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Worthington Biochemical act
Act, supplied by Worthington Biochemical, used in various techniques. Bioz Stars score: 99/100, based on 505 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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act - by Bioz Stars, 2026-11

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Article Title: Growing from Shame: Positive Psychology Interventions as a way to treat Moral Injury informed by acts of Commission and Omission
Article Snippet: Moral injury is a condition that can occur after incidents in which individuals perform an action that violates their own deeply held moral beliefs, or fail to prevent such actions from occurring. in the wake of these incidents, negative self-evaluations can lead to intense feelings of shame and self-loathing; hallmarks of the condition of moral injury.. Unfortunately, potentially morally injurious circumstances are plentiful for the modern-day service member and veterans of recent conflicts. existing treatment options for moral injury are currently insufficient, and there is a lack of attention paid to the condition in psychology research due in part to moral injury’s absence in the DSM 5.. Moral injury has been erroneously conceptualized as an element of PtSD, and is commonly treated by trauma-processing modalities that, while effective in trauma-focused treatment, are ineffective in reducing symptoms of moral injury. the present article details how Positive Psychology interventions may be effective in the treatment of moral injury (heretofore untested and unexplored), and is a call for such research to be conducted.

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Manipulated expression of VISTA in cancer cells caused cell morphological change. (A) Phenotypic and protein expression changes in cancer cells with knockdown of VISTA. In each experiment, control (shCtrl) and knockdown (shVISTA) cells were collected and subjected to immunoblotting (IB). β-ACT was used as a loading control. (B) Phenotypic and protein expression changes in cancer cells in response to overexpression of VISTA. In each experiment, control cells (Ctrl) and cells with VISTA overexpression (VISTA) were collected and subjected to IB. β-ACT was used as a loading control. (C) Rescue of the morphological alteration in A375 cells resulting from VISTA knockdown by overexpression of mouse Vista (mVista) via transfection of virus at different MOIs as indicated.

Journal: bioRxiv

Article Title: Expression of immune checkpoint VISTA represents a differentiated state of cancer cells and plays a role in regulating actin cytoskeleton

doi: 10.64898/2026.08.24.746888

Figure Lengend Snippet: Manipulated expression of VISTA in cancer cells caused cell morphological change. (A) Phenotypic and protein expression changes in cancer cells with knockdown of VISTA. In each experiment, control (shCtrl) and knockdown (shVISTA) cells were collected and subjected to immunoblotting (IB). β-ACT was used as a loading control. (B) Phenotypic and protein expression changes in cancer cells in response to overexpression of VISTA. In each experiment, control cells (Ctrl) and cells with VISTA overexpression (VISTA) were collected and subjected to IB. β-ACT was used as a loading control. (C) Rescue of the morphological alteration in A375 cells resulting from VISTA knockdown by overexpression of mouse Vista (mVista) via transfection of virus at different MOIs as indicated.

Article Snippet: The primary antibodies were: β-ACT (Abclonal, #AC004.

Techniques: Expressing, Knockdown, Control, Western Blot, Over Expression, Transfection, Virus

Differential regulation of VISTA by non-neural differentiation factors and oncoproteins. (A) Regulatory effect on VISTA of forced expression of non-neural differentiation factors, as revealed by IB. (B) Regulation of VISTA by forced expression of proteins promoting cancer, as revealed by IB. In each experiment in (A) or (B), control cells (Ctrl) and cells with forced expression of a protein were collected and subjected to IB. β-ACT was used as a loading control.

Journal: bioRxiv

Article Title: Expression of immune checkpoint VISTA represents a differentiated state of cancer cells and plays a role in regulating actin cytoskeleton

doi: 10.64898/2026.08.24.746888

Figure Lengend Snippet: Differential regulation of VISTA by non-neural differentiation factors and oncoproteins. (A) Regulatory effect on VISTA of forced expression of non-neural differentiation factors, as revealed by IB. (B) Regulation of VISTA by forced expression of proteins promoting cancer, as revealed by IB. In each experiment in (A) or (B), control cells (Ctrl) and cells with forced expression of a protein were collected and subjected to IB. β-ACT was used as a loading control.

Article Snippet: The primary antibodies were: β-ACT (Abclonal, #AC004.

