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Merck & Co human ventricular cardiomyocytes
A fraction of DPP3 is transported via EVs and upregulated during septic shock in humans (A) Western blot qualitative analysis of cluster of differentiation 63 (CD63) at 26 KD (bottom), heat shock protein 70 (HSC70) at 73 KD (middle), and DPP3 at 83 KD (above), in protein extracts of EVs derived from bone marrow supernatant (BM SN) from Ctrl mice (left) and ISO mice (right). DPP3 activity (U/L) in large (lEVs) and small (sEVs) EVs derived from (B) plasma of control mice (Ctrl) ( n = 6) and isoproterenol-treated mice (ISO) ( n = 5), or from (C) BM SN of Ctrl ( n = 6) and ISO mice ( n = 6). (D) DPP3 activity in lEVs and sEVs derived from BM SN of WT mice injected with bone marrow cells from Dpp3-KO (WT BM KO ) and Dpp3-KO mice injected with bone marrow cells from WT mice (KO BM WT ) ( n = 5) for each. (E) Quantification of Nano track analysis (NTA) results of plasma derived-lEVs and sEVs concentration (vesicle/ml) in healthy individuals ( n = 7), septic shock (SS) ( n = 6) and cardiogenic shock (CS) patients ( n = 5). (F) DPP3 activity (U/L) in lEVs and sEVs derived from plasma of healthy individuals ( n = 8) and septic shock (SS) patients ( n = 6). (G) DPP3 activity (U/L) in lEVs and sEVs derived from plasma of healthy individuals ( n = 8) and cardiogenic shock (CS) patients ( n = 11). DPP3 activity (U/L) in lEVs and sEVs derived from cell culture supernatant of (H) human <t>cardiomyocytes</t> <t>AC16</t> ( n = 6) and (I) human monocytes THP-1 ( n = 2). In all bars, data are presented as mean ± standard error of the mean (SEM). Comparisons were made by Multiple Mann-Whitney tests in B, C, F, and G, and by two-way ANOVA in D and E. Significance was presented as follows (∗ p < 0.05, ∗∗ p < 0.01, and ns for non-significant differences).
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1) Product Images from "Crosstalk between circulating DPP3 and immune cells in the context of cardio-systemic stress"

Article Title: Crosstalk between circulating DPP3 and immune cells in the context of cardio-systemic stress

