected with COL2A1 siRNAs or negative control siRNA ( e ). f − h SW1353 and Hs819.T cells were pretreated with 10 μg·mL −1 ITGB1 blocking antibody or anti-human IgG antibody for 1 h and then treated with COL2A1 or vehicle for 1 h. Immunoblotting evaluation of p-ITGB1, p-SMAD1 S463/465 , ITGB1, and SMAD1 ( f ), and qPCR evaluation of ID1 , ID2 , DLX5 , RUNX2 , and COL10A1 ( g, h ) were performed. i Immunoblotting evaluation of SMAD1 in both nuclear (Nuc) and cytoplasmic (Cyto) extracts was performed in SW1353 and Hs819.T cells pretreated with ITGB1 blocking antibody or anti-human IgG and then treated with COL2A1 or vehicle. Data in ( g ) and ( h ) are presented as the mean ± SD ( n = 3). * P

    Techniques Used: Immunoprecipitation, Mutagenesis, Mouse Assay, Transfection, Negative Control, Blocking Assay, Real-time Polymerase Chain Reaction

    COL2A1 suppressed chondrocyte hypertrophy through regulation of the BMP-SMAD1 pathway. a KEGG pathway functional annotations of the differentially expressed genes according to the qPCR analysis. Enrichment scores are displayed as −log( P value). A pathway was considered to be significantly enriched only if it passed the count threshold of five genes per annotation term and presented an EASE score, with the Benjamini−Hochberg correction set to 0.05. b , c Immunoblotting evaluation of p-Smad1 S463/465 , Smad1, Smad4, p-Smad2, p-Smad3, and Smad2/3 in chondrocytes of all three genotypes from Col2a1 p.Gly1170Ser mutant mice. d , e qPCR quantification of Id1 , Id2 , Dlx5 , Acvr1 , Stat1 , and Serpine1 in chondrocytes of Col2a1 mutant mice. f , g Immunoblotting evaluation of p-SMAD1 S463/465 , p-SMAD2, p-SMAD3, SMAD1, and SMAD2/3 ( f ), and qPCR quantification of ID1 , ID2 , DLX5 , ACVR1 , STAT1 , and SERPINE1 ( g ) were carried out in SW1353 and Hs819.T cells treated with 100 μg·mL −1 purified COL2A1 or vehicle (0.05 mol·L −1 acetic acid). h Immunoblotting evaluation of p-SMAD1 S463/465 , SMAD1, RUNX2, and COL10A1 in SW1353 and Hs819.T cells treated with vehicle (0.05 mol·L −1 acetic acid), 100 μg·mL −1 COL2A1, or 10 ng·mL −1 BMP2. i Human articular chondrocytes were treated with the indicated concentrations of BMP2 and 100 μg·mL −1 purified COL2A1, and the expression levels of p-SMAD1 S463/465 , SMAD1, RUNX2, and COL10A1 were detected by immunoblotting. j Confocal laser scanning was used to demonstrate SMAD1 nuclear localization in SW1353 and Hs819.T cells treated with COL2A1 or vehicle. Scale bars: 20 μm. k − m Injured cartilage samples from 50 OA patients underwent immunohistochemical staining using anti-COL2A1, p-SMAD1 S463/465 , and COL10A1 antibodies. k Representative micrographs of two patients are shown. Scale bars: 100 μm. l , m The correlation among the expression levels of three proteins was analyzed by the chi-squared test. Data in ( d ), ( e ), and ( g ) are presented as the mean ± SD ( n = 3). * P
    Figure Legend Snippet: COL2A1 suppressed chondrocyte hypertrophy through regulation of the BMP-SMAD1 pathway. a KEGG pathway functional annotations of the differentially expressed genes according to the qPCR analysis. Enrichment scores are displayed as −log( P value). A pathway was considered to be significantly enriched only if it passed the count threshold of five genes per annotation term and presented an EASE score, with the Benjamini−Hochberg correction set to 0.05. b , c Immunoblotting evaluation of p-Smad1 S463/465 , Smad1, Smad4, p-Smad2, p-Smad3, and Smad2/3 in chondrocytes of all three genotypes from Col2a1 p.Gly1170Ser mutant mice. d , e qPCR quantification of Id1 , Id2 , Dlx5 , Acvr1 , Stat1 , and Serpine1 in chondrocytes of Col2a1 mutant mice. f , g Immunoblotting evaluation of p-SMAD1 S463/465 , p-SMAD2, p-SMAD3, SMAD1, and SMAD2/3 ( f ), and qPCR quantification of ID1 , ID2 , DLX5 , ACVR1 , STAT1 , and SERPINE1 ( g ) were carried out in SW1353 and Hs819.T cells treated with 100 μg·mL −1 purified COL2A1 or vehicle (0.05 mol·L −1 acetic acid). h Immunoblotting evaluation of p-SMAD1 S463/465 , SMAD1, RUNX2, and COL10A1 in SW1353 and Hs819.T cells treated with vehicle (0.05 mol·L −1 acetic acid), 100 μg·mL −1 COL2A1, or 10 ng·mL −1 BMP2. i Human articular chondrocytes were treated with the indicated concentrations of BMP2 and 100 μg·mL −1 purified COL2A1, and the expression levels of p-SMAD1 S463/465 , SMAD1, RUNX2, and COL10A1 were detected by immunoblotting. j Confocal laser scanning was used to demonstrate SMAD1 nuclear localization in SW1353 and Hs819.T cells treated with COL2A1 or vehicle. Scale bars: 20 μm. k − m Injured cartilage samples from 50 OA patients underwent immunohistochemical staining using anti-COL2A1, p-SMAD1 S463/465 , and COL10A1 antibodies. k Representative micrographs of two patients are shown. Scale bars: 100 μm. l , m The correlation among the expression levels of three proteins was analyzed by the chi-squared test. Data in ( d ), ( e ), and ( g ) are presented as the mean ± SD ( n = 3). * P