Techniques: Expressing, Control

USP11 expression in colon cancer patients. OS (A), PPS (B), RFS (C) in colon cancer patients. USP11 mRNA expression in colon cancer cell lines (D). USP11 protein expression in colon cancer cell lines (Western blotting, E). **, P<0.01; ***, P<0.001. CI, confidence interval; HR, hazard ratio; OS, overall survival; PPS, post-progression survival; RFS, recurrence-free survival.

Journal: Translational Cancer Research

Article Title: The m6A/METTL3 modifies USP11 to promote Warburg effect progression of colon cancer undifferentiated by HIF-1α/YAP signaling pathway

doi: 10.21037/tcr-2026-1567

Figure Lengend Snippet: USP11 expression in colon cancer patients. OS (A), PPS (B), RFS (C) in colon cancer patients. USP11 mRNA expression in colon cancer cell lines (D). USP11 protein expression in colon cancer cell lines (Western blotting, E). **, P<0.01; ***, P<0.001. CI, confidence interval; HR, hazard ratio; OS, overall survival; PPS, post-progression survival; RFS, recurrence-free survival.

Article Snippet: SW480 cells were transfected with USP11 plasmid (sc-403368-ACT, Santa Cruz Biotechnology, Inc.), and HCT-116 cells were transfected with si-USP11 plasmid (sc-63193-SH, Santa Cruz Biotechnology, Inc.) using Lipofectamine 3000.

Techniques: Expressing, Western Blot

USP11 expression in colon cancer using single-cell sequencing data. (A) Cell information of single-cell sequencing data; (B) gene expression of single-cell sequencing data; (C) cancer cell; (D) B cells; (E) T cells; (F) macrophage cells; (G) USP11/Ki67 in cancer tissue of colon cancer. *, P<0.05. USP11, ubiquitin-specific peptidase 11.

Journal: Translational Cancer Research

Article Title: The m6A/METTL3 modifies USP11 to promote Warburg effect progression of colon cancer undifferentiated by HIF-1α/YAP signaling pathway

doi: 10.21037/tcr-2026-1567

Figure Lengend Snippet: USP11 expression in colon cancer using single-cell sequencing data. (A) Cell information of single-cell sequencing data; (B) gene expression of single-cell sequencing data; (C) cancer cell; (D) B cells; (E) T cells; (F) macrophage cells; (G) USP11/Ki67 in cancer tissue of colon cancer. *, P<0.05. USP11, ubiquitin-specific peptidase 11.

Techniques: Expressing, Single-Cell Sequencing, Gene Expression, Tissue, Ubiquitin Proteomics

USP11 promotes cell growth progression of colon cancer. Tumor volume and weight (A,B), tumor tissue (C), Ki67 levels (D; immunohistochemistry, magnification: ×20), COX-2 and TNF-α mRNA levels (E,F), caspase-3 and caspase-9 activity levels (G,H). **, P<0.01; ***, P<0.001. mRNA, messenger RNA; TNF-α, tumor necrosis factor-alpha; USP11, ubiquitin-specific peptidase 11.

Journal: Translational Cancer Research

Article Title: The m6A/METTL3 modifies USP11 to promote Warburg effect progression of colon cancer undifferentiated by HIF-1α/YAP signaling pathway

doi: 10.21037/tcr-2026-1567

Figure Lengend Snippet: USP11 promotes cell growth progression of colon cancer. Tumor volume and weight (A,B), tumor tissue (C), Ki67 levels (D; immunohistochemistry, magnification: ×20), COX-2 and TNF-α mRNA levels (E,F), caspase-3 and caspase-9 activity levels (G,H). **, P<0.01; ***, P<0.001. mRNA, messenger RNA; TNF-α, tumor necrosis factor-alpha; USP11, ubiquitin-specific peptidase 11.

Techniques: Tissue, Immunohistochemistry, Activity Assay, Ubiquitin Proteomics

USP11 promotes Warburg effect progression of colon cancer. USP11 mRNA expression (A), cell proliferation (B), migration (C; staining method: Transwell chambers), EdU positive (D; EDU staining; ×20) and wound healing (E, ×20), glucose uptake (F), lactate production (G), ATP level (H), PK activity (I), HK activity (J), PFK-1 activity (K), ECAR (L), OCR levels (M) in BCPAP cells were transfected with USP11 plasmid. **, P<0.01; ***, P<0.001. ATP, adenosine triphosphate; DAPI, 4',6-diamidino-2-phenylindole; ECAR, extracellular acidification rate; EdU, 5-Ethynyl-2'-deoxyuridine; FCCP, carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone; HK, hexokinase; mRNA, messenger RNA; OCR, oxygen consumption rate; PFK-1, phosphofructokinase-1; PK, pyruvate kinase; USP11, ubiquitin-specific peptidase 11.

