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Cell Signaling Technology Inc rabbit monoclonal anti human p16

Expression of autophagy and senescence markers in fibroblasts derived from IPF and control lungs. ( A ) Western blot analysis of EPDR1, lysosomal marker (LAMP1), autophagy markers (LC3B, p62), and senescence markers (p21, <t>p16)</t> in primary lung fibroblasts from controls ( n = 10) and IPF patients ( n = 10). ( B ) Quantification of protein levels normalized to β-actin. Group comparisons were analyzed using Quade’s ANCOVA with age as a covariate. Data are presented as mean ± SEM.

Rabbit Monoclonal Anti Human P16, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 104 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "EPDR1 Links Fibroblast Dysfunction to Disease Severity in Idiopathic Pulmonary Fibrosis"

Article Title: EPDR1 Links Fibroblast Dysfunction to Disease Severity in Idiopathic Pulmonary Fibrosis

Journal: Cells

doi: 10.3390/cells14191515

Figure Legend Snippet: Expression of autophagy and senescence markers in fibroblasts derived from IPF and control lungs. ( A ) Western blot analysis of EPDR1, lysosomal marker (LAMP1), autophagy markers (LC3B, p62), and senescence markers (p21, p16) in primary lung fibroblasts from controls ( n = 10) and IPF patients ( n = 10). ( B ) Quantification of protein levels normalized to β-actin. Group comparisons were analyzed using Quade’s ANCOVA with age as a covariate. Data are presented as mean ± SEM.

Techniques Used: Expressing, Derivative Assay, Control, Western Blot, Marker

Effect of EPDR1 knockdown on autophagy and senescence marker expression in fibroblasts derived from IPF lungs. Primary lung fibroblasts were transfected with scramble (SCR) or EPDR1 siRNA. ( A ) Representative images of SA-β-gal staining in fibroblasts transfected with SCR or EPDR1 siRNA. ( B ) Quantification of SA-β-gal staining in fibroblasts transfected with SCR or EPDR1 siRNA. Quantification was performed using primary fibroblasts from three different patients. For each sample, six randomly selected fields were imaged under a light microscope at 100× magnification. ( C ) Western blot analysis of EPDR1, lysosomal marker (LAMP1), autophagy markers (LC3B, p62), and senescence markers (p21, p16) in six fibroblasts transfected with SCR or EPDR1 siRNA. ( D ) Densitometric quantification normalized to β-actin from six independent experiments.

Figure Legend Snippet: Effect of EPDR1 knockdown on autophagy and senescence marker expression in fibroblasts derived from IPF lungs. Primary lung fibroblasts were transfected with scramble (SCR) or EPDR1 siRNA. ( A ) Representative images of SA-β-gal staining in fibroblasts transfected with SCR or EPDR1 siRNA. ( B ) Quantification of SA-β-gal staining in fibroblasts transfected with SCR or EPDR1 siRNA. Quantification was performed using primary fibroblasts from three different patients. For each sample, six randomly selected fields were imaged under a light microscope at 100× magnification. ( C ) Western blot analysis of EPDR1, lysosomal marker (LAMP1), autophagy markers (LC3B, p62), and senescence markers (p21, p16) in six fibroblasts transfected with SCR or EPDR1 siRNA. ( D ) Densitometric quantification normalized to β-actin from six independent experiments.

Techniques Used: Knockdown, Marker, Expressing, Derivative Assay, Transfection, Staining, Light Microscopy, Western Blot

Inhibition:

Article Title: Involvement of ERCC1 in the Pathogenesis of Osteoarthritis Through the Modulation of Apoptosis and Cellular Senescence
Article Snippet: Sodium Dodecyl Sulfate (SDS)–Polyacrylamide Gel Electrophoresis and Immunoblotting Chondrocytes were lysed and SDS–polyacrylamide gel electrophoresis and immunoblotting were performed as reported previously.Sodium Dodecyl Sulfate (SDS)–Polyacrylamide Gel Electrophoresis and Immunoblotting Chondrocytes were lysed and SDS–polyacrylamide gel electrophoresis and immunoblotting were performed as reported previously.. 20 , 21 The following antibodies were used: rabbit anti-human ERCC1, rabbit anti-human p16, rabbit anti-human cleaved poly (ADP-ribose) polymerase (PARP; all from Cell Signaling), rabbit anti-human matrix metallopeptidase (MMP)13, rabbit anti-human IL-6 (both from Abcam, Cambridge, England), mouse anti-human collagen type II, alpha 1 (COL2A1; Millipore, Billerica, MA), HRP-conjugated goat anti-rabbit IgG, and HRP-conjugated goat anti-mouse IgG (both from Cell Signaling).. The intensities of the bands were quantified using ImageJ software (National Institutes of Health).The intensities of the bands were quantified using ImageJ software (National Institutes of Health).