    Techniques Used: Functional Assay, Real-time Polymerase Chain Reaction, Mutagenesis, Mouse Assay, Purification, Expressing, Immunohistochemistry, Staining

    4) Product Images from "Collagen type II suppresses articular chondrocyte hypertrophy and osteoarthritis progression by promoting integrin β1−SMAD1 interaction"

    Article Title: Collagen type II suppresses articular chondrocyte hypertrophy and osteoarthritis progression by promoting integrin β1−SMAD1 interaction

    Journal: Bone Research

    doi: 10.1038/s41413-019-0046-y

    COL2A1 phosphorylated SMAD1 S206 by activating ERK1/2, which negatively influenced BMP-SMAD1 activity. a , b Immunoblotting evaluation of p-SMAD1 S463/465 , p-SMAD1 S206 , and SMAD1 in chondrocytes from Col2a1 mutant mice ( a ) and SW1353 and Hs819.T cells treated with 100 μg·mL −1 COL2A1 or vehicle (0.05 mol·L −1 acetic acid) for 1 h ( b ). c , d Immunoblotting evaluation of p-ERK1/2, ERK1/2, p-MAPK14, MAPK14, p-JNK1/2, and JNK1/2 in chondrocytes from Col2a1 mutant mice ( c ), and SW1353 and Hs819.T cells treated with COL2A1 or vehicle ( d ). e − g The expression levels of p-ERK1/2, p-SMAD1 S463/465 , p-SMAD1 S206 , ERK1/2, and SMAD1 proteins were detected by immunoblotting ( e ), and the expression levels of ID1 , ID2 , DLX5 , RUNX2 , and COL10A1 were tested by qPCR in SW1353 ( f ) and Hs819.T cells ( g ) pretreated with 10 μmol·L −1 U0126 or vehicle 1 (dimethylsulfoxide) for 1 h and then treated with 100 μg·mL −1 COL2A1 or vehicle 2 (0.05 mol·L −1 acetic acid) for 1 h. h , i Immunoprecipitation was performed on 293T cells treated with COL2A1 or vehicle with anti-SMAD1 antibody ( h ) or anti-ERK1/2 antibody ( i ), followed by immunoblotting with anti-ERK1/2 and anti-SMAD1 antibodies. j Immunoblotting evaluation of SMAD1 in both nuclear (Nuc) and cytoplasmic (Cyto) extracts in SW1353 and Hs819.T cells pretreated with U0126 or vehicle 1 and then treated with COL2A1 or vehicle 2. k, l Immunoprecipitation was performed on 293T cells treated with COL2A1 or vehicle with anti-SMAD1 antibody ( k ) or anti-SMAD4 antibody ( l ), followed by immunoblotting with anti-SMAD4 antibody and anti-SMAD1 antibody. Data in ( f ) and ( g ) are presented as the mean ± SD ( n = 3). * P
    Figure Legend Snippet: COL2A1 phosphorylated SMAD1 S206 by activating ERK1/2, which negatively influenced BMP-SMAD1 activity. a , b Immunoblotting evaluation of p-SMAD1 S463/465 , p-SMAD1 S206 , and SMAD1 in chondrocytes from Col2a1 mutant mice ( a ) and SW1353 and Hs819.T cells treated with 100 μg·mL −1 COL2A1 or vehicle (0.05 mol·L −1 acetic acid) for 1 h ( b ). c , d Immunoblotting evaluation of p-ERK1/2, ERK1/2, p-MAPK14, MAPK14, p-JNK1/2, and JNK1/2 in chondrocytes from Col2a1 mutant mice ( c ), and SW1353 and Hs819.T cells treated with COL2A1 or vehicle ( d ). e − g The expression levels of p-ERK1/2, p-SMAD1 S463/465 , p-SMAD1 S206 , ERK1/2, and SMAD1 proteins were detected by immunoblotting ( e ), and the expression levels of ID1 , ID2 , DLX5 , RUNX2 , and COL10A1 were tested by qPCR in SW1353 ( f ) and Hs819.T cells ( g ) pretreated with 10 μmol·L −1 U0126 or vehicle 1 (dimethylsulfoxide) for 1 h and then treated with 100 μg·mL −1 COL2A1 or vehicle 2 (0.05 mol·L −1 acetic acid) for 1 h. h , i Immunoprecipitation was performed on 293T cells treated with COL2A1 or vehicle with anti-SMAD1 antibody ( h ) or anti-ERK1/2 antibody ( i ), followed by immunoblotting with anti-ERK1/2 and anti-SMAD1 antibodies. j Immunoblotting evaluation of SMAD1 in both nuclear (Nuc) and cytoplasmic (Cyto) extracts in SW1353 and Hs819.T cells pretreated with U0126 or vehicle 1 and then treated with COL2A1 or vehicle 2. k, l Immunoprecipitation was performed on 293T cells treated with COL2A1 or vehicle with anti-SMAD1 antibody ( k ) or anti-SMAD4 antibody ( l ), followed by immunoblotting with anti-SMAD4 antibody and anti-SMAD1 antibody. Data in ( f ) and ( g ) are presented as the mean ± SD ( n = 3). * P

