rnascope probe-rn-cdkn2a Search Results


rnascope probe-rn-cdkn2a  (Cosmo Bio USA)
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Senescent satellite cells and mesenchymal progenitor cells were present in DMD rats. ( a – c ) Quantification of mRNA levels of senescence markers (p16, p19, and p21) in WT and DMD rat TA muscles (n = 6, each). ( d ) In situ hybridisation of <t>CDKN2A</t> mRNA using RNAscope on TA muscle sections from 6-month-old WT and DMD rats. Shown are representative images of tissues from WT (top) and DMD rats (middle) with CDKN2A mRNA appearing as brown dots. Scale bar = 50 μm. A higher magnification image from the dotted area is shown in the bottom frame. Scale bar = 10 μm. The white arrowheads show the mononucleated CDKN2A mRNA + cells. ( e ) Skeletal muscle primary cells from 6-month-old DMD rats were subjected to CDKN2A mRNA in situ hybridisation using RNAscope before the immunocytochemistry of Pax7, CSPG4, CD45, and CD31. Scale bar = 10 μm. White arrowheads indicate DAB signal. White arrows indicate CD45 + or CD31 + cells. ( f ) Quantification of CDKN2A + Pax7 + cells per all Pax7 + cells (shown as SC) and CDKN2A + CSPG4 + cells per all CSPG4 + cells (shown as MPC) in skeletal muscle primary cells from DMD rats (n = 4, each). Data are expressed as mean + SEM, and were compared by Tukey Kramer’s test. For ( a – c ), the result of statistical comparison only between the genotypes at each indicated ages was displayed. When a significant age-related difference was observed by the Tukey–Kramer’s test, the † mark was added beside the legend of the graph. *p < 0.05. **p < 0.01. ***p < 0.001.
Rnascope Probe Rn Cdkn2a, supplied by Cosmo Bio USA, 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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Senescent satellite cells and mesenchymal progenitor cells were present in DMD rats. ( a – c ) Quantification of mRNA levels of senescence markers (p16, p19, and p21) in WT and DMD rat TA muscles (n = 6, each). ( d ) In situ hybridisation of CDKN2A mRNA using RNAscope on TA muscle sections from 6-month-old WT and DMD rats. Shown are representative images of tissues from WT (top) and DMD rats (middle) with CDKN2A mRNA appearing as brown dots. Scale bar = 50 μm. A higher magnification image from the dotted area is shown in the bottom frame. Scale bar = 10 μm. The white arrowheads show the mononucleated CDKN2A mRNA + cells. ( e ) Skeletal muscle primary cells from 6-month-old DMD rats were subjected to CDKN2A mRNA in situ hybridisation using RNAscope before the immunocytochemistry of Pax7, CSPG4, CD45, and CD31. Scale bar = 10 μm. White arrowheads indicate DAB signal. White arrows indicate CD45 + or CD31 + cells. ( f ) Quantification of CDKN2A + Pax7 + cells per all Pax7 + cells (shown as SC) and CDKN2A + CSPG4 + cells per all CSPG4 + cells (shown as MPC) in skeletal muscle primary cells from DMD rats (n = 4, each). Data are expressed as mean + SEM, and were compared by Tukey Kramer’s test. For ( a – c ), the result of statistical comparison only between the genotypes at each indicated ages was displayed. When a significant age-related difference was observed by the Tukey–Kramer’s test, the † mark was added beside the legend of the graph. *p < 0.05. **p < 0.01. ***p < 0.001.

Journal: Scientific Reports

Article Title: Cellular senescence-mediated exacerbation of Duchenne muscular dystrophy