Journal: iScience

doi: 10.1016/j.isci.2026.115114

A fraction of DPP3 is transported via EVs and upregulated during septic shock in humans (A) Western blot qualitative analysis of cluster of differentiation 63 (CD63) at 26 KD (bottom), heat shock protein 70 (HSC70) at 73 KD (middle), and DPP3 at 83 KD (above), in protein extracts of EVs derived from bone marrow supernatant (BM SN) from Ctrl mice (left) and ISO mice (right). DPP3 activity (U/L) in large (lEVs) and small (sEVs) EVs derived from (B) plasma of control mice (Ctrl) ( n = 6) and isoproterenol-treated mice (ISO) ( n = 5), or from (C) BM SN of Ctrl ( n = 6) and ISO mice ( n = 6). (D) DPP3 activity in lEVs and sEVs derived from BM SN of WT mice injected with bone marrow cells from Dpp3-KO (WT BM KO ) and Dpp3-KO mice injected with bone marrow cells from WT mice (KO BM WT ) ( n = 5) for each. (E) Quantification of Nano track analysis (NTA) results of plasma derived-lEVs and sEVs concentration (vesicle/ml) in healthy individuals ( n = 7), septic shock (SS) ( n = 6) and cardiogenic shock (CS) patients ( n = 5). (F) DPP3 activity (U/L) in lEVs and sEVs derived from plasma of healthy individuals ( n = 8) and septic shock (SS) patients ( n = 6). (G) DPP3 activity (U/L) in lEVs and sEVs derived from plasma of healthy individuals ( n = 8) and cardiogenic shock (CS) patients ( n = 11). DPP3 activity (U/L) in lEVs and sEVs derived from cell culture supernatant of (H) human cardiomyocytes AC16 ( n = 6) and (I) human monocytes THP-1 ( n = 2). In all bars, data are presented as mean ± standard error of the mean (SEM). Comparisons were made by Multiple Mann-Whitney tests in B, C, F, and G, and by two-way ANOVA in D and E. Significance was presented as follows (∗ p < 0.05, ∗∗ p < 0.01, and ns for non-significant differences).
Figure Legend Snippet: A fraction of DPP3 is transported via EVs and upregulated during septic shock in humans (A) Western blot qualitative analysis of cluster of differentiation 63 (CD63) at 26 KD (bottom), heat shock protein 70 (HSC70) at 73 KD (middle), and DPP3 at 83 KD (above), in protein extracts of EVs derived from bone marrow supernatant (BM SN) from Ctrl mice (left) and ISO mice (right). DPP3 activity (U/L) in large (lEVs) and small (sEVs) EVs derived from (B) plasma of control mice (Ctrl) ( n = 6) and isoproterenol-treated mice (ISO) ( n = 5), or from (C) BM SN of Ctrl ( n = 6) and ISO mice ( n = 6). (D) DPP3 activity in lEVs and sEVs derived from BM SN of WT mice injected with bone marrow cells from Dpp3-KO (WT BM KO ) and Dpp3-KO mice injected with bone marrow cells from WT mice (KO BM WT ) ( n = 5) for each. (E) Quantification of Nano track analysis (NTA) results of plasma derived-lEVs and sEVs concentration (vesicle/ml) in healthy individuals ( n = 7), septic shock (SS) ( n = 6) and cardiogenic shock (CS) patients ( n = 5). (F) DPP3 activity (U/L) in lEVs and sEVs derived from plasma of healthy individuals ( n = 8) and septic shock (SS) patients ( n = 6). (G) DPP3 activity (U/L) in lEVs and sEVs derived from plasma of healthy individuals ( n = 8) and cardiogenic shock (CS) patients ( n = 11). DPP3 activity (U/L) in lEVs and sEVs derived from cell culture supernatant of (H) human cardiomyocytes AC16 ( n = 6) and (I) human monocytes THP-1 ( n = 2). In all bars, data are presented as mean ± standard error of the mean (SEM). Comparisons were made by Multiple Mann-Whitney tests in B, C, F, and G, and by two-way ANOVA in D and E. Significance was presented as follows (∗ p < 0.05, ∗∗ p < 0.01, and ns for non-significant differences).

Techniques Used: Western Blot, Derivative Assay, Activity Assay, Clinical Proteomics, Control, Injection, Concentration Assay, Cell Culture, MANN-WHITNEY