    Techniques Used: Activity Assay, Mutagenesis, Mouse Assay, Expressing, Real-time Polymerase Chain Reaction, Immunoprecipitation

    COL2A1 exerted suppression on chondrocyte hypertrophy and on the production of matrix-degrading enzymes. a , b SW1353 and Hs819.T cells were treated with COL2A1 (100 μg·mL −1 ) or vehicle (0.05 mol·L −1 acetic acid) for 48 h, and the expression levels of RUNX2 and COL10A1 were detected by qPCR ( a ) and immunoblotting ( b ). c , d Human articular chondrocytes were transfected with COL2A1 siRNA or negative control siRNA, and the expression levels of RUNX2 and COL10A1 were detected by qPCR ( c ) and immunoblotting ( d ). e − g Pellet cultures of MSCs were induced to undergo chondrogenesis for 14 d and then induced for hypertrophic differentiation for another 14 d with purified COL2A1 or vehicle. In addition, pellet cultures of MSCs induced to undergo chondrogenesis for 28 d were used as chondrogenic controls. e Gross appearance, HE staining, safranin O staining, and Alcian blue staining were evaluated. Scale bars in the images of gross appearance: 1 mm; other scale bars in ( e ): 200 μm. The expression levels of COL10A1, RUNX2, and MMP13 were detected by qPCR ( f ) and immunoblotting ( g ). Data in ( a ), ( c ), and ( f ) are presented as the mean ± SD ( n = 3). * P
    Figure Legend Snippet: COL2A1 exerted suppression on chondrocyte hypertrophy and on the production of matrix-degrading enzymes. a , b SW1353 and Hs819.T cells were treated with COL2A1 (100 μg·mL −1 ) or vehicle (0.05 mol·L −1 acetic acid) for 48 h, and the expression levels of RUNX2 and COL10A1 were detected by qPCR ( a ) and immunoblotting ( b ). c , d Human articular chondrocytes were transfected with COL2A1 siRNA or negative control siRNA, and the expression levels of RUNX2 and COL10A1 were detected by qPCR ( c ) and immunoblotting ( d ). e − g Pellet cultures of MSCs were induced to undergo chondrogenesis for 14 d and then induced for hypertrophic differentiation for another 14 d with purified COL2A1 or vehicle. In addition, pellet cultures of MSCs induced to undergo chondrogenesis for 28 d were used as chondrogenic controls. e Gross appearance, HE staining, safranin O staining, and Alcian blue staining were evaluated. Scale bars in the images of gross appearance: 1 mm; other scale bars in ( e ): 200 μm. The expression levels of COL10A1, RUNX2, and MMP13 were detected by qPCR ( f ) and immunoblotting ( g ). Data in ( a ), ( c ), and ( f ) are presented as the mean ± SD ( n = 3). * P

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction, Transfection, Negative Control, Purification, Staining