Article Title: Involvement of ERCC1 in the Pathogenesis of Osteoarthritis Through the Modulation of Apoptosis and Cellular Senescence
Article Snippet: Chondrocytes were lysed and SDS–polyacrylamide gel electrophoresis and immunoblotting were performed as reported previously.Chondrocytes were lysed and SDS–polyacrylamide gel electrophoresis and immunoblotting were performed as reported previously.. 20 , 21 The following antibodies were used: rabbit anti-human ERCC1, rabbit anti-human p16, rabbit anti-human cleaved poly (ADP-ribose) polymerase (PARP; all from Cell Signaling), rabbit anti-human matrix metallopeptidase (MMP)13, rabbit anti-human IL-6 (both from Abcam, Cambridge, England), mouse anti-human collagen type II, alpha 1 (COL2A1; Millipore, Billerica, MA), HRP-conjugated goat anti-rabbit IgG, and HRP-conjugated goat anti-mouse IgG (both from Cell Signaling).. The intensities of the bands were quantified using ImageJ software (National Institutes of Health).The intensities of the bands were quantified using ImageJ software (National Institutes of Health).

Western Blot:

Expressing:

Image Search Results

Senescence induction in BC cells following OxxySlab lysate treatment. Cell lines were treated with OxxySlab lysate (75–150 μg/mL) for 48 h. Senescent cells were identified by β-galactosidase staining (β-gal). Representative phase-contrast images of T24 ( A ), 5637 ( E ) and SV-HUC-1 ( I ) β-gal-positive cells (blue staining) are shown. Quantification of senescence was performed by measuring the Mean Gray Value of blue staining intensity using ImageJ software, with data expressed as Inverted Mean Gray Value (255 − MGV), which directly reflects β-gal activity. Data are expressed as mean ± SEM of two independent experiments in triplicate. Western blot analysis of the senescence markers p21, p53 and p16 was performed in untreated (CNTR) and OxxySlab -treated T24 ( B – D ), 5637 ( F – H ), and SV-HUC1 ( J – L ) cells. Protein levels were quantified by densitometry, normalized to GAPDH, and expressed as fold change relative to CNTR of three independent experiments (mean ± SEM). Statistical significance was assessed by one-way ANOVA followed by Tukey post hoc test (* p < 0.05, ** p < 0.01).

Journal: Antioxidants

Article Title: Exploring the Anticancer Potential of the Multistrain Probiotic Formulation OxxySlab in Bladder Cancer Cell Lines

doi: 10.3390/antiox14111282

Figure Lengend Snippet: Senescence induction in BC cells following OxxySlab lysate treatment. Cell lines were treated with OxxySlab lysate (75–150 μg/mL) for 48 h. Senescent cells were identified by β-galactosidase staining (β-gal). Representative phase-contrast images of T24 ( A ), 5637 ( E ) and SV-HUC-1 ( I ) β-gal-positive cells (blue staining) are shown. Quantification of senescence was performed by measuring the Mean Gray Value of blue staining intensity using ImageJ software, with data expressed as Inverted Mean Gray Value (255 − MGV), which directly reflects β-gal activity. Data are expressed as mean ± SEM of two independent experiments in triplicate. Western blot analysis of the senescence markers p21, p53 and p16 was performed in untreated (CNTR) and OxxySlab -treated T24 ( B – D ), 5637 ( F – H ), and SV-HUC1 ( J – L ) cells. Protein levels were quantified by densitometry, normalized to GAPDH, and expressed as fold change relative to CNTR of three independent experiments (mean ± SEM). Statistical significance was assessed by one-way ANOVA followed by Tukey post hoc test (* p < 0.05, ** p < 0.01).