doi: 10.1038/s41598-020-73315-6

Figure Lengend Snippet: Senescent satellite cells and mesenchymal progenitor cells were present in DMD rats. ( a – c ) Quantification of mRNA levels of senescence markers (p16, p19, and p21) in WT and DMD rat TA muscles (n = 6, each). ( d ) In situ hybridisation of CDKN2A mRNA using RNAscope on TA muscle sections from 6-month-old WT and DMD rats. Shown are representative images of tissues from WT (top) and DMD rats (middle) with CDKN2A mRNA appearing as brown dots. Scale bar = 50 μm. A higher magnification image from the dotted area is shown in the bottom frame. Scale bar = 10 μm. The white arrowheads show the mononucleated CDKN2A mRNA + cells. ( e ) Skeletal muscle primary cells from 6-month-old DMD rats were subjected to CDKN2A mRNA in situ hybridisation using RNAscope before the immunocytochemistry of Pax7, CSPG4, CD45, and CD31. Scale bar = 10 μm. White arrowheads indicate DAB signal. White arrows indicate CD45 + or CD31 + cells. ( f ) Quantification of CDKN2A + Pax7 + cells per all Pax7 + cells (shown as SC) and CDKN2A + CSPG4 + cells per all CSPG4 + cells (shown as MPC) in skeletal muscle primary cells from DMD rats (n = 4, each). Data are expressed as mean + SEM, and were compared by Tukey Kramer’s test. For ( a – c ), the result of statistical comparison only between the genotypes at each indicated ages was displayed. When a significant age-related difference was observed by the Tukey–Kramer’s test, the † mark was added beside the legend of the graph. *p < 0.05. **p < 0.01. ***p < 0.001.

Article Snippet: Then, the samples were hybridised with RNAscope Probe-Rn-CDKN2A (for rat samples; Cosmo Bio) or RNAscope Probe-Hs-CDKN2A (for human samples; Cosmo Bio) for 2 h, and signals were amplified with AMP1 to 6 (Cosmo Bio).

Techniques: In Situ, Hybridization, Immunocytochemistry

Senolytic drug ABT263 inhibits the exacerbation of muscular dystrophy in DMD rats. ( a ) Quantification of mRNA levels of senescence markers (p16, p19, and p21) in vehicle- and ABT263-treated rats (n = 7, 9). ( b ) In situ hybridisation of CDKN2A mRNA using RNAscope on TA muscle sections from vehicle- or ABT263-treated rats, with CDKN2A mRNA appearing as red dots. The white arrowheads show the CDKN2A mRNA + cells. Scale bar = 50 μm. ( c ) Quantification of the number of CDKN2A mRNA positive mononucleated cells per section from vehicle- or ABT263-treated rats. ( d ) Body weight comparison before and after treatment with vehicle (left panel) or ABT263 (right panel) (n = 7, 9). ( e ) Quantification of maximum muscle strength by grip test before and after treatment with vehicle (left panel) or ABT263 (right panel) (n = 7, 9). ( f ) Immunoblotting analysis of perilipin expression in vehicle- and ABT263-treated rats. Full-length blots are presented in Supplementary Figure a. ( g ) Quantification of perilipin protein expression (n = 7, 9). ( h ) Masson Trichrome stains of TA muscles from vehicle and ABT263-treated rats. Scale bar = 100 μm. ( i ) Quantification of Masson Trichrome staining positive area per section (n = 7, 9). ( j ) Immunohistochemical analysis of eMHC in TA muscle sections from vehicle- and ABT263-treated rats. Scale bar = 100 μm. ( k ) Quantification of eMHC positive fibres per section (n = 7, 9). ( l , m ) Quantification of ( l ) Pax7 + cells and ( m ) MyoD + cells of skeletal muscle primary cells from vehicle- and ABT263-treated rats (n = 7, 9). ( n ) Quantification of mRNA levels of SASP markers (IL-6, TGF-β 1 , IL-1β, CTGF, and MMP2) in vehicle- and ABT263-treated rats (n = 7, 9). Data are expressed as mean ± SEM. The p-value was determined by paired Student’s t test for ( d ) and ( e ), and unpaired Student’s t test for others. *p < 0.05, **p < 0.01. n.s. not significant.

Journal: Scientific Reports

Article Title: Cellular senescence-mediated exacerbation of Duchenne muscular dystrophy