    The ITGB1 receptor mediated the effect of COL2A1 on the BMP pathway and chondrocyte hypertrophy. a , b Immunoprecipitation with anti-BMPR1A ( a ) or anti-BMPR1B ( b ) antibody was performed in extracts of 293T cells treated with 100 μg·mL −1 COL2A1 or vehicle (0.05 mol·L −1 acetic acid) for 1 h, and then, immunoblotting was conducted with anti-phospho-serine/threonine and anti-BMPR1A/B antibodies. c − e Immunoblotting evaluation of p-ITGB1 and ITGB1 in chondrocytes of Col2a1 p.Gly1170Ser mutant mice ( c ), SW1353 and Hs819.T cells treated with COL2A1 or vehicle ( d ), and human articular chondrocytes transfected with COL2A1 siRNAs or negative control siRNA ( e ). f − h SW1353 and Hs819.T cells were pretreated with 10 μg·mL −1 ITGB1 blocking antibody or anti-human IgG antibody for 1 h and then treated with COL2A1 or vehicle for 1 h. Immunoblotting evaluation of p-ITGB1, p-SMAD1 S463/465 , ITGB1, and SMAD1 ( f ), and qPCR evaluation of ID1 , ID2 , DLX5 , RUNX2 , and COL10A1 ( g, h ) were performed. i Immunoblotting evaluation of SMAD1 in both nuclear (Nuc) and cytoplasmic (Cyto) extracts was performed in SW1353 and Hs819.T cells pretreated with ITGB1 blocking antibody or anti-human IgG and then treated with COL2A1 or vehicle. Data in ( g ) and ( h ) are presented as the mean ± SD ( n = 3). * P
    Figure Legend Snippet: The ITGB1 receptor mediated the effect of COL2A1 on the BMP pathway and chondrocyte hypertrophy. a , b Immunoprecipitation with anti-BMPR1A ( a ) or anti-BMPR1B ( b ) antibody was performed in extracts of 293T cells treated with 100 μg·mL −1 COL2A1 or vehicle (0.05 mol·L −1 acetic acid) for 1 h, and then, immunoblotting was conducted with anti-phospho-serine/threonine and anti-BMPR1A/B antibodies. c − e Immunoblotting evaluation of p-ITGB1 and ITGB1 in chondrocytes of Col2a1 p.Gly1170Ser mutant mice ( c ), SW1353 and Hs819.T cells treated with COL2A1 or vehicle ( d ), and human articular chondrocytes transfected with COL2A1 siRNAs or negative control siRNA ( e ). f − h SW1353 and Hs819.T cells were pretreated with 10 μg·mL −1 ITGB1 blocking antibody or anti-human IgG antibody for 1 h and then treated with COL2A1 or vehicle for 1 h. Immunoblotting evaluation of p-ITGB1, p-SMAD1 S463/465 , ITGB1, and SMAD1 ( f ), and qPCR evaluation of ID1 , ID2 , DLX5 , RUNX2 , and COL10A1 ( g, h ) were performed. i Immunoblotting evaluation of SMAD1 in both nuclear (Nuc) and cytoplasmic (Cyto) extracts was performed in SW1353 and Hs819.T cells pretreated with ITGB1 blocking antibody or anti-human IgG and then treated with COL2A1 or vehicle. Data in ( g ) and ( h ) are presented as the mean ± SD ( n = 3). * P

    Techniques Used: Immunoprecipitation, Mutagenesis, Mouse Assay, Transfection, Negative Control, Blocking Assay, Real-time Polymerase Chain Reaction