Article Snippet: Following incubation with 5% non-fat dry milk in Tris-buffered saline for 1 h at room temperature, the membranes were incubated overnight at 4 °C with primary antibodies: goat anti-human vimentin polyclonal antibody (Chemicon International, Temecula, CA, USA; dilution 1:100), mouse anti-human E-cadherin monoclonal antibody (Cell Signaling Technology; dilution 1:1000), rabbit anti-human β-catenin monoclonal antibody (Cell Signaling Technology; dilution 1:1000), rabbit anti-human p21 polyclonal antibody (Santa Cruz Biotechnology, Dallas, TX, USA dilution 1:1000); rabbit anti-human phospho-Nrf2 monoclonal antibody (S40) (1:2000, Abcam, Cambridge, UK); rabbit anti-human p16 polyclonal antibody (Santa Cruz Biotechnology, dilution 1:200); mouse anti-human p53 monoclonal antibody (Santa Cruz Biotechnology, dilution 1:1000); mouse anti-human GAPDH monoclonal antibody (Immunological Sciences, Rome, Italy; dilution 1:1000).

Techniques: Staining, Software, Activity Assay, Western Blot

Journal: Cells

Article Title: EPDR1 Links Fibroblast Dysfunction to Disease Severity in Idiopathic Pulmonary Fibrosis

doi: 10.3390/cells14191515

Figure Lengend Snippet: Expression of autophagy and senescence markers in fibroblasts derived from IPF and control lungs. ( A ) Western blot analysis of EPDR1, lysosomal marker (LAMP1), autophagy markers (LC3B, p62), and senescence markers (p21, p16) in primary lung fibroblasts from controls ( n = 10) and IPF patients ( n = 10). ( B ) Quantification of protein levels normalized to β-actin. Group comparisons were analyzed using Quade’s ANCOVA with age as a covariate. Data are presented as mean ± SEM.

Article Snippet: Following blocking, the membranes were incubated with primary antibodies: rabbit polyclonal anti-EPDR1 (1:1000; Abcam, Cambridge, UK), mouse monoclonal anti-LC3B (1:1000; Santa Cruz Biotechnology, Dallas, TX, USA), mouse monoclonal anti-human p62 (1:1000; Santa Cruz Biotechnology, Santa Cruz, CA, USA), rabbit polyclonal anti-human p21 (1:1000; Abcam, Cambridge, UK), rabbit monoclonal anti-human p16 (1:1000; Cell Signaling Technology, Danvers, MA, USA), rabbit polyclonal anti-human α-smooth muscle actin (α-SMA) (1:2000; Abcam, Cambridge, UK), rabbit polyclonal anti-human COL1A1 (1:1000; Abcam, Cambridge, UK), rabbit polyclonal anti-human fibronectin (FN1) (1:2000; Abcam, Cambridge, UK), and mouse monoclonal anti-human β-actin (1:50,000; Sigma-Aldrich).

Techniques: Expressing, Derivative Assay, Control, Western Blot, Marker

Journal: Cells

Article Title: EPDR1 Links Fibroblast Dysfunction to Disease Severity in Idiopathic Pulmonary Fibrosis

doi: 10.3390/cells14191515

Figure Lengend Snippet: Effect of EPDR1 knockdown on autophagy and senescence marker expression in fibroblasts derived from IPF lungs. Primary lung fibroblasts were transfected with scramble (SCR) or EPDR1 siRNA. ( A ) Representative images of SA-β-gal staining in fibroblasts transfected with SCR or EPDR1 siRNA. ( B ) Quantification of SA-β-gal staining in fibroblasts transfected with SCR or EPDR1 siRNA. Quantification was performed using primary fibroblasts from three different patients. For each sample, six randomly selected fields were imaged under a light microscope at 100× magnification. ( C ) Western blot analysis of EPDR1, lysosomal marker (LAMP1), autophagy markers (LC3B, p62), and senescence markers (p21, p16) in six fibroblasts transfected with SCR or EPDR1 siRNA. ( D ) Densitometric quantification normalized to β-actin from six independent experiments.

