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rabbit anti pde2a  (Novus Biologicals)


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    Novus Biologicals rabbit anti pde2a
    Figure 2. Gene therapy with <t>PDE2A</t> prevents cardiac remodeling and dysfunction induced by chronic isoproterenol infusion. A, Schematic representation of the experimental protocol. Mice were injected in the tail vein with 1012 viral particles of a serotype 9 adeno-associated viruses encoding for luciferase or phosphodiesterase 2A3. Fourteen days later, mice injected with AAV9-LUC were implanted subcutaneously with osmotic pumps diffusing either NaCl (NaCl-LUC) or isoproterenol at 60 mg/kg per day (isoproterenol- LUC) and animals injected with AAV9-PDE2A were implanted with pumps delivering isoproterenol at 60 mg/kg per day (isoproterenol- PDE2A). Treatment duration was 14 days (hatched bars). Minipumps were then removed and mice were kept for 2 additional weeks before euthanasia. Cardiac function was evaluated by serial echocardiography before injection of the virus as well as at 14, 28, 35, and 42 days. B, Left panel shows representative blots of PDE2A and vinculin. PDE2A protein expression in heart tissues extracts measured by Western blot and the bar graph represents the ratios of PDE2A over vinculin quantified expressed as mean±SEM in NaCl-LUC, isoproterenol-LUC and isoproterenol-PDE2A groups. C, Heart weight and lung weight over tibia length ratio expressed as mean±SEM. D, Time course of the normalized ratio of calculated left ventricular weight over body weight and normalized ejection fraction in NaCl-LUC, isoproterenol-LUC and isoproterenol-PDE2A mice. Number of mice is indicated in the brackets. E, Panel on the left, representative images of Masson’s trichrome staining (scale bar 100 μm), bar graph on the left represents quantifications of interstitial fibrosis as mean±SEM in NaCl-LUC (n=9), isoproterenol-LUC (n=9), and isoproterenol+PDE2A (n=9) groups. Statistical significance is indicated by the P value (* vs NaCl-LUC and † vs isoproterenol-LUC) determined using Welch’s t test (B), Kruskal– Wallis followed by a Dunn’s test (C panel bottom and E), 2-way ANOVA followed by a Tukey’s test (D), 1-way ANOVA followed by a Tukey’s test (C panel top). AAV9 indicates serotype 9 adeno-associated viruses; BW, body weight; HW, heart weight; Iso-LUC, isoproterenol-luciferase; Iso-PDE2A, isoproterenol-phosphodiesterase 2A; LUC, luciferase; LVW, left ventricular weight; LW, lung weight; PDE2A, phosphodiesterase 2A; and TL, tibia length.
    Rabbit Anti Pde2a, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti pde2a/product/Novus Biologicals
    Average 93 stars, based on 1 article reviews
    rabbit anti pde2a - by Bioz Stars, 2026-05
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    Images

    1) Product Images from "Cardiac Gene Therapy With Phosphodiesterase 2A Limits Remodeling and Arrhythmias in Mouse Models of Heart Failure"

    Article Title: Cardiac Gene Therapy With Phosphodiesterase 2A Limits Remodeling and Arrhythmias in Mouse Models of Heart Failure