    COL2A1 suppressed chondrocyte hypertrophy through regulation of the BMP-SMAD1 pathway. a KEGG pathway functional annotations of the differentially expressed genes according to the qPCR analysis. Enrichment scores are displayed as −log( P value). A pathway was considered to be significantly enriched only if it passed the count threshold of five genes per annotation term and presented an EASE score, with the Benjamini−Hochberg correction set to 0.05. b , c Immunoblotting evaluation of p-Smad1 S463/465 , Smad1, Smad4, p-Smad2, p-Smad3, and Smad2/3 in chondrocytes of all three genotypes from Col2a1 p.Gly1170Ser mutant mice. d , e qPCR quantification of Id1 , Id2 , Dlx5 , Acvr1 , Stat1 , and Serpine1 in chondrocytes of Col2a1 mutant mice. f , g Immunoblotting evaluation of p-SMAD1 S463/465 , p-SMAD2, p-SMAD3, SMAD1, and SMAD2/3 ( f ), and qPCR quantification of ID1 , ID2 , DLX5 , ACVR1 , STAT1 , and SERPINE1 ( g ) were carried out in SW1353 and Hs819.T cells treated with 100 μg·mL −1 purified COL2A1 or vehicle (0.05 mol·L −1 acetic acid). h Immunoblotting evaluation of p-SMAD1 S463/465 , SMAD1, RUNX2, and COL10A1 in SW1353 and Hs819.T cells treated with vehicle (0.05 mol·L −1 acetic acid), 100 μg·mL −1 COL2A1, or 10 ng·mL −1 BMP2. i Human articular chondrocytes were treated with the indicated concentrations of BMP2 and 100 μg·mL −1 purified COL2A1, and the expression levels of p-SMAD1 S463/465 , SMAD1, RUNX2, and COL10A1 were detected by immunoblotting. j Confocal laser scanning was used to demonstrate SMAD1 nuclear localization in SW1353 and Hs819.T cells treated with COL2A1 or vehicle. Scale bars: 20 μm. k − m Injured cartilage samples from 50 OA patients underwent immunohistochemical staining using anti-COL2A1, p-SMAD1 S463/465 , and COL10A1 antibodies. k Representative micrographs of two patients are shown. Scale bars: 100 μm. l , m The correlation among the expression levels of three proteins was analyzed by the chi-squared test. Data in ( d ), ( e ), and ( g ) are presented as the mean ± SD ( n = 3). * P
    Figure Legend Snippet: COL2A1 suppressed chondrocyte hypertrophy through regulation of the BMP-SMAD1 pathway. a KEGG pathway functional annotations of the differentially expressed genes according to the qPCR analysis. Enrichment scores are displayed as −log( P value). A pathway was considered to be significantly enriched only if it passed the count threshold of five genes per annotation term and presented an EASE score, with the Benjamini−Hochberg correction set to 0.05. b , c Immunoblotting evaluation of p-Smad1 S463/465 , Smad1, Smad4, p-Smad2, p-Smad3, and Smad2/3 in chondrocytes of all three genotypes from Col2a1 p.Gly1170Ser mutant mice. d , e qPCR quantification of Id1 , Id2 , Dlx5 , Acvr1 , Stat1 , and Serpine1 in chondrocytes of Col2a1 mutant mice. f , g Immunoblotting evaluation of p-SMAD1 S463/465 , p-SMAD2, p-SMAD3, SMAD1, and SMAD2/3 ( f ), and qPCR quantification of ID1 , ID2 , DLX5 , ACVR1 , STAT1 , and SERPINE1 ( g ) were carried out in SW1353 and Hs819.T cells treated with 100 μg·mL −1 purified COL2A1 or vehicle (0.05 mol·L −1 acetic acid). h Immunoblotting evaluation of p-SMAD1 S463/465 , SMAD1, RUNX2, and COL10A1 in SW1353 and Hs819.T cells treated with vehicle (0.05 mol·L −1 acetic acid), 100 μg·mL −1 COL2A1, or 10 ng·mL −1 BMP2. i Human articular chondrocytes were treated with the indicated concentrations of BMP2 and 100 μg·mL −1 purified COL2A1, and the expression levels of p-SMAD1 S463/465 , SMAD1, RUNX2, and COL10A1 were detected by immunoblotting. j Confocal laser scanning was used to demonstrate SMAD1 nuclear localization in SW1353 and Hs819.T cells treated with COL2A1 or vehicle. Scale bars: 20 μm. k − m Injured cartilage samples from 50 OA patients underwent immunohistochemical staining using anti-COL2A1, p-SMAD1 S463/465 , and COL10A1 antibodies. k Representative micrographs of two patients are shown. Scale bars: 100 μm. l , m The correlation among the expression levels of three proteins was analyzed by the chi-squared test. Data in ( d ), ( e ), and ( g ) are presented as the mean ± SD ( n = 3). * P

    Techniques Used: Functional Assay, Real-time Polymerase Chain Reaction, Mutagenesis, Mouse Assay, Purification, Expressing, Immunohistochemistry, Staining