Techniques: Knockdown, Marker, Expressing, Derivative Assay, Transfection, Staining, Light Microscopy, Western Blot

( A ) Representative images of SA-β-gal–stained retina sections from blank mice, and EAU mice treated with vehicle or DNase I (red arrows indicate stained vascular wall). Scale bar: 100 μm. ( B ) Representative images of SA-β-gal–stained RMECs treated with PBS, NETs, or NETs pretreated by DNase I for 24 hours. Scale bar: 100 μm. ( C ) The secretion of IL-6, IL-1β, IL-8 and CCL20 from RMECs was detected and measured via ELISA ( n = 4). ( D ) Flow cytometry analysis of P53, phospho-P53 (p-P53), P16, and P21 in RMECs ( n = 4). ( E ) The mRNA expression levels of P21, P16, and P53 in retinas from the 2 groups and blank mice were detected via RT-qPCR ( n = 4). ( F ) Functional protein association network of cGAS ( CGAS ), STING, IRF3, P21, P16, and P53 in humans. ( G ) Flow cytometry analysis of phospho-STING (p-STING) and phospho-IRF3 (p-IRF3) in RMECs 24 hours after treatment ( n = 4). ( H ) CD69, TNF-α, IFN-γ, and IL-17A expression on human CD4 + T cells (CD3 + CD8 – ) after coculture with RMECs pretreated with PBS, NETs, or NETs plus dasatinib, quercetin, fisetin, or H151 ( n = 4). Representative data are from at least 3 independent experiments. Data are presented as the mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001 for Mann-Whitney test ( E ) and 1-way ANOVA ( C , D , and G ).

Journal: JCI Insight

Article Title: Neutrophil extracellular traps potentiate effector T cells via endothelial senescence in uveitis

doi: 10.1172/jci.insight.180248

Figure Lengend Snippet: ( A ) Representative images of SA-β-gal–stained retina sections from blank mice, and EAU mice treated with vehicle or DNase I (red arrows indicate stained vascular wall). Scale bar: 100 μm. ( B ) Representative images of SA-β-gal–stained RMECs treated with PBS, NETs, or NETs pretreated by DNase I for 24 hours. Scale bar: 100 μm. ( C ) The secretion of IL-6, IL-1β, IL-8 and CCL20 from RMECs was detected and measured via ELISA ( n = 4). ( D ) Flow cytometry analysis of P53, phospho-P53 (p-P53), P16, and P21 in RMECs ( n = 4). ( E ) The mRNA expression levels of P21, P16, and P53 in retinas from the 2 groups and blank mice were detected via RT-qPCR ( n = 4). ( F ) Functional protein association network of cGAS ( CGAS ), STING, IRF3, P21, P16, and P53 in humans. ( G ) Flow cytometry analysis of phospho-STING (p-STING) and phospho-IRF3 (p-IRF3) in RMECs 24 hours after treatment ( n = 4). ( H ) CD69, TNF-α, IFN-γ, and IL-17A expression on human CD4 + T cells (CD3 + CD8 – ) after coculture with RMECs pretreated with PBS, NETs, or NETs plus dasatinib, quercetin, fisetin, or H151 ( n = 4). Representative data are from at least 3 independent experiments. Data are presented as the mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001 for Mann-Whitney test ( E ) and 1-way ANOVA ( C , D , and G ).

Article Snippet: For indirect labeling, the cells were first incubated with anti-human P16 (Cell Signaling Technology, 18769), anti-human P21 (Cell Signaling Technology, 2947), or anti-human pIRF3 (Cell Signaling Technology, 29047) antibodies overnight in 4°C and then with Alexa Fluor–conjugated secondary antibodies (Invitrogen, F-2765 and P-2771) overnight at 4°C the next day.

Techniques: Staining, Enzyme-linked Immunosorbent Assay, Flow Cytometry, Expressing, Quantitative RT-PCR, Functional Assay, MANN-WHITNEY

Overview of TaqMan® primer‐probes sets used in qPCR reactions.

Journal: Journal of Experimental Orthopaedics

Article Title: Microfragmented abdominal adipose tissue‐derived stem cells from knee osteoarthritis patients aged 29–65 years demonstrate in vitro stemness and low levels of cellular senescence

doi: 10.1002/jeo2.12056

Figure Lengend Snippet: Overview of TaqMan® primer‐probes sets used in qPCR reactions.