Journal: Translational Cancer Research

Article Title: The m6A/METTL3 modifies USP11 to promote Warburg effect progression of colon cancer undifferentiated by HIF-1α/YAP signaling pathway

doi: 10.21037/tcr-2026-1567

Figure Lengend Snippet: USP11 promotes Warburg effect progression of colon cancer. USP11 mRNA expression (A), cell proliferation (B), migration (C; staining method: Transwell chambers), EdU positive (D; EDU staining; ×20) and wound healing (E, ×20), glucose uptake (F), lactate production (G), ATP level (H), PK activity (I), HK activity (J), PFK-1 activity (K), ECAR (L), OCR levels (M) in BCPAP cells were transfected with USP11 plasmid. **, P<0.01; ***, P<0.001. ATP, adenosine triphosphate; DAPI, 4',6-diamidino-2-phenylindole; ECAR, extracellular acidification rate; EdU, 5-Ethynyl-2'-deoxyuridine; FCCP, carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone; HK, hexokinase; mRNA, messenger RNA; OCR, oxygen consumption rate; PFK-1, phosphofructokinase-1; PK, pyruvate kinase; USP11, ubiquitin-specific peptidase 11.

Techniques: Expressing, Migration, Staining, Activity Assay, Transfection, Plasmid Preparation, Ubiquitin Proteomics

Si-USP11 reduces Warburg effect progression of colon cancer. USP11 mRNA expression (A), cell proliferation (B), migration (C; staining method: Transwell chambers), EdU positive (D; EDU staining ; ×20) and wound healing (E, ×20), glucose uptake (F), lactate production (G), ATP level (H), PK activity (I), HK activity (J), PFK-1 activity (K), ECAR (L), OCR levels (M) in HCT-116 cells were transfected with si-USP11 plasmid. *, P<0.05; **, P<0.01, ***, P<0.001. ATP, adenosine triphosphate; DAPI, 4',6-diamidino-2-phenylindole; ECAR, extracellular acidification rate; EdU, 5-Ethynyl-2'-deoxyuridine; FCCP, carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone; HK, hexokinase; mRNA, messenger RNA; NC, negative control; OCR, oxygen consumption rate; PFK-1, phosphofructokinase-1; PK, pyruvate kinase; USP11, ubiquitin-specific peptidase 11.

Journal: Translational Cancer Research

Article Title: The m6A/METTL3 modifies USP11 to promote Warburg effect progression of colon cancer undifferentiated by HIF-1α/YAP signaling pathway

doi: 10.21037/tcr-2026-1567

Figure Lengend Snippet: Si-USP11 reduces Warburg effect progression of colon cancer. USP11 mRNA expression (A), cell proliferation (B), migration (C; staining method: Transwell chambers), EdU positive (D; EDU staining ; ×20) and wound healing (E, ×20), glucose uptake (F), lactate production (G), ATP level (H), PK activity (I), HK activity (J), PFK-1 activity (K), ECAR (L), OCR levels (M) in HCT-116 cells were transfected with si-USP11 plasmid. *, P<0.05; **, P<0.01, ***, P<0.001. ATP, adenosine triphosphate; DAPI, 4',6-diamidino-2-phenylindole; ECAR, extracellular acidification rate; EdU, 5-Ethynyl-2'-deoxyuridine; FCCP, carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone; HK, hexokinase; mRNA, messenger RNA; NC, negative control; OCR, oxygen consumption rate; PFK-1, phosphofructokinase-1; PK, pyruvate kinase; USP11, ubiquitin-specific peptidase 11.

Techniques: Expressing, Migration, Staining, Activity Assay, Transfection, Plasmid Preparation, Negative Control, Ubiquitin Proteomics

USP11 induced HIF-1α expression in colon cancer. Heat map (A), HIF-1α (B; immunofluorescence; ×20) in mice model; HIF-1α expression (immunohistochemical), USP11/HIF-1α/YAP protein expression (C), USP11/HIF-1α expression (D; immunofluorescence; ×20) in mice model of colon cancer. USP11/HIF-1α/YAP protein expression (E,F), USP11/HIF-1α expression (G,H; immunofluorescence; ×50) in vitro model of colon cancer. **, P<0.01, ***, P<0.001. HIF-1α, hypoxia-inducible factor 1-alpha; USP11, ubiquitin-specific peptidase 11.