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  • hs 819  (ATCC)
    93
    ATCC hs 819
    Nuclear YAP1 is required for the growth of CHS cells. A  IHC analysis of YAP1 expression in tissue arrays of CHS of different grades. Representative images are shown. Scale bar: 50 μm. Well (well-differentiated,  N  = 43), moderate (moderately differentiated, = 17), poor (poorly differentiated,  N  = 20).  B  Quantification of YAP1 expression scores in ( A ).  C  The expression scores of YAP1 in the cytoplasm and nucleus in poorly differentiated CHS (Poor) were quantified.  D  The percentage of YAP1 expression in the cytoplasm and nucleus in the chondrocytic cell line (CHON-001) and CHS cell lines (SW 1353 and Hs 819.T). C: cytoplasm, N: nucleus.  E  Representative IF image of YAP1 localization (green) in SW 1353 cells. DAPI (blue) indicates the nucleus, while F-actin (red) defines the cytoskeleton. Scale bar: 10 μm.  F  IB analysis of YAP1 and HA-tagged expression in primary chondrocytes infected with lentivirus-delivered HA-vector (Vector), HA-YAP1 (YAP1), or HA-YAP1-5SA (5SA). Red arrows indicated both the endogenous and exogenous YAP1 expression. The elastic modulus and adhesion properties of the indicated cells were analyzed by AFM for at least three individual cells; representative images are shown below.  G  SW 1353 cells stably expressing control shRNA or YAP1-specific shRNAs (shYAP#1, #2, #3, #4) were established, and the knockdown efficiency was confirmed using an antibody against YAP1 for IB (above). The cell viabilities of each construct at varying time points were determined by a CCK-8 assay (below).  H  Colony formation ability (number of colonies) of the indicated stable cells is shown (above). Representative images are shown below. Data are presented as the mean ± SD of at least three independent experiments in panel ( B – D ,  F – H ). One-way ANOVA followed by Dunnett’s test was applied for ( B ,  F ,  H ). Student’s  t -test for ( C ,  D ). Two-way ANOVA followed by Tukey’s test for ( G ). n.s. nonsignificant, * P
    Hs 819, supplied by ATCC, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC sf ehec o157 nm 819 02
    Comparison of bacterial ammonia production after 24 h of culture in urea broth. Means ± standard deviations of ammonia measurements for E. coli strain ATCC 25922, <t>EHEC</t> <t>O157:H7</t> strain 4413/95, SF O157:NM strain 493/89, and EHEC O157:H7 strain EDL933 are shown. The data presented are from three independent experiments.
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    96
    ATCC sw1353 cell lines
    Analysis of miR-525 levels in CHS tissues and cells. (A) RT-qPCR analysis of miR-525 expression in normal control tissues and CHS tissues. (B) RT-qPCR analysis of miR-525 level in CHON-002, JJ012, Hs 819.T and <t>SW1353</t> cells. *P
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    Nuclear YAP1 is required for the growth of CHS cells. A  IHC analysis of YAP1 expression in tissue arrays of CHS of different grades. Representative images are shown. Scale bar: 50 μm. Well (well-differentiated,  N  = 43), moderate (moderately differentiated, = 17), poor (poorly differentiated,  N  = 20).  B  Quantification of YAP1 expression scores in ( A ).  C  The expression scores of YAP1 in the cytoplasm and nucleus in poorly differentiated CHS (Poor) were quantified.  D  The percentage of YAP1 expression in the cytoplasm and nucleus in the chondrocytic cell line (CHON-001) and CHS cell lines (SW 1353 and Hs 819.T). C: cytoplasm, N: nucleus.  E  Representative IF image of YAP1 localization (green) in SW 1353 cells. DAPI (blue) indicates the nucleus, while F-actin (red) defines the cytoskeleton. Scale bar: 10 μm.  F  IB analysis of YAP1 and HA-tagged expression in primary chondrocytes infected with lentivirus-delivered HA-vector (Vector), HA-YAP1 (YAP1), or HA-YAP1-5SA (5SA). Red arrows indicated both the endogenous and exogenous YAP1 expression. The elastic modulus and adhesion properties of the indicated cells were analyzed by AFM for at least three individual cells; representative images are shown below.  G  SW 1353 cells stably expressing control shRNA or YAP1-specific shRNAs (shYAP#1, #2, #3, #4) were established, and the knockdown efficiency was confirmed using an antibody against YAP1 for IB (above). The cell viabilities of each construct at varying time points were determined by a CCK-8 assay (below).  H  Colony formation ability (number of colonies) of the indicated stable cells is shown (above). Representative images are shown below. Data are presented as the mean ± SD of at least three independent experiments in panel ( B – D ,  F – H ). One-way ANOVA followed by Dunnett’s test was applied for ( B ,  F ,  H ). Student’s  t -test for ( C ,  D ). Two-way ANOVA followed by Tukey’s test for ( G ). n.s. nonsignificant, * P

    Journal: Cell Death & Disease

    Article Title: Sequential targeting of YAP1 and p21 enhances the elimination of senescent cells induced by the BET inhibitor JQ1

    doi: 10.1038/s41419-021-03416-1

    Figure Lengend Snippet: Nuclear YAP1 is required for the growth of CHS cells. A IHC analysis of YAP1 expression in tissue arrays of CHS of different grades. Representative images are shown. Scale bar: 50 μm. Well (well-differentiated, N  = 43), moderate (moderately differentiated, = 17), poor (poorly differentiated, N  = 20). B Quantification of YAP1 expression scores in ( A ). C The expression scores of YAP1 in the cytoplasm and nucleus in poorly differentiated CHS (Poor) were quantified. D The percentage of YAP1 expression in the cytoplasm and nucleus in the chondrocytic cell line (CHON-001) and CHS cell lines (SW 1353 and Hs 819.T). C: cytoplasm, N: nucleus. E Representative IF image of YAP1 localization (green) in SW 1353 cells. DAPI (blue) indicates the nucleus, while F-actin (red) defines the cytoskeleton. Scale bar: 10 μm. F IB analysis of YAP1 and HA-tagged expression in primary chondrocytes infected with lentivirus-delivered HA-vector (Vector), HA-YAP1 (YAP1), or HA-YAP1-5SA (5SA). Red arrows indicated both the endogenous and exogenous YAP1 expression. The elastic modulus and adhesion properties of the indicated cells were analyzed by AFM for at least three individual cells; representative images are shown below. G SW 1353 cells stably expressing control shRNA or YAP1-specific shRNAs (shYAP#1, #2, #3, #4) were established, and the knockdown efficiency was confirmed using an antibody against YAP1 for IB (above). The cell viabilities of each construct at varying time points were determined by a CCK-8 assay (below). H Colony formation ability (number of colonies) of the indicated stable cells is shown (above). Representative images are shown below. Data are presented as the mean ± SD of at least three independent experiments in panel ( B – D , F – H ). One-way ANOVA followed by Dunnett’s test was applied for ( B , F , H ). Student’s t -test for ( C , D ). Two-way ANOVA followed by Tukey’s test for ( G ). n.s. nonsignificant, * P