Article Snippet: Additionally, anti‐human p16 antibody Alexa flour® 647 conjugate (Cell Signaling Technology, Cat# 43161S) and anti‐human p21 antibody Alexa flour® 488 conjugate (Cell Signaling Technology, Cat# 5487S) were added in a 1:50 dilution.

Techniques: Control

Flow cytometry gating strategy for (a–e) the intracellular senescence markers p16 and p21 after 1 h of labelling MF‐ADSCs, at passage 4, with p16 antibody Alexa fluor® 647 conjugate and p21 antibody Alexa fluor® 488 conjugate. (a, c) MF‐ADSCs induced to undergo stress‐induced premature senescence for 8 days using 200 μM H 2 O 2 for 2 h, followed by 10 μM H 2 O 2 for maintenance (positive control used for gating). (b, d) A representative (untreated) sample of MF‐ADSCs at passage 4. Cells to the right of the vertical lines were determined to be p16 and p21 positive. (e) Selection of cells of interest by removal of debris based on SSC‐A and FSC‐A. Purple dots indicated cells positive for p16 and green dots indicated cells positive for p21. Gating strategy for (f–h) the SA‐β‐GAL activity assay after 2 h of spiking passage 4 MF‐ADSCs with senescence dye at pH 6. (f) MF‐ADSCs induced to undergo replicative senescence (positive control used for gating). (g) A representative sample of (untreated) MF‐ADSCs at passage 4. Cells to the right of the vertical line were determined to be SA‐β‐GAL positive. (h) Selection of cells of interest by removal of debris based on SSC‐H and FSC‐H. Green dots indicated cells with SA‐β‐GAL activity. ADSC, adipose tissue‐derived stem cell; FSC‐A, forward scatter‐area; MF, microfragmented; SSC‐A, sideward scatter‐area.

Journal: Journal of Experimental Orthopaedics

doi: 10.1002/jeo2.12056

Figure Lengend Snippet: Flow cytometry gating strategy for (a–e) the intracellular senescence markers p16 and p21 after 1 h of labelling MF‐ADSCs, at passage 4, with p16 antibody Alexa fluor® 647 conjugate and p21 antibody Alexa fluor® 488 conjugate. (a, c) MF‐ADSCs induced to undergo stress‐induced premature senescence for 8 days using 200 μM H 2 O 2 for 2 h, followed by 10 μM H 2 O 2 for maintenance (positive control used for gating). (b, d) A representative (untreated) sample of MF‐ADSCs at passage 4. Cells to the right of the vertical lines were determined to be p16 and p21 positive. (e) Selection of cells of interest by removal of debris based on SSC‐A and FSC‐A. Purple dots indicated cells positive for p16 and green dots indicated cells positive for p21. Gating strategy for (f–h) the SA‐β‐GAL activity assay after 2 h of spiking passage 4 MF‐ADSCs with senescence dye at pH 6. (f) MF‐ADSCs induced to undergo replicative senescence (positive control used for gating). (g) A representative sample of (untreated) MF‐ADSCs at passage 4. Cells to the right of the vertical line were determined to be SA‐β‐GAL positive. (h) Selection of cells of interest by removal of debris based on SSC‐H and FSC‐H. Green dots indicated cells with SA‐β‐GAL activity. ADSC, adipose tissue‐derived stem cell; FSC‐A, forward scatter‐area; MF, microfragmented; SSC‐A, sideward scatter‐area.

Techniques: Flow Cytometry, Positive Control, Selection, Activity Assay, Derivative Assay

Journal: Journal of Experimental Orthopaedics

doi: 10.1002/jeo2.12056

Figure Lengend Snippet: Overview of results.