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A fraction of DPP3 is transported via EVs and upregulated during septic shock in humans (A) Western blot qualitative analysis of cluster of differentiation 63 (CD63) at 26 KD (bottom), heat shock protein 70 (HSC70) at 73 KD (middle), and DPP3 at 83 KD (above), in protein extracts of EVs derived from bone marrow supernatant (BM SN) from Ctrl mice (left) and ISO mice (right). DPP3 activity (U/L) in large (lEVs) and small (sEVs) EVs derived from (B) plasma of control mice (Ctrl) ( n = 6) and isoproterenol-treated mice (ISO) ( n = 5), or from (C) BM SN of Ctrl ( n = 6) and ISO mice ( n = 6). (D) DPP3 activity in lEVs and sEVs derived from BM SN of WT mice injected with bone marrow cells from Dpp3-KO (WT BM KO ) and Dpp3-KO mice injected with bone marrow cells from WT mice (KO BM WT ) ( n = 5) for each. (E) Quantification of Nano track analysis (NTA) results of plasma derived-lEVs and sEVs concentration (vesicle/ml) in healthy individuals ( n = 7), septic shock (SS) ( n = 6) and cardiogenic shock (CS) patients ( n = 5). (F) DPP3 activity (U/L) in lEVs and sEVs derived from plasma of healthy individuals ( n = 8) and septic shock (SS) patients ( n = 6). (G) DPP3 activity (U/L) in lEVs and sEVs derived from plasma of healthy individuals ( n = 8) and cardiogenic shock (CS) patients ( n = 11). DPP3 activity (U/L) in lEVs and sEVs derived from cell culture supernatant of (H) human cardiomyocytes <t>AC16</t> ( n = 6) and (I) human monocytes THP-1 ( n = 2). In all bars, data are presented as mean ± standard error of the mean (SEM). Comparisons were made by Multiple Mann-Whitney tests in B, C, F, and G, and by two-way ANOVA in D and E. Significance was presented as follows (∗ p < 0.05, ∗∗ p < 0.01, and ns for non-significant differences).
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A fraction of DPP3 is transported via EVs and upregulated during septic shock in humans (A) Western blot qualitative analysis of cluster of differentiation 63 (CD63) at 26 KD (bottom), heat shock protein 70 (HSC70) at 73 KD (middle), and DPP3 at 83 KD (above), in protein extracts of EVs derived from bone marrow supernatant (BM SN) from Ctrl mice (left) and ISO mice (right). DPP3 activity (U/L) in large (lEVs) and small (sEVs) EVs derived from (B) plasma of control mice (Ctrl) ( n = 6) and isoproterenol-treated mice (ISO) ( n = 5), or from (C) BM SN of Ctrl ( n = 6) and ISO mice ( n = 6). (D) DPP3 activity in lEVs and sEVs derived from BM SN of WT mice injected with bone marrow cells from Dpp3-KO (WT BM KO ) and Dpp3-KO mice injected with bone marrow cells from WT mice (KO BM WT ) ( n = 5) for each. (E) Quantification of Nano track analysis (NTA) results of plasma derived-lEVs and sEVs concentration (vesicle/ml) in healthy individuals ( n = 7), septic shock (SS) ( n = 6) and cardiogenic shock (CS) patients ( n = 5). (F) DPP3 activity (U/L) in lEVs and sEVs derived from plasma of healthy individuals ( n = 8) and septic shock (SS) patients ( n = 6). (G) DPP3 activity (U/L) in lEVs and sEVs derived from plasma of healthy individuals ( n = 8) and cardiogenic shock (CS) patients ( n = 11). DPP3 activity (U/L) in lEVs and sEVs derived from cell culture supernatant of (H) human cardiomyocytes <t>AC16</t> ( n = 6) and (I) human monocytes THP-1 ( n = 2). In all bars, data are presented as mean ± standard error of the mean (SEM). Comparisons were made by Multiple Mann-Whitney tests in B, C, F, and G, and by two-way ANOVA in D and E. Significance was presented as follows (∗ p < 0.05, ∗∗ p < 0.01, and ns for non-significant differences).
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Image Search Results


KO schematic in cardiomyocytes B-D: Oxygen consumption rate (OCR) is significantly increased in siSMN-treated cardiomyocytes compared with siScramble controls and extracellular acidification rate (ECAR) is significantly decreased in siSMN-treated cardiomyocytes. n = 16 technical replicates. * p <0.05. **p < 0.01. Mitochondrial and glycolytic ATP production rates show no significant difference between siSMN and siScramble conditions (ns). E: Volcano plot of differential gene expression following SMN knockdown. F: Heatmap and hierarchical clustering of differentially expressed genes demonstrate distinct transcriptional profiles between siSMN and siScramble cardiomyocytes. G: Pathway enrichment analysis of differentially expressed genes identifies significant perturbation of multiple signaling pathways, including enrichment of PTEN signaling.