    Article Snippet: CHON-001, SW 1353, Hs 819.T, and U2 OS cells were obtained from the American Type Culture Collection (ATCC, VA, USA) and authenticated by a polymerase chain reaction of short tandem repeat (STR) sequences, as we described previously .

    Techniques: Immunohistochemistry, Expressing, Infection, Plasmid Preparation, Stable Transfection, shRNA, Construct, CCK-8 Assay

    YAP1/TEAD controls cell cycle exit and induces cellular senescence. A  Cell cycle distribution analysis in the groups of control shRNA and YAP1-specific shRNAs (shYAP#2, #3, #4).  B ,  C  Control shRNA or YAP1-depleted SW 1353 cells were stained with SA-β-gal, and the representative images are shown in ( B ); the percentage of SA-β-gal-positive cells was quantified and shown in ( C ), scale bars: 10 μm.  D  Hs 819.T cells were infected with lentivirus of control shRNA or YAP1-specific shRNAs (shYAP#3, #4), and then the percentage of SA-β-gal-positive cells was quantified.  E ,  F  YAP1 depletion inhibits cell proliferation. Cell proliferation was determined by the EdU incorporation assay ( E ), scale bar: 10 μm. DAPI was used as a nuclear counterstain. The percentage of cells that incorporated EdU was quantified ( F ).  G  Knockdown of YAP1 induces the increase of p21 expression, independent of cell density. Expression of the indicated proteins was determined by IB.  H – J  YAP1-TEAD plays a role in regulating CHS cell senescence. control shRNA or YAP1-depleted SW 1353 cells were transiently transfected with HA-vector (Vector), HA-YAP1-5SA (YAP1-5SA), or HA-YAP1-5SA/S94A (YAP1-5SA/S94A) for 72 h, and then the protein levels of HA, Cyr61, and p21 were determined by IB ( H ). The percentage of SA-β-gal-positive cells was quantified ( I ), and representative images are shown in ( J ); scale bars: 10 μm. Data are presented as the mean ± SD of at least three independent experiments in ( A ,  C ,  D ,  F ,  I ). One-way ANOVA followed by Dunnett’s test was applied for ( A ,  C ,  D ,  F ). Two-way ANOVA followed by Tukey’s test for ( I ). n.s. nonsignificant, * P

    Journal: Cell Death & Disease

    Article Title: Sequential targeting of YAP1 and p21 enhances the elimination of senescent cells induced by the BET inhibitor JQ1

    doi: 10.1038/s41419-021-03416-1

    Figure Lengend Snippet: YAP1/TEAD controls cell cycle exit and induces cellular senescence. A Cell cycle distribution analysis in the groups of control shRNA and YAP1-specific shRNAs (shYAP#2, #3, #4). B , C Control shRNA or YAP1-depleted SW 1353 cells were stained with SA-β-gal, and the representative images are shown in ( B ); the percentage of SA-β-gal-positive cells was quantified and shown in ( C ), scale bars: 10 μm. D Hs 819.T cells were infected with lentivirus of control shRNA or YAP1-specific shRNAs (shYAP#3, #4), and then the percentage of SA-β-gal-positive cells was quantified. E , F YAP1 depletion inhibits cell proliferation. Cell proliferation was determined by the EdU incorporation assay ( E ), scale bar: 10 μm. DAPI was used as a nuclear counterstain. The percentage of cells that incorporated EdU was quantified ( F ). G Knockdown of YAP1 induces the increase of p21 expression, independent of cell density. Expression of the indicated proteins was determined by IB. H – J YAP1-TEAD plays a role in regulating CHS cell senescence. control shRNA or YAP1-depleted SW 1353 cells were transiently transfected with HA-vector (Vector), HA-YAP1-5SA (YAP1-5SA), or HA-YAP1-5SA/S94A (YAP1-5SA/S94A) for 72 h, and then the protein levels of HA, Cyr61, and p21 were determined by IB ( H ). The percentage of SA-β-gal-positive cells was quantified ( I ), and representative images are shown in ( J ); scale bars: 10 μm. Data are presented as the mean ± SD of at least three independent experiments in ( A , C , D , F , I ). One-way ANOVA followed by Dunnett’s test was applied for ( A , C , D , F ). Two-way ANOVA followed by Tukey’s test for ( I ). n.s. nonsignificant, * P

    Article Snippet: CHON-001, SW 1353, Hs 819.T, and U2 OS cells were obtained from the American Type Culture Collection (ATCC, VA, USA) and authenticated by a polymerase chain reaction of short tandem repeat (STR) sequences, as we described previously .