Techniques: Flow Cytometry

Percentage (%) of MF‐ADSCs at passage 4 with (a) intracellular senescence marker p16 and (b) p21, as a function of patient age after 1 h of spiking with p16 antibody Alexa fluor® 647 conjugate and p21 antibody Alexa fluor 488® conjugate. The positive senescent cell control showing stress‐induced premature senescence using H 2 O 2 is represented by a red dot. (c) Percentage of MF‐ADSCs with SA‐β‐GAL activity as a function of patient age after 2 h of spiking with senescence dye at pH 6. The positive senescent cell control showing replicative senescence is represented by a red dot. (d) Percentage of proliferating MF‐ADSCs as a function of patient age. Proliferating cells were detected using a fluorescence microscope after spiking the cells with EdU for 24 h. Replicative senescent cells, as positive control, are represented by a red dot. Note: difference in y‐axis (a, c). Yo.: year old. (e) Representative images of MF‐ADSCs at passage 4 after 24 h of spiking with EdU. From the left; proliferating cell nuclei stained with Alexa Fluor 594 picolyl azide (red/pink) fluorescently detected with an Alexa Fluor 594 filter; nuclear cells counterstained with DAPI (blue) fluorescently detected with a DAPI filter; overlapping of the two stainings; overlapping of the two stainings and a bright field image (20×) showing the cells. (f) Brightfield (20×) and fluorescent overlapping (DAPI and Alexa 594) images of the positive senescence control of MF‐ADSCs induced to undergo replicative senescence after 24 h of spiking with EdU. ADSC, adipose tissue‐derived stem cell; MF, microfragmented.

Journal: Journal of Experimental Orthopaedics

doi: 10.1002/jeo2.12056

Figure Lengend Snippet: Percentage (%) of MF‐ADSCs at passage 4 with (a) intracellular senescence marker p16 and (b) p21, as a function of patient age after 1 h of spiking with p16 antibody Alexa fluor® 647 conjugate and p21 antibody Alexa fluor 488® conjugate. The positive senescent cell control showing stress‐induced premature senescence using H 2 O 2 is represented by a red dot. (c) Percentage of MF‐ADSCs with SA‐β‐GAL activity as a function of patient age after 2 h of spiking with senescence dye at pH 6. The positive senescent cell control showing replicative senescence is represented by a red dot. (d) Percentage of proliferating MF‐ADSCs as a function of patient age. Proliferating cells were detected using a fluorescence microscope after spiking the cells with EdU for 24 h. Replicative senescent cells, as positive control, are represented by a red dot. Note: difference in y‐axis (a, c). Yo.: year old. (e) Representative images of MF‐ADSCs at passage 4 after 24 h of spiking with EdU. From the left; proliferating cell nuclei stained with Alexa Fluor 594 picolyl azide (red/pink) fluorescently detected with an Alexa Fluor 594 filter; nuclear cells counterstained with DAPI (blue) fluorescently detected with a DAPI filter; overlapping of the two stainings; overlapping of the two stainings and a bright field image (20×) showing the cells. (f) Brightfield (20×) and fluorescent overlapping (DAPI and Alexa 594) images of the positive senescence control of MF‐ADSCs induced to undergo replicative senescence after 24 h of spiking with EdU. ADSC, adipose tissue‐derived stem cell; MF, microfragmented.

Techniques: Marker, Control, Activity Assay, Fluorescence, Microscopy, Positive Control, Staining, Derivative Assay

DNA damage, telomere shortening, disruption of chromatin organization, oncogene activation, oxidative stress, and mitochondrial dysfunction may accumulate in the cell over time. This may ultimately cause the cells to turn cancerous. To avoid this, the cell can either undergo apoptosis or become senescent. Continuous activation of the p53‐p21 or the p16 pathways inhibits transcription of cell cycle genes, irreversibly preventing cell proliferation, inducing cellular senescence and the associated characteristics. Based on Kumari and Jat and Huang et al. .

Journal: Journal of Experimental Orthopaedics

doi: 10.1002/jeo2.12056

Figure Lengend Snippet: DNA damage, telomere shortening, disruption of chromatin organization, oncogene activation, oxidative stress, and mitochondrial dysfunction may accumulate in the cell over time. This may ultimately cause the cells to turn cancerous. To avoid this, the cell can either undergo apoptosis or become senescent. Continuous activation of the p53‐p21 or the p16 pathways inhibits transcription of cell cycle genes, irreversibly preventing cell proliferation, inducing cellular senescence and the associated characteristics. Based on Kumari and Jat and Huang et al. .