Journal: Translational Cancer Research

Article Title: The m6A/METTL3 modifies USP11 to promote Warburg effect progression of colon cancer undifferentiated by HIF-1α/YAP signaling pathway

doi: 10.21037/tcr-2026-1567

Figure Lengend Snippet: USP11 induced HIF-1α expression in colon cancer. Heat map (A), HIF-1α (B; immunofluorescence; ×20) in mice model; HIF-1α expression (immunohistochemical), USP11/HIF-1α/YAP protein expression (C), USP11/HIF-1α expression (D; immunofluorescence; ×20) in mice model of colon cancer. USP11/HIF-1α/YAP protein expression (E,F), USP11/HIF-1α expression (G,H; immunofluorescence; ×50) in vitro model of colon cancer. **, P<0.01, ***, P<0.001. HIF-1α, hypoxia-inducible factor 1-alpha; USP11, ubiquitin-specific peptidase 11.

Techniques: Expressing, Immunofluorescence, Immunohistochemical staining, In Vitro, Ubiquitin Proteomics

HIF-1α mediates the stimulatory effect of USP11 on proliferation and migration in colon cancer. HIF-1α/YAP protein expression (A), cell proliferation (B), migration (C, ×20), EdU positive (D, ×20) and wound healing (E, ×20) in BCPAP cells were transfected with USP11 plasmid+ HIF-1α inhibitor; HIF-1α/YAP protein expression (F), cell proliferation (G), migration (H, ×20), Edu positive (I, ×20) and wound healing (J, ×20) in HCT-116 cells were transfected with si-USP11 plasmid+ HIF-1α agonist. *, P<0.05, **, P<0.01, ***, P<0.001. EdU, 5-Ethynyl-2'-deoxyuridine; HIF-1α, hypoxia-inducible factor 1-alpha; USP11, ubiquitin-specific peptidase 11.

Journal: Translational Cancer Research

Article Title: The m6A/METTL3 modifies USP11 to promote Warburg effect progression of colon cancer undifferentiated by HIF-1α/YAP signaling pathway

doi: 10.21037/tcr-2026-1567

Figure Lengend Snippet: HIF-1α mediates the stimulatory effect of USP11 on proliferation and migration in colon cancer. HIF-1α/YAP protein expression (A), cell proliferation (B), migration (C, ×20), EdU positive (D, ×20) and wound healing (E, ×20) in BCPAP cells were transfected with USP11 plasmid+ HIF-1α inhibitor; HIF-1α/YAP protein expression (F), cell proliferation (G), migration (H, ×20), Edu positive (I, ×20) and wound healing (J, ×20) in HCT-116 cells were transfected with si-USP11 plasmid+ HIF-1α agonist. *, P<0.05, **, P<0.01, ***, P<0.001. EdU, 5-Ethynyl-2'-deoxyuridine; HIF-1α, hypoxia-inducible factor 1-alpha; USP11, ubiquitin-specific peptidase 11.

Techniques: Migration, Expressing, Transfection, Plasmid Preparation, Ubiquitin Proteomics

HIF-1α mediates the stimulatory effect of USP11 on Warburg effect progression in colon cancer. Glucose uptake (A), lactate production (B), ATP level (C), ECAR (D), OCR levels (E) in BCPAP cells were transfected with USP11 plasmid + HIF-1α inhibitor; glucose uptake (F), lactate production (G), ATP level (H), ECAR (I), OCR levels (J) in HCT-116 cells were transfected with si-USP11 plasmid+ HIF-1α agonist. **, P<0.01, ***, P<0.001. ATP, adenosine triphosphate; ECAR, extracellular acidification rate; HIF-1α, hypoxia-inducible factor 1-alpha; OCR, oxygen consumption rate; USP11, ubiquitin-specific peptidase 11.