    Journal: Journal of the American Heart Association

    doi: 10.1161/jaha.124.037343

    Figure 2. Gene therapy with PDE2A prevents cardiac remodeling and dysfunction induced by chronic isoproterenol infusion. A, Schematic representation of the experimental protocol. Mice were injected in the tail vein with 1012 viral particles of a serotype 9 adeno-associated viruses encoding for luciferase or phosphodiesterase 2A3. Fourteen days later, mice injected with AAV9-LUC were implanted subcutaneously with osmotic pumps diffusing either NaCl (NaCl-LUC) or isoproterenol at 60 mg/kg per day (isoproterenol- LUC) and animals injected with AAV9-PDE2A were implanted with pumps delivering isoproterenol at 60 mg/kg per day (isoproterenol- PDE2A). Treatment duration was 14 days (hatched bars). Minipumps were then removed and mice were kept for 2 additional weeks before euthanasia. Cardiac function was evaluated by serial echocardiography before injection of the virus as well as at 14, 28, 35, and 42 days. B, Left panel shows representative blots of PDE2A and vinculin. PDE2A protein expression in heart tissues extracts measured by Western blot and the bar graph represents the ratios of PDE2A over vinculin quantified expressed as mean±SEM in NaCl-LUC, isoproterenol-LUC and isoproterenol-PDE2A groups. C, Heart weight and lung weight over tibia length ratio expressed as mean±SEM. D, Time course of the normalized ratio of calculated left ventricular weight over body weight and normalized ejection fraction in NaCl-LUC, isoproterenol-LUC and isoproterenol-PDE2A mice. Number of mice is indicated in the brackets. E, Panel on the left, representative images of Masson’s trichrome staining (scale bar 100 μm), bar graph on the left represents quantifications of interstitial fibrosis as mean±SEM in NaCl-LUC (n=9), isoproterenol-LUC (n=9), and isoproterenol+PDE2A (n=9) groups. Statistical significance is indicated by the P value (* vs NaCl-LUC and † vs isoproterenol-LUC) determined using Welch’s t test (B), Kruskal– Wallis followed by a Dunn’s test (C panel bottom and E), 2-way ANOVA followed by a Tukey’s test (D), 1-way ANOVA followed by a Tukey’s test (C panel top). AAV9 indicates serotype 9 adeno-associated viruses; BW, body weight; HW, heart weight; Iso-LUC, isoproterenol-luciferase; Iso-PDE2A, isoproterenol-phosphodiesterase 2A; LUC, luciferase; LVW, left ventricular weight; LW, lung weight; PDE2A, phosphodiesterase 2A; and TL, tibia length.
    Figure Legend Snippet: Figure 2. Gene therapy with PDE2A prevents cardiac remodeling and dysfunction induced by chronic isoproterenol infusion. A, Schematic representation of the experimental protocol. Mice were injected in the tail vein with 1012 viral particles of a serotype 9 adeno-associated viruses encoding for luciferase or phosphodiesterase 2A3. Fourteen days later, mice injected with AAV9-LUC were implanted subcutaneously with osmotic pumps diffusing either NaCl (NaCl-LUC) or isoproterenol at 60 mg/kg per day (isoproterenol- LUC) and animals injected with AAV9-PDE2A were implanted with pumps delivering isoproterenol at 60 mg/kg per day (isoproterenol- PDE2A). Treatment duration was 14 days (hatched bars). Minipumps were then removed and mice were kept for 2 additional weeks before euthanasia. Cardiac function was evaluated by serial echocardiography before injection of the virus as well as at 14, 28, 35, and 42 days. B, Left panel shows representative blots of PDE2A and vinculin. PDE2A protein expression in heart tissues extracts measured by Western blot and the bar graph represents the ratios of PDE2A over vinculin quantified expressed as mean±SEM in NaCl-LUC, isoproterenol-LUC and isoproterenol-PDE2A groups. C, Heart weight and lung weight over tibia length ratio expressed as mean±SEM. D, Time course of the normalized ratio of calculated left ventricular weight over body weight and normalized ejection fraction in NaCl-LUC, isoproterenol-LUC and isoproterenol-PDE2A mice. Number of mice is indicated in the brackets. E, Panel on the left, representative images of Masson’s trichrome staining (scale bar 100 μm), bar graph on the left represents quantifications of interstitial fibrosis as mean±SEM in NaCl-LUC (n=9), isoproterenol-LUC (n=9), and isoproterenol+PDE2A (n=9) groups. Statistical significance is indicated by the P value (* vs NaCl-LUC and † vs isoproterenol-LUC) determined using Welch’s t test (B), Kruskal– Wallis followed by a Dunn’s test (C panel bottom and E), 2-way ANOVA followed by a Tukey’s test (D), 1-way ANOVA followed by a Tukey’s test (C panel top). AAV9 indicates serotype 9 adeno-associated viruses; BW, body weight; HW, heart weight; Iso-LUC, isoproterenol-luciferase; Iso-PDE2A, isoproterenol-phosphodiesterase 2A; LUC, luciferase; LVW, left ventricular weight; LW, lung weight; PDE2A, phosphodiesterase 2A; and TL, tibia length.