Techniques: Disruption, Activation Assay

MSCs treatment changed thymus morphology, tissue structure, secretory function, and P16 and CK14 expression in aged macaque monkeys. A Comparison of the appearance and morphology of thymus between the Elderly and the Treated: the above figure shows the appearance of thymus of the aged macaque monkeys, represents the area of adipose tissue in the thymus. The figure on the below shows the appearance of the thymus after MSCs treatment, and represents the thymus tissue area. B HE staining of thymus tissue from the senescent elderly group and treatment group (100×, Image 1 represents thymus cortex, Image 2 represents the thymus medulla; Image 3 represents the Hassel body). C and D Comparison of thymus index and the contents of thymopoietin α and thymosin in the elderly and treatment group. E Expression of P16 in the elderly and treatment group (400×). F The expression of CK14 in thymus tissue was detected by immunohistochemistry (400×, brown indicates antibody-positive reaction) (the measured values represent the mean ± standard deviation (`X ± s) of three replicate experiments. ∗∗P < 0.01, ∗∗∗P < 0.001).

Journal: Regenerative Therapy

Article Title: Mesenchymal stem cells reverse thymus aging by reprogramming the DNA methylation of thymic epithelial cells

doi: 10.1016/j.reth.2024.03.008

Figure Lengend Snippet: MSCs treatment changed thymus morphology, tissue structure, secretory function, and P16 and CK14 expression in aged macaque monkeys. A Comparison of the appearance and morphology of thymus between the Elderly and the Treated: the above figure shows the appearance of thymus of the aged macaque monkeys, represents the area of adipose tissue in the thymus. The figure on the below shows the appearance of the thymus after MSCs treatment, and represents the thymus tissue area. B HE staining of thymus tissue from the senescent elderly group and treatment group (100×, Image 1 represents thymus cortex, Image 2 represents the thymus medulla; Image 3 represents the Hassel body). C and D Comparison of thymus index and the contents of thymopoietin α and thymosin in the elderly and treatment group. E Expression of P16 in the elderly and treatment group (400×). F The expression of CK14 in thymus tissue was detected by immunohistochemistry (400×, brown indicates antibody-positive reaction) (the measured values represent the mean ± standard deviation (`X ± s) of three replicate experiments. ∗∗P < 0.01, ∗∗∗P < 0.001).

Article Snippet: Primary anti-rabbit anti-human P16 (1RV 1000, ab32503), P21 (1RV 1000, ab32351), SRC (1RV 300000 ab179473 ab109381), and ITGB3 (1RV 1000 ab179473) antibodies were obtained from Abcam.

Techniques: Expressing, Comparison, Staining, Immunohistochemistry, Standard Deviation

Intervention effect of MSCs on aging TECs. A SA-β-gal staining of TECs after MSCs coculture (100 ×, represents increased activity of SA-β-gal). B Ultrastructural changes in TECs after MSC coculture (nucleus (N), mitochondria (M), and autophagosome (ASS); the upper scale is 2 μm). C After coculture with MSCs, the TEC senescence genes P16 and P21 were expressed. D TUNEL staining was used to detect the effect of MSCs on H 2 O 2 -induced apoptosis (the measured values represent the mean ± standard deviation (`X ± s) of three replicate experiments. ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001).

Journal: Regenerative Therapy

Article Title: Mesenchymal stem cells reverse thymus aging by reprogramming the DNA methylation of thymic epithelial cells

doi: 10.1016/j.reth.2024.03.008

Figure Lengend Snippet: Intervention effect of MSCs on aging TECs. A SA-β-gal staining of TECs after MSCs coculture (100 ×, represents increased activity of SA-β-gal). B Ultrastructural changes in TECs after MSC coculture (nucleus (N), mitochondria (M), and autophagosome (ASS); the upper scale is 2 μm). C After coculture with MSCs, the TEC senescence genes P16 and P21 were expressed. D TUNEL staining was used to detect the effect of MSCs on H 2 O 2 -induced apoptosis (the measured values represent the mean ± standard deviation (`X ± s) of three replicate experiments. ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001).

Techniques: Staining, Activity Assay, TUNEL Assay, Standard Deviation

Summary of antibodies used for immunofluorescence and Imagestream

Journal: GeroScience

Article Title: Vascular senescence and leak are features of the early breakdown of the blood–brain barrier in Alzheimer’s disease models

doi: 10.1007/s11357-023-00927-x

Figure Lengend Snippet: Summary of antibodies used for immunofluorescence and Imagestream

Article Snippet: Rabbit anti-human p16 , Origene , 1:100.