Journal: bioRxiv

Article Title: Cardiac defects in spinal muscular atrophy and the role of SMN in cardiomyocyte homeostasis

doi: 10.64898/2026.03.20.713246

Figure Lengend Snippet: KO schematic in cardiomyocytes B-D: Oxygen consumption rate (OCR) is significantly increased in siSMN-treated cardiomyocytes compared with siScramble controls and extracellular acidification rate (ECAR) is significantly decreased in siSMN-treated cardiomyocytes. n = 16 technical replicates. * p <0.05. **p < 0.01. Mitochondrial and glycolytic ATP production rates show no significant difference between siSMN and siScramble conditions (ns). E: Volcano plot of differential gene expression following SMN knockdown. F: Heatmap and hierarchical clustering of differentially expressed genes demonstrate distinct transcriptional profiles between siSMN and siScramble cardiomyocytes. G: Pathway enrichment analysis of differentially expressed genes identifies significant perturbation of multiple signaling pathways, including enrichment of PTEN signaling.

Article Snippet: Human cardiomyocytes (Axol Bioscience Limited, Cambridgeshire, England; Cat. No. ax2520; Lot No. 2520310317) were cultured and differentiated in coated plates using supplemented media from the Human iPSC-Derived Ventricular Cardiomyocyte Kit (Axol Bioscience Limited, Cambridgeshire, England).

Techniques: Gene Expression, Knockdown, Protein-Protein interactions

Ingenuity pathway analysis of differentially expressed genes after SMN2 knockdown in human cardiomyocytes, showing the top 20 significantly enriched canonical pathways ranked by –log(p value). Bar color denotes predicted directionality based on z-score: black indicates negative z-score (predicted pathway inhibition), red indicates positive z-score (predicted pathway activation), and gray indicates no consistent activation pattern.

Journal: bioRxiv

Article Title: Cardiac defects in spinal muscular atrophy and the role of SMN in cardiomyocyte homeostasis

doi: 10.64898/2026.03.20.713246

Figure Lengend Snippet: Ingenuity pathway analysis of differentially expressed genes after SMN2 knockdown in human cardiomyocytes, showing the top 20 significantly enriched canonical pathways ranked by –log(p value). Bar color denotes predicted directionality based on z-score: black indicates negative z-score (predicted pathway inhibition), red indicates positive z-score (predicted pathway activation), and gray indicates no consistent activation pattern.

Article Snippet: Human cardiomyocytes (Axol Bioscience Limited, Cambridgeshire, England; Cat. No. ax2520; Lot No. 2520310317) were cultured and differentiated in coated plates using supplemented media from the Human iPSC-Derived Ventricular Cardiomyocyte Kit (Axol Bioscience Limited, Cambridgeshire, England).

Techniques: Knockdown, Inhibition, Activation Assay

A fraction of DPP3 is transported via EVs and upregulated during septic shock in humans (A) Western blot qualitative analysis of cluster of differentiation 63 (CD63) at 26 KD (bottom), heat shock protein 70 (HSC70) at 73 KD (middle), and DPP3 at 83 KD (above), in protein extracts of EVs derived from bone marrow supernatant (BM SN) from Ctrl mice (left) and ISO mice (right). DPP3 activity (U/L) in large (lEVs) and small (sEVs) EVs derived from (B) plasma of control mice (Ctrl) ( n = 6) and isoproterenol-treated mice (ISO) ( n = 5), or from (C) BM SN of Ctrl ( n = 6) and ISO mice ( n = 6). (D) DPP3 activity in lEVs and sEVs derived from BM SN of WT mice injected with bone marrow cells from Dpp3-KO (WT BM KO ) and Dpp3-KO mice injected with bone marrow cells from WT mice (KO BM WT ) ( n = 5) for each. (E) Quantification of Nano track analysis (NTA) results of plasma derived-lEVs and sEVs concentration (vesicle/ml) in healthy individuals ( n = 7), septic shock (SS) ( n = 6) and cardiogenic shock (CS) patients ( n = 5). (F) DPP3 activity (U/L) in lEVs and sEVs derived from plasma of healthy individuals ( n = 8) and septic shock (SS) patients ( n = 6). (G) DPP3 activity (U/L) in lEVs and sEVs derived from plasma of healthy individuals ( n = 8) and cardiogenic shock (CS) patients ( n = 11). DPP3 activity (U/L) in lEVs and sEVs derived from cell culture supernatant of (H) human cardiomyocytes AC16 ( n = 6) and (I) human monocytes THP-1 ( n = 2). In all bars, data are presented as mean ± standard error of the mean (SEM). Comparisons were made by Multiple Mann-Whitney tests in B, C, F, and G, and by two-way ANOVA in D and E. Significance was presented as follows (∗ p < 0.05, ∗∗ p < 0.01, and ns for non-significant differences).