doi: 10.1038/s41598-020-73315-6

Figure Lengend Snippet: Senolytic drug ABT263 inhibits the exacerbation of muscular dystrophy in DMD rats. ( a ) Quantification of mRNA levels of senescence markers (p16, p19, and p21) in vehicle- and ABT263-treated rats (n = 7, 9). ( b ) In situ hybridisation of CDKN2A mRNA using RNAscope on TA muscle sections from vehicle- or ABT263-treated rats, with CDKN2A mRNA appearing as red dots. The white arrowheads show the CDKN2A mRNA + cells. Scale bar = 50 μm. ( c ) Quantification of the number of CDKN2A mRNA positive mononucleated cells per section from vehicle- or ABT263-treated rats. ( d ) Body weight comparison before and after treatment with vehicle (left panel) or ABT263 (right panel) (n = 7, 9). ( e ) Quantification of maximum muscle strength by grip test before and after treatment with vehicle (left panel) or ABT263 (right panel) (n = 7, 9). ( f ) Immunoblotting analysis of perilipin expression in vehicle- and ABT263-treated rats. Full-length blots are presented in Supplementary Figure a. ( g ) Quantification of perilipin protein expression (n = 7, 9). ( h ) Masson Trichrome stains of TA muscles from vehicle and ABT263-treated rats. Scale bar = 100 μm. ( i ) Quantification of Masson Trichrome staining positive area per section (n = 7, 9). ( j ) Immunohistochemical analysis of eMHC in TA muscle sections from vehicle- and ABT263-treated rats. Scale bar = 100 μm. ( k ) Quantification of eMHC positive fibres per section (n = 7, 9). ( l , m ) Quantification of ( l ) Pax7 + cells and ( m ) MyoD + cells of skeletal muscle primary cells from vehicle- and ABT263-treated rats (n = 7, 9). ( n ) Quantification of mRNA levels of SASP markers (IL-6, TGF-β 1 , IL-1β, CTGF, and MMP2) in vehicle- and ABT263-treated rats (n = 7, 9). Data are expressed as mean ± SEM. The p-value was determined by paired Student’s t test for ( d ) and ( e ), and unpaired Student’s t test for others. *p < 0.05, **p < 0.01. n.s. not significant.

Article Snippet: Then, the samples were hybridised with RNAscope Probe-Rn-CDKN2A (for rat samples; Cosmo Bio) or RNAscope Probe-Hs-CDKN2A (for human samples; Cosmo Bio) for 2 h, and signals were amplified with AMP1 to 6 (Cosmo Bio).

Techniques: In Situ, Hybridization, Western Blot, Expressing, Staining, Immunohistochemical staining

Senescence markers were elevated in human DMD patients. ( a – c ) Quantification of mRNA levels of senescence markers (p16, p14, and p21) in non-DMD control individuals and patients with DMD. Individual data from non-DMD control individuals and DMD patients are expressed as bar graphs (n = 10, 35). The grey band behind the graph indicates the mean ± SEM value range of the non-DMD control group. The figure without a grey band indicate that the target gene expression was not observed in the non-DMD control group. ( d , e ) Skeletal muscle sections from DMD patients were subjected to in situ hybridisation of CDKN2A mRNA using RNAscope before immunocytochemical analysis of ( d ) Pax7 or ( e ) PDGFRα with laminin. CDKN2A mRNA appears as brown dots. Scale bar = 10 μm. White arrowheads indicate DAB signal. N.D. not detected.

Journal: Scientific Reports

Article Title: Cellular senescence-mediated exacerbation of Duchenne muscular dystrophy

doi: 10.1038/s41598-020-73315-6

Figure Lengend Snippet: Senescence markers were elevated in human DMD patients. ( a – c ) Quantification of mRNA levels of senescence markers (p16, p14, and p21) in non-DMD control individuals and patients with DMD. Individual data from non-DMD control individuals and DMD patients are expressed as bar graphs (n = 10, 35). The grey band behind the graph indicates the mean ± SEM value range of the non-DMD control group. The figure without a grey band indicate that the target gene expression was not observed in the non-DMD control group. ( d , e ) Skeletal muscle sections from DMD patients were subjected to in situ hybridisation of CDKN2A mRNA using RNAscope before immunocytochemical analysis of ( d ) Pax7 or ( e ) PDGFRα with laminin. CDKN2A mRNA appears as brown dots. Scale bar = 10 μm. White arrowheads indicate DAB signal. N.D. not detected.

Article Snippet: Then, the samples were hybridised with RNAscope Probe-Rn-CDKN2A (for rat samples; Cosmo Bio) or RNAscope Probe-Hs-CDKN2A (for human samples; Cosmo Bio) for 2 h, and signals were amplified with AMP1 to 6 (Cosmo Bio).

Techniques: Expressing, In Situ, Hybridization