Techniques: Immunofluorescence

Validation of senescence green probe (SGP) as a marker of senescence. Ai-vi shows a representative gating strategy used to identify senescent cells populations in H 2 O 2 -treated cells. Focused cells were gated into single cell population (green box). DAPI + cells (magenta box) was analyzed for p16 expression followed by SGP expression against cell area/size. Small p16 + cells (yellow box) shows a population with high SGP expression (intermediate senescent cells) and another population negative for SGP expression (non-senescent cells). A majority of the large cells with high expression of p16 (orange box) also had high expression of SGP (committed senescent cells). Untreated, H 2 O 2 -treated, and unstained HUVECs were analyzed by Amnis ImageStream and gated in the same fashion. B Representative images of unstained HUVECs, non-senescent HUVECs, and HUVECs at different stages of senescence according to their cell size in brightfield (BF) and side scatter (SSC) as well as expression of senescent markers SGP (green) and p16 (red). Committed senescent cell in the representative image shown here has two DAPI (purple) positive nucleus. C Quantification of the percentage of SGP + and p16 + large senescent cells in untreated and H 2 O 2 -treated HUVECs. D Representative images of HUVECs at different stages of senescence according to cell size and senescent markers SGP (green) and p21 (red). E Quantification of the percentage of SGP + and p21 + large senescent cells in untreated and H 2 O 2 -treated HUVECs. In vitro data presented for p16- or p21-independent experiments are from 2 different HUVEC lines and are presented as mean ± standard deviation, scale bar = 20 µm. F Representative images of traditional SA-β-gal (blue) and SGP (green) stain in the brain taken from APP/PS1 mice after amyloid plaque development. Amyloid beta (gray) staining shows that SGP (green) staining on CD31 + vasculature (red) is localized to vascular cells, not plaques deposited on the blood vessel. Scale bar = 50 µm

Journal: GeroScience

Article Title: Vascular senescence and leak are features of the early breakdown of the blood–brain barrier in Alzheimer’s disease models

doi: 10.1007/s11357-023-00927-x

Figure Lengend Snippet: Validation of senescence green probe (SGP) as a marker of senescence. Ai-vi shows a representative gating strategy used to identify senescent cells populations in H 2 O 2 -treated cells. Focused cells were gated into single cell population (green box). DAPI + cells (magenta box) was analyzed for p16 expression followed by SGP expression against cell area/size. Small p16 + cells (yellow box) shows a population with high SGP expression (intermediate senescent cells) and another population negative for SGP expression (non-senescent cells). A majority of the large cells with high expression of p16 (orange box) also had high expression of SGP (committed senescent cells). Untreated, H 2 O 2 -treated, and unstained HUVECs were analyzed by Amnis ImageStream and gated in the same fashion. B Representative images of unstained HUVECs, non-senescent HUVECs, and HUVECs at different stages of senescence according to their cell size in brightfield (BF) and side scatter (SSC) as well as expression of senescent markers SGP (green) and p16 (red). Committed senescent cell in the representative image shown here has two DAPI (purple) positive nucleus. C Quantification of the percentage of SGP + and p16 + large senescent cells in untreated and H 2 O 2 -treated HUVECs. D Representative images of HUVECs at different stages of senescence according to cell size and senescent markers SGP (green) and p21 (red). E Quantification of the percentage of SGP + and p21 + large senescent cells in untreated and H 2 O 2 -treated HUVECs. In vitro data presented for p16- or p21-independent experiments are from 2 different HUVEC lines and are presented as mean ± standard deviation, scale bar = 20 µm. F Representative images of traditional SA-β-gal (blue) and SGP (green) stain in the brain taken from APP/PS1 mice after amyloid plaque development. Amyloid beta (gray) staining shows that SGP (green) staining on CD31 + vasculature (red) is localized to vascular cells, not plaques deposited on the blood vessel. Scale bar = 50 µm

Article Snippet: Rabbit anti-human p16 , Origene , 1:100.

Techniques: Biomarker Discovery, Marker, Expressing, In Vitro, Standard Deviation, Staining

Review

rabbit monoclonal anti human p16 (Cell Signaling Technology Inc)

Structured Review

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1) Product Images from "EPDR1 Links Fibroblast Dysfunction to Disease Severity in Idiopathic Pulmonary Fibrosis"

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