Journal: Translational Cancer Research

Article Title: The m6A/METTL3 modifies USP11 to promote Warburg effect progression of colon cancer undifferentiated by HIF-1α/YAP signaling pathway

doi: 10.21037/tcr-2026-1567

Figure Lengend Snippet: HIF-1α mediates the stimulatory effect of USP11 on Warburg effect progression in colon cancer. Glucose uptake (A), lactate production (B), ATP level (C), ECAR (D), OCR levels (E) in BCPAP cells were transfected with USP11 plasmid + HIF-1α inhibitor; glucose uptake (F), lactate production (G), ATP level (H), ECAR (I), OCR levels (J) in HCT-116 cells were transfected with si-USP11 plasmid+ HIF-1α agonist. **, P<0.01, ***, P<0.001. ATP, adenosine triphosphate; ECAR, extracellular acidification rate; HIF-1α, hypoxia-inducible factor 1-alpha; OCR, oxygen consumption rate; USP11, ubiquitin-specific peptidase 11.

Techniques: Transfection, Plasmid Preparation, Ubiquitin Proteomics

HIF-1α mediates the stimulatory effect of USP11 on cell growth progression in colon cancer. HIF-1α/YAP protein expression (A), tumor tissue (B), tumor volume and weight (C,D), Ki67 levels (E; immunohistochemistry; ×20), COX-2 and TNF-α mRNA levels (F,G), caspase-3 and caspase-9 activity levels (H,I). **, P<0.01; ***, P<0.001. HIF-1α, hypoxia-inducible factor 1-alpha; TNF-α, tumor necrosis factor-alpha; USP11, ubiquitin-specific peptidase 11.

Journal: Translational Cancer Research

Article Title: The m6A/METTL3 modifies USP11 to promote Warburg effect progression of colon cancer undifferentiated by HIF-1α/YAP signaling pathway

doi: 10.21037/tcr-2026-1567

Figure Lengend Snippet: HIF-1α mediates the stimulatory effect of USP11 on cell growth progression in colon cancer. HIF-1α/YAP protein expression (A), tumor tissue (B), tumor volume and weight (C,D), Ki67 levels (E; immunohistochemistry; ×20), COX-2 and TNF-α mRNA levels (F,G), caspase-3 and caspase-9 activity levels (H,I). **, P<0.01; ***, P<0.001. HIF-1α, hypoxia-inducible factor 1-alpha; TNF-α, tumor necrosis factor-alpha; USP11, ubiquitin-specific peptidase 11.

Techniques: Expressing, Tissue, Immunohistochemistry, Activity Assay, Ubiquitin Proteomics

USP11 interacts with HIF-1α complex and stabilizes HIF-1α in colon cancer. USP11 interacts with HIF-1α complex (3D, A), USP11 WT/Mut and HIF-1α WT/Mut (B), USP11 WT/Mut interacts with HIF-1α WT/Mut complex (IP, C), HIF-1α ubiquitin (D), USP11 WT/Mut interacts with HIF-1α ubiquitin (E); YAP protein expression (F), USP11 interacts with YAP complex (G), YAP ubiquitin (H). HIF-1α, hypoxia-inducible factor 1-alpha; IgG, immunoglobulin G; IP, Immunoprecipitation; Mut, mutant; WT, wild type; USP11, ubiquitin-specific peptidase 11.

Journal: Translational Cancer Research

Article Title: The m6A/METTL3 modifies USP11 to promote Warburg effect progression of colon cancer undifferentiated by HIF-1α/YAP signaling pathway

doi: 10.21037/tcr-2026-1567

Figure Lengend Snippet: USP11 interacts with HIF-1α complex and stabilizes HIF-1α in colon cancer. USP11 interacts with HIF-1α complex (3D, A), USP11 WT/Mut and HIF-1α WT/Mut (B), USP11 WT/Mut interacts with HIF-1α WT/Mut complex (IP, C), HIF-1α ubiquitin (D), USP11 WT/Mut interacts with HIF-1α ubiquitin (E); YAP protein expression (F), USP11 interacts with YAP complex (G), YAP ubiquitin (H). HIF-1α, hypoxia-inducible factor 1-alpha; IgG, immunoglobulin G; IP, Immunoprecipitation; Mut, mutant; WT, wild type; USP11, ubiquitin-specific peptidase 11.

Techniques: Ubiquitin Proteomics, Expressing, Immunoprecipitation, Mutagenesis

METTL3-mediated m6A modification increases USP11 stability in an YTHDF1-dependent manner. Methylation modification sites near (A), USP11 mRNA enrichment in colon cancer cells by METTL3 (B), the stability of USP11 mRNA in colon cancer cells (C), m6A of USP11 (D), 3'-UTR of USP11 (E), luciferase activity level (F), m6A modification (G,H). **, P<0.01, ***, P<0.001. IgG, immunoglobulin G; m6A, N6-methyladenosine; USP11, ubiquitin-specific peptidase 11; UTR, untranslated region.