    Techniques Used: Injection, Luciferase, Virus, Expressing, Western Blot, Staining

    Figure 3. PDE2A overexpression limits maladaptive remodeling and cardiac dysfunction induced by chronic isoproterenol and phenylephrine infusion. A, Schematic representation of the experimental protocol. Mice were injected with 1012 viral particles of serotype 9 adeno-associated viruses encoding for Luciferase or phosphodiesterase 2A3. Fourteen days later, mice were implanted with osmotic minipumps diffusing either NaCl (NaCl-LUC) or isoproterenol+phenylephrine at 30 mg/kg per day each (isoproterenol+phenylephrine-LUC and isoproterenol + phenylephrine-PDE2A). Minipumps were removed 2 weeks later and mice were euthanized. Cardiac function was assessed throughout the protocol using echocardiography before the injection of the virus and at 2, 3, 4, and 6 weeks. B, Representative blots of PDE2A and GAPDH on the left panel are shown and the bar graph represents ratios of PDE2A over GAPDH quantifications expressed as mean±SEM in a subset of the animals treated with NaCl-LUC, isoproterenol+phenylephrine-LUC, and isoproterenol+phenylephrine-PDE2A. C, Heart weight and lung weight over tibia length ratios expressed as mean±SEM. D, Time course of the normalized ratios of calculated left ventricular weight (over body weight and normalized ejection fraction in NaCl-LUC, isoproterenol+phenylephrine-LUC, and isoproterenol+phenylephrine-PDE2A mice). Number of mice is indicated in the brackets. E, Top panel shows representative images of Masson’s trichrome staining (scale bar 200 μm), the middle panel depicts representative images of terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay (scale bar 100 μm) detecting apoptotic nuclei in green costained with the glycocalix marker wheat germ agglutinin in red and nuclei in blue colored with Hoechst. Bar graphs representing mean±SEM quantifications of interstitial fibrosis and apoptotic nuclei in NaCl-LUC (10), isoproterenol+phenylephrine- LUC (9) and isoproterenol+phenylephrine-PDE2A (9) mice are depicted. Statistical significance indicated by the P value (* vs NaCl- LUC and † vs isoproterenol+phenylephrine-LUC) was determined using Welch’s t test (B), Kruskal–Wallis followed by a Dunn’s test (C), 2-way ANOVA followed by a Tukey’s test (D), Welch’s 1-way ANOVA followed by a Dunnett’s test (E). AAV9 indicates serotype 9 adeno-associated viruses; BW, body weight; HW, heart weight; Iso-Phe-LUC, isoproterenol-phenylephrine-luciferase; Iso-Phe- PDE2A, isoproterenol-phenylephrine-phosphodiesterase 2A; LUC, luciferase; LVW, left ventricular weight; LW, lung weight; ns, not significant; PDE2A, phosphodiesterase 2A; and TL, tibia length.
    Figure Legend Snippet: Figure 3. PDE2A overexpression limits maladaptive remodeling and cardiac dysfunction induced by chronic isoproterenol and phenylephrine infusion. A, Schematic representation of the experimental protocol. Mice were injected with 1012 viral particles of serotype 9 adeno-associated viruses encoding for Luciferase or phosphodiesterase 2A3. Fourteen days later, mice were implanted with osmotic minipumps diffusing either NaCl (NaCl-LUC) or isoproterenol+phenylephrine at 30 mg/kg per day each (isoproterenol+phenylephrine-LUC and isoproterenol + phenylephrine-PDE2A). Minipumps were removed 2 weeks later and mice were euthanized. Cardiac function was assessed throughout the protocol using echocardiography before the injection of the virus and at 2, 3, 4, and 6 weeks. B, Representative blots of PDE2A and GAPDH on the left panel are shown and the bar graph represents ratios of PDE2A over GAPDH quantifications expressed as mean±SEM in a subset of the animals treated with NaCl-LUC, isoproterenol+phenylephrine-LUC, and isoproterenol+phenylephrine-PDE2A. C, Heart weight and lung weight over tibia length ratios expressed as mean±SEM. D, Time course of the normalized ratios of calculated left ventricular weight (over body weight and normalized ejection fraction in NaCl-LUC, isoproterenol+phenylephrine-LUC, and isoproterenol+phenylephrine-PDE2A mice). Number of mice is indicated in the brackets. E, Top panel shows representative images of Masson’s trichrome staining (scale bar 200 μm), the middle panel depicts representative images of terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay (scale bar 100 μm) detecting apoptotic nuclei in green costained with the glycocalix marker wheat germ agglutinin in red and nuclei in blue colored with Hoechst. Bar graphs representing mean±SEM quantifications of interstitial fibrosis and apoptotic nuclei in NaCl-LUC (10), isoproterenol+phenylephrine- LUC (9) and isoproterenol+phenylephrine-PDE2A (9) mice are depicted. Statistical significance indicated by the P value (* vs NaCl- LUC and † vs isoproterenol+phenylephrine-LUC) was determined using Welch’s t test (B), Kruskal–Wallis followed by a Dunn’s test (C), 2-way ANOVA followed by a Tukey’s test (D), Welch’s 1-way ANOVA followed by a Dunnett’s test (E). AAV9 indicates serotype 9 adeno-associated viruses; BW, body weight; HW, heart weight; Iso-Phe-LUC, isoproterenol-phenylephrine-luciferase; Iso-Phe- PDE2A, isoproterenol-phenylephrine-phosphodiesterase 2A; LUC, luciferase; LVW, left ventricular weight; LW, lung weight; ns, not significant; PDE2A, phosphodiesterase 2A; and TL, tibia length.