Journal: iScience

Article Title: Crosstalk between circulating DPP3 and immune cells in the context of cardio-systemic stress

doi: 10.1016/j.isci.2026.115114

Figure Lengend Snippet: A fraction of DPP3 is transported via EVs and upregulated during septic shock in humans (A) Western blot qualitative analysis of cluster of differentiation 63 (CD63) at 26 KD (bottom), heat shock protein 70 (HSC70) at 73 KD (middle), and DPP3 at 83 KD (above), in protein extracts of EVs derived from bone marrow supernatant (BM SN) from Ctrl mice (left) and ISO mice (right). DPP3 activity (U/L) in large (lEVs) and small (sEVs) EVs derived from (B) plasma of control mice (Ctrl) ( n = 6) and isoproterenol-treated mice (ISO) ( n = 5), or from (C) BM SN of Ctrl ( n = 6) and ISO mice ( n = 6). (D) DPP3 activity in lEVs and sEVs derived from BM SN of WT mice injected with bone marrow cells from Dpp3-KO (WT BM KO ) and Dpp3-KO mice injected with bone marrow cells from WT mice (KO BM WT ) ( n = 5) for each. (E) Quantification of Nano track analysis (NTA) results of plasma derived-lEVs and sEVs concentration (vesicle/ml) in healthy individuals ( n = 7), septic shock (SS) ( n = 6) and cardiogenic shock (CS) patients ( n = 5). (F) DPP3 activity (U/L) in lEVs and sEVs derived from plasma of healthy individuals ( n = 8) and septic shock (SS) patients ( n = 6). (G) DPP3 activity (U/L) in lEVs and sEVs derived from plasma of healthy individuals ( n = 8) and cardiogenic shock (CS) patients ( n = 11). DPP3 activity (U/L) in lEVs and sEVs derived from cell culture supernatant of (H) human cardiomyocytes AC16 ( n = 6) and (I) human monocytes THP-1 ( n = 2). In all bars, data are presented as mean ± standard error of the mean (SEM). Comparisons were made by Multiple Mann-Whitney tests in B, C, F, and G, and by two-way ANOVA in D and E. Significance was presented as follows (∗ p < 0.05, ∗∗ p < 0.01, and ns for non-significant differences).

Article Snippet: Three cell lines were used: human ventricular cardiomyocytes (AC16, Merck SCC109), murine ovarian cancer cells (ID8, Merck SCC145), and human monocytes (THP-1, kindly provided by Prof. Jean-Sébastien Silvestre).

Techniques: Western Blot, Derivative Assay, Activity Assay, Clinical Proteomics, Control, Injection, Concentration Assay, Cell Culture, MANN-WHITNEY