Journal: Translational Cancer Research

Article Title: The m6A/METTL3 modifies USP11 to promote Warburg effect progression of colon cancer undifferentiated by HIF-1α/YAP signaling pathway

doi: 10.21037/tcr-2026-1567

Figure Lengend Snippet: METTL3-mediated m6A modification increases USP11 stability in an YTHDF1-dependent manner. Methylation modification sites near (A), USP11 mRNA enrichment in colon cancer cells by METTL3 (B), the stability of USP11 mRNA in colon cancer cells (C), m6A of USP11 (D), 3'-UTR of USP11 (E), luciferase activity level (F), m6A modification (G,H). **, P<0.01, ***, P<0.001. IgG, immunoglobulin G; m6A, N6-methyladenosine; USP11, ubiquitin-specific peptidase 11; UTR, untranslated region.

Techniques: Modification, Stability, Methylation, Luciferase, Activity Assay, Ubiquitin Proteomics

The m6A/METTL3 modifies USP11 promotes Warburg effect progression of colon cancer undifferentiated by HIF-1α/YAP signaling pathway. HIF-1α, hypoxia-inducible factor 1-alpha; USP11, ubiquitin-specific peptidase 11.

Journal: Translational Cancer Research

Article Title: The m6A/METTL3 modifies USP11 to promote Warburg effect progression of colon cancer undifferentiated by HIF-1α/YAP signaling pathway

doi: 10.21037/tcr-2026-1567

Figure Lengend Snippet: The m6A/METTL3 modifies USP11 promotes Warburg effect progression of colon cancer undifferentiated by HIF-1α/YAP signaling pathway. HIF-1α, hypoxia-inducible factor 1-alpha; USP11, ubiquitin-specific peptidase 11.

Techniques: Ubiquitin Proteomics

Analysis of ligands and receptors in senescent and receiving cells. (A) Schematic depicting BulkSignalR pipeline which uses known ligand‐receptor interactions and affected downstream pathways to analyze their activation based on our bulk RNAseq data from DMSO and BrdU treated human cell lines (created with BioRender). (B) Venn diagram showing the number of receptors inferred from BulkSignalR to be activated across each of the five human cell types. Three receptors were identified in common between astrocytes (purple), endothelial cells (pink), and microglia (yellow) which were the cell types shown (Figure ) to be capable of receiving senescence signals and becoming SA β‐gal positive: CXCR7, KREMEN2, and GIPR. Only CXCR7 was expressed in the cell types capable of entering secondary senescence (astrocytes, endothelial cells, microglia) (Figure , Figure ). (C) TPM expression values of CXCR7 , its ligand CXCL12 , and DPP4 which cleaves and inactivates CXCL12 in DMSO (gray) and BrdU (red) treated cell lines ( n = 3 replicates). (D) Schematic of the four selected SASP inhibitors mechanisms of action: Bindarit is a CCL2 synthesis inhibitor which prevents p65 activation of the CCL2 gene at the promoter region, ISO‐1 is a MIF antagonist, ACT‐1004‐1239 is a CXCR7 antagonist, and Sitagliptin inhibits DPP4 preventing its action of cleaving and inactivating CXCL12 (created with BioRender). Data were analyzed by two‐way ANOVA with Tukey's multiple comparisons test (C). All graphs show mean with error bars depicting standard deviation (ns, p > 0.05, ** p < 0.01, *** p < 0.001).

Journal: Aging Cell

Article Title: Characterizing the SASP ‐Dependent Paracrine Spreading of Senescence Between Human Brain Cell Types