    Techniques Used: Over Expression, Injection, Luciferase, Virus, Staining, TUNEL Assay, Marker



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    FabGennix rabbit anti-pde2 antibody pde2a-101ap
    Figure 2. Gene therapy with <t>PDE2A</t> prevents cardiac remodeling and dysfunction induced by chronic isoproterenol infusion. A, Schematic representation of the experimental protocol. Mice were injected in the tail vein with 1012 viral particles of a serotype 9 adeno-associated viruses encoding for luciferase or phosphodiesterase 2A3. Fourteen days later, mice injected with AAV9-LUC were implanted subcutaneously with osmotic pumps diffusing either NaCl (NaCl-LUC) or isoproterenol at 60 mg/kg per day (isoproterenol- LUC) and animals injected with AAV9-PDE2A were implanted with pumps delivering isoproterenol at 60 mg/kg per day (isoproterenol- PDE2A). Treatment duration was 14 days (hatched bars). Minipumps were then removed and mice were kept for 2 additional weeks before euthanasia. Cardiac function was evaluated by serial echocardiography before injection of the virus as well as at 14, 28, 35, and 42 days. B, Left panel shows representative blots of PDE2A and vinculin. PDE2A protein expression in heart tissues extracts measured by Western blot and the bar graph represents the ratios of PDE2A over vinculin quantified expressed as mean±SEM in NaCl-LUC, isoproterenol-LUC and isoproterenol-PDE2A groups. C, Heart weight and lung weight over tibia length ratio expressed as mean±SEM. D, Time course of the normalized ratio of calculated left ventricular weight over body weight and normalized ejection fraction in NaCl-LUC, isoproterenol-LUC and isoproterenol-PDE2A mice. Number of mice is indicated in the brackets. E, Panel on the left, representative images of Masson’s trichrome staining (scale bar 100 μm), bar graph on the left represents quantifications of interstitial fibrosis as mean±SEM in NaCl-LUC (n=9), isoproterenol-LUC (n=9), and isoproterenol+PDE2A (n=9) groups. Statistical significance is indicated by the P value (* vs NaCl-LUC and † vs isoproterenol-LUC) determined using Welch’s t test (B), Kruskal– Wallis followed by a Dunn’s test (C panel bottom and E), 2-way ANOVA followed by a Tukey’s test (D), 1-way ANOVA followed by a Tukey’s test (C panel top). AAV9 indicates serotype 9 adeno-associated viruses; BW, body weight; HW, heart weight; Iso-LUC, isoproterenol-luciferase; Iso-PDE2A, isoproterenol-phosphodiesterase 2A; LUC, luciferase; LVW, left ventricular weight; LW, lung weight; PDE2A, phosphodiesterase 2A; and TL, tibia length.
    Rabbit Anti Pde2 Antibody Pde2a 101ap, supplied by FabGennix, 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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    rabbit anti-pde2 antibody pde2a-101ap - by Bioz Stars, 2026-05
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    rabbit anti-pde2a pab abn1486  (Millipore)