    Techniques: shRNA, Staining, Infection, Expressing, Transfection, Plasmid Preparation

    Comparison of bacterial ammonia production after 24 h of culture in urea broth. Means ± standard deviations of ammonia measurements for E. coli strain ATCC 25922, EHEC O157:H7 strain 4413/95, SF O157:NM strain 493/89, and EHEC O157:H7 strain EDL933 are shown. The data presented are from three independent experiments.

    Journal: Journal of Clinical Microbiology

    Article Title: Distribution of the Urease Gene Cluster among and Urease Activities of Enterohemorrhagic Escherichia coli O157 Isolates from Humans

    doi: 10.1128/JCM.43.2.546-550.2005

    Figure Lengend Snippet: Comparison of bacterial ammonia production after 24 h of culture in urea broth. Means ± standard deviations of ammonia measurements for E. coli strain ATCC 25922, EHEC O157:H7 strain 4413/95, SF O157:NM strain 493/89, and EHEC O157:H7 strain EDL933 are shown. The data presented are from three independent experiments.

    Article Snippet: After 24 h of culture in urea broth, ammonia production by strain 4413/95 was significantly higher than that by strains EDL933, SF EHEC O157:NM 819/02, and ATCC 25922, which were all negative on Christensen agar (Fig. ).

    Techniques:

    Analysis of miR-525 levels in CHS tissues and cells. (A) RT-qPCR analysis of miR-525 expression in normal control tissues and CHS tissues. (B) RT-qPCR analysis of miR-525 level in CHON-002, JJ012, Hs 819.T and SW1353 cells. *P

    Journal: Oncology Letters

    Article Title: MicroRNA-525 enhances chondrosarcoma malignancy by targeting F-spondin 1

    doi: 10.3892/ol.2018.9711

    Figure Lengend Snippet: Analysis of miR-525 levels in CHS tissues and cells. (A) RT-qPCR analysis of miR-525 expression in normal control tissues and CHS tissues. (B) RT-qPCR analysis of miR-525 level in CHON-002, JJ012, Hs 819.T and SW1353 cells. *P

    Article Snippet: The human chondrosarcoma JJ012, Hs 819.T and SW1353 cell lines were purchased from the American Type Culture Collection (ATCC; Manassas, VA, USA).

    Techniques: Quantitative RT-PCR, Expressing

    Enhanced SPON1 expression in CHS tissues and cells. (A) Western blot analysis was performed to evaluate the protein levels of SPON1 in the CHS tissues and the normal control tissues. (B) Western blotting assay was conducted to explore the protein levels of SPON1 in JJ012, Hs 819.T, SW1353 and CHON-002 cells. The Hs819.T lane was run discontinuously with the other lanes in the gel and the separation is indicated by a dashed line. *P

    Journal: Oncology Letters

    Article Title: MicroRNA-525 enhances chondrosarcoma malignancy by targeting F-spondin 1

    doi: 10.3892/ol.2018.9711

    Figure Lengend Snippet: Enhanced SPON1 expression in CHS tissues and cells. (A) Western blot analysis was performed to evaluate the protein levels of SPON1 in the CHS tissues and the normal control tissues. (B) Western blotting assay was conducted to explore the protein levels of SPON1 in JJ012, Hs 819.T, SW1353 and CHON-002 cells. The Hs819.T lane was run discontinuously with the other lanes in the gel and the separation is indicated by a dashed line. *P

    Article Snippet: The human chondrosarcoma JJ012, Hs 819.T and SW1353 cell lines were purchased from the American Type Culture Collection (ATCC; Manassas, VA, USA).

    Techniques: Expressing, Western Blot

    MiR-525 suppressed SW1353 cell migration and invasion and prompted cell apoptosis. (A) Cell migration and (B) invasion assay of the overexpression of miR-525 (C) Flow cytometry analyses revealed that miR-525 significantly increased the population of apoptotic cells. **P

    Journal: Oncology Letters

    Article Title: MicroRNA-525 enhances chondrosarcoma malignancy by targeting F-spondin 1

    doi: 10.3892/ol.2018.9711

    Figure Lengend Snippet: MiR-525 suppressed SW1353 cell migration and invasion and prompted cell apoptosis. (A) Cell migration and (B) invasion assay of the overexpression of miR-525 (C) Flow cytometry analyses revealed that miR-525 significantly increased the population of apoptotic cells. **P

    Article Snippet: The human chondrosarcoma JJ012, Hs 819.T and SW1353 cell lines were purchased from the American Type Culture Collection (ATCC; Manassas, VA, USA).

    Techniques: Migration, Invasion Assay, Over Expression, Flow Cytometry, Cytometry