doi: 10.1111/acel.70673

Figure Lengend Snippet: Analysis of ligands and receptors in senescent and receiving cells. (A) Schematic depicting BulkSignalR pipeline which uses known ligand‐receptor interactions and affected downstream pathways to analyze their activation based on our bulk RNAseq data from DMSO and BrdU treated human cell lines (created with BioRender). (B) Venn diagram showing the number of receptors inferred from BulkSignalR to be activated across each of the five human cell types. Three receptors were identified in common between astrocytes (purple), endothelial cells (pink), and microglia (yellow) which were the cell types shown (Figure ) to be capable of receiving senescence signals and becoming SA β‐gal positive: CXCR7, KREMEN2, and GIPR. Only CXCR7 was expressed in the cell types capable of entering secondary senescence (astrocytes, endothelial cells, microglia) (Figure , Figure ). (C) TPM expression values of CXCR7 , its ligand CXCL12 , and DPP4 which cleaves and inactivates CXCL12 in DMSO (gray) and BrdU (red) treated cell lines ( n = 3 replicates). (D) Schematic of the four selected SASP inhibitors mechanisms of action: Bindarit is a CCL2 synthesis inhibitor which prevents p65 activation of the CCL2 gene at the promoter region, ISO‐1 is a MIF antagonist, ACT‐1004‐1239 is a CXCR7 antagonist, and Sitagliptin inhibits DPP4 preventing its action of cleaving and inactivating CXCL12 (created with BioRender). Data were analyzed by two‐way ANOVA with Tukey's multiple comparisons test (C). All graphs show mean with error bars depicting standard deviation (ns, p > 0.05, ** p < 0.01, *** p < 0.001).

Article Snippet: Treatment with CXCR7 antagonist ACT‐1004‐1239 (MedChemExpress, Catalog No. HY‐142617) was utilized to prevent CXCR7‐associated communication between senescence inducers and receiving cells.

Techniques: Activation Assay, RNA sequencing, Expressing, Standard Deviation

Targeting SASP ligands and receptors to prevent the spreading of senescence. (A) Quantification of percentage of SA β‐gal positive astrocytes following 7‐day treatment with 100 μM BrdU (red) along with 200 μM Bindarit (pink), 50 μM ISO‐1 (blue), 200 μM ACT‐1004‐1239 (orange), or 2 μM Sitagliptin (green) ( n = 6 replicates). (B) Quantification of percentage of SA β‐gal positive microglia following 7‐day treatment with 100 μM BrdU (red) along with 200 μM Bindarit (pink), 50 μM ISO‐1 (blue), 200 μM ACT‐1004‐1239 (orange), or 2 μM Sitagliptin (green) ( n = 6 replicates). (C) Timeline showing treatment with DMSO + Bindarit CM or BrdU + Bindarit CM for 7 days. Timeline showing treatment with DMSO or 100 μM BrdU along with SASP inhibitors (ISO‐1, ACT‐1004‐1239, or Sitagliptin) for 7 days. Features of senescence were analyzed 8 days after the initial plating of cells (created with BioRender). (D) Quantification of percentage of SA β‐gal positive astrocytes following 7‐day treatment with DMSO + Bindarit CM from astrocytes (gray), BrdU + Bindarit CM from astrocytes (red), DMSO CM from astrocytes + SASP inhibitor (gray), or BrdU CM from astrocytes + SASP inhibitor (red) ( n = 4 replicates). Quantification of percentage of SA β‐gal positive astrocytes following 7‐day treatment with DMSO CM from astrocytes + Bindarit (gray) or BrdU CM from astrocytes + Bindarit (red) ( n = 4 replicates). (E) Quantification of percentage of SA β‐gal positive astrocytes following 7‐day treatment with DMSO + Bindarit CM from microglia (gray), BrdU + Bindarit CM from microglia (red), DMSO CM from microglia + SASP inhibitor (gray), or BrdU CM from microglia + SASP inhibitor (red) ( n = 4 replicates). Quantification of percentage of SA β‐gal positive astrocytes following 7‐day treatment with DMSO CM from microglia + Bindarit (gray) or BrdU CM from microglia + Bindarit (red) ( n = 4 replicates). (F) Quantification of percentage of SA β‐gal positive microglia following 7‐day treatment with DMSO + Bindarit CM from microglia (gray), BrdU + Bindarit CM from microglia (red), DMSO CM from microglia + SASP inhibitor (gray), or BrdU CM from microglia + SASP inhibitor (red) ( n = 4 replicates). Quantification of percentage of SA β‐gal positive astrocytes following 7‐day treatment with DMSO CM from microglia + Bindarit (gray) or BrdU CM from microglia + Bindarit (red) ( n = 4 replicates). (G) Quantification of percentage of SA β‐gal positive microglia following 7‐day treatment with DMSO + Bindarit CM from astrocytes (gray), BrdU + Bindarit CM from astrocytes (red), DMSO CM from astrocytes + SASP inhibitor (gray), or BrdU CM from astrocytes + SASP inhibitor (red) ( n = 4 replicates). Quantification of percentage of SA β‐gal positive astrocytes following 7‐day treatment with DMSO CM from astrocytes + Bindarit (gray) or BrdU CM from astrocytes + Bindarit (red) ( n = 4 replicates). Data analyzed by unpaired t ‐test (A, B) and two‐way ANOVA with Tukey's or Šídák's multiple comparisons test (D–G). All graphs show mean with error bars depicting standard deviation (ns, p > 0.05, * p < 0.05, ** p < 0.01, *** p < 0.001).