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    Figure 2. Gene therapy with <t>PDE2A</t> prevents cardiac remodeling and dysfunction induced by chronic isoproterenol infusion. A, Schematic representation of the experimental protocol. Mice were injected in the tail vein with 1012 viral particles of a serotype 9 adeno-associated viruses encoding for luciferase or phosphodiesterase 2A3. Fourteen days later, mice injected with AAV9-LUC were implanted subcutaneously with osmotic pumps diffusing either NaCl (NaCl-LUC) or isoproterenol at 60 mg/kg per day (isoproterenol- LUC) and animals injected with AAV9-PDE2A were implanted with pumps delivering isoproterenol at 60 mg/kg per day (isoproterenol- PDE2A). Treatment duration was 14 days (hatched bars). Minipumps were then removed and mice were kept for 2 additional weeks before euthanasia. Cardiac function was evaluated by serial echocardiography before injection of the virus as well as at 14, 28, 35, and 42 days. B, Left panel shows representative blots of PDE2A and vinculin. PDE2A protein expression in heart tissues extracts measured by Western blot and the bar graph represents the ratios of PDE2A over vinculin quantified expressed as mean±SEM in NaCl-LUC, isoproterenol-LUC and isoproterenol-PDE2A groups. C, Heart weight and lung weight over tibia length ratio expressed as mean±SEM. D, Time course of the normalized ratio of calculated left ventricular weight over body weight and normalized ejection fraction in NaCl-LUC, isoproterenol-LUC and isoproterenol-PDE2A mice. Number of mice is indicated in the brackets. E, Panel on the left, representative images of Masson’s trichrome staining (scale bar 100 μm), bar graph on the left represents quantifications of interstitial fibrosis as mean±SEM in NaCl-LUC (n=9), isoproterenol-LUC (n=9), and isoproterenol+PDE2A (n=9) groups. Statistical significance is indicated by the P value (* vs NaCl-LUC and † vs isoproterenol-LUC) determined using Welch’s t test (B), Kruskal– Wallis followed by a Dunn’s test (C panel bottom and E), 2-way ANOVA followed by a Tukey’s test (D), 1-way ANOVA followed by a Tukey’s test (C panel top). AAV9 indicates serotype 9 adeno-associated viruses; BW, body weight; HW, heart weight; Iso-LUC, isoproterenol-luciferase; Iso-PDE2A, isoproterenol-phosphodiesterase 2A; LUC, luciferase; LVW, left ventricular weight; LW, lung weight; PDE2A, phosphodiesterase 2A; and TL, tibia length.
    Rabbit Anti Pde2a Pab Abn1486, supplied by Millipore, 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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    Figure 2. Gene therapy with <t>PDE2A</t> prevents cardiac remodeling and dysfunction induced by chronic isoproterenol infusion. A, Schematic representation of the experimental protocol. Mice were injected in the tail vein with 1012 viral particles of a serotype 9 adeno-associated viruses encoding for luciferase or phosphodiesterase 2A3. Fourteen days later, mice injected with AAV9-LUC were implanted subcutaneously with osmotic pumps diffusing either NaCl (NaCl-LUC) or isoproterenol at 60 mg/kg per day (isoproterenol- LUC) and animals injected with AAV9-PDE2A were implanted with pumps delivering isoproterenol at 60 mg/kg per day (isoproterenol- PDE2A). Treatment duration was 14 days (hatched bars). Minipumps were then removed and mice were kept for 2 additional weeks before euthanasia. Cardiac function was evaluated by serial echocardiography before injection of the virus as well as at 14, 28, 35, and 42 days. B, Left panel shows representative blots of PDE2A and vinculin. PDE2A protein expression in heart tissues extracts measured by