A fraction of DPP3 is transported via EVs and upregulated during septic shock in humans (A) Western blot qualitative analysis of cluster of differentiation 63 (CD63) at 26 KD (bottom), heat shock protein 70 (HSC70) at 73 KD (middle), and DPP3 at 83 KD (above), in protein extracts of EVs derived from bone marrow supernatant (BM SN) from Ctrl mice (left) and ISO mice (right). DPP3 activity (U/L) in large (lEVs) and small (sEVs) EVs derived from (B) plasma of control mice (Ctrl) ( n = 6) and isoproterenol-treated mice (ISO) ( n = 5), or from (C) BM SN of Ctrl ( n = 6) and ISO mice ( n = 6). (D) DPP3 activity in lEVs and sEVs derived from BM SN of WT mice injected with bone marrow cells from Dpp3-KO (WT BM KO ) and Dpp3-KO mice injected with bone marrow cells from WT mice (KO BM WT ) ( n = 5) for each. (E) Quantification of Nano track analysis (NTA) results of plasma derived-lEVs and sEVs concentration (vesicle/ml) in healthy individuals ( n = 7), septic shock (SS) ( n = 6) and cardiogenic shock (CS) patients ( n = 5). (F) DPP3 activity (U/L) in lEVs and sEVs derived from plasma of healthy individuals ( n = 8) and septic shock (SS) patients ( n = 6). (G) DPP3 activity (U/L) in lEVs and sEVs derived from plasma of healthy individuals ( n = 8) and cardiogenic shock (CS) patients ( n = 11). DPP3 activity (U/L) in lEVs and sEVs derived from cell culture supernatant of (H) human cardiomyocytes AC16 ( n = 6) and (I) human monocytes THP-1 ( n = 2). In all bars, data are presented as mean ± standard error of the mean (SEM). Comparisons were made by Multiple Mann-Whitney tests in B, C, F, and G, and by two-way ANOVA in D and E. Significance was presented as follows (∗ p < 0.05, ∗∗ p < 0.01, and ns for non-significant differences).

Journal: iScience

Article Title: Crosstalk between circulating DPP3 and immune cells in the context of cardio-systemic stress

doi: 10.1016/j.isci.2026.115114

Figure Lengend Snippet: A fraction of DPP3 is transported via EVs and upregulated during septic shock in humans (A) Western blot qualitative analysis of cluster of differentiation 63 (CD63) at 26 KD (bottom), heat shock protein 70 (HSC70) at 73 KD (middle), and DPP3 at 83 KD (above), in protein extracts of EVs derived from bone marrow supernatant (BM SN) from Ctrl mice (left) and ISO mice (right). DPP3 activity (U/L) in large (lEVs) and small (sEVs) EVs derived from (B) plasma of control mice (Ctrl) ( n = 6) and isoproterenol-treated mice (ISO) ( n = 5), or from (C) BM SN of Ctrl ( n = 6) and ISO mice ( n = 6). (D) DPP3 activity in lEVs and sEVs derived from BM SN of WT mice injected with bone marrow cells from Dpp3-KO (WT BM KO ) and Dpp3-KO mice injected with bone marrow cells from WT mice (KO BM WT ) ( n = 5) for each. (E) Quantification of Nano track analysis (NTA) results of plasma derived-lEVs and sEVs concentration (vesicle/ml) in healthy individuals ( n = 7), septic shock (SS) ( n = 6) and cardiogenic shock (CS) patients ( n = 5). (F) DPP3 activity (U/L) in lEVs and sEVs derived from plasma of healthy individuals ( n = 8) and septic shock (SS) patients ( n = 6). (G) DPP3 activity (U/L) in lEVs and sEVs derived from plasma of healthy individuals ( n = 8) and cardiogenic shock (CS) patients ( n = 11). DPP3 activity (U/L) in lEVs and sEVs derived from cell culture supernatant of (H) human cardiomyocytes AC16 ( n = 6) and (I) human monocytes THP-1 ( n = 2). In all bars, data are presented as mean ± standard error of the mean (SEM). Comparisons were made by Multiple Mann-Whitney tests in B, C, F, and G, and by two-way ANOVA in D and E. Significance was presented as follows (∗ p < 0.05, ∗∗ p < 0.01, and ns for non-significant differences).

Article Snippet: Human ventricular cardiomyocytes (AC16) , Merck , SCC109.

Techniques: Western Blot, Derivative Assay, Activity Assay, Clinical Proteomics, Control, Injection, Concentration Assay, Cell Culture, MANN-WHITNEY