Journal: Aging Cell

Article Title: Characterizing the SASP ‐Dependent Paracrine Spreading of Senescence Between Human Brain Cell Types

doi: 10.1111/acel.70673

Figure Lengend Snippet: Targeting SASP ligands and receptors to prevent the spreading of senescence. (A) Quantification of percentage of SA β‐gal positive astrocytes following 7‐day treatment with 100 μM BrdU (red) along with 200 μM Bindarit (pink), 50 μM ISO‐1 (blue), 200 μM ACT‐1004‐1239 (orange), or 2 μM Sitagliptin (green) ( n = 6 replicates). (B) Quantification of percentage of SA β‐gal positive microglia following 7‐day treatment with 100 μM BrdU (red) along with 200 μM Bindarit (pink), 50 μM ISO‐1 (blue), 200 μM ACT‐1004‐1239 (orange), or 2 μM Sitagliptin (green) ( n = 6 replicates). (C) Timeline showing treatment with DMSO + Bindarit CM or BrdU + Bindarit CM for 7 days. Timeline showing treatment with DMSO or 100 μM BrdU along with SASP inhibitors (ISO‐1, ACT‐1004‐1239, or Sitagliptin) for 7 days. Features of senescence were analyzed 8 days after the initial plating of cells (created with BioRender). (D) Quantification of percentage of SA β‐gal positive astrocytes following 7‐day treatment with DMSO + Bindarit CM from astrocytes (gray), BrdU + Bindarit CM from astrocytes (red), DMSO CM from astrocytes + SASP inhibitor (gray), or BrdU CM from astrocytes + SASP inhibitor (red) ( n = 4 replicates). Quantification of percentage of SA β‐gal positive astrocytes following 7‐day treatment with DMSO CM from astrocytes + Bindarit (gray) or BrdU CM from astrocytes + Bindarit (red) ( n = 4 replicates). (E) Quantification of percentage of SA β‐gal positive astrocytes following 7‐day treatment with DMSO + Bindarit CM from microglia (gray), BrdU + Bindarit CM from microglia (red), DMSO CM from microglia + SASP inhibitor (gray), or BrdU CM from microglia + SASP inhibitor (red) ( n = 4 replicates). Quantification of percentage of SA β‐gal positive astrocytes following 7‐day treatment with DMSO CM from microglia + Bindarit (gray) or BrdU CM from microglia + Bindarit (red) ( n = 4 replicates). (F) Quantification of percentage of SA β‐gal positive microglia following 7‐day treatment with DMSO + Bindarit CM from microglia (gray), BrdU + Bindarit CM from microglia (red), DMSO CM from microglia + SASP inhibitor (gray), or BrdU CM from microglia + SASP inhibitor (red) ( n = 4 replicates). Quantification of percentage of SA β‐gal positive astrocytes following 7‐day treatment with DMSO CM from microglia + Bindarit (gray) or BrdU CM from microglia + Bindarit (red) ( n = 4 replicates). (G) Quantification of percentage of SA β‐gal positive microglia following 7‐day treatment with DMSO + Bindarit CM from astrocytes (gray), BrdU + Bindarit CM from astrocytes (red), DMSO CM from astrocytes + SASP inhibitor (gray), or BrdU CM from astrocytes + SASP inhibitor (red) ( n = 4 replicates). Quantification of percentage of SA β‐gal positive astrocytes following 7‐day treatment with DMSO CM from astrocytes + Bindarit (gray) or BrdU CM from astrocytes + Bindarit (red) ( n = 4 replicates). Data analyzed by unpaired t ‐test (A, B) and two‐way ANOVA with Tukey's or Šídák's multiple comparisons test (D–G). All graphs show mean with error bars depicting standard deviation (ns, p > 0.05, * p < 0.05, ** p < 0.01, *** p < 0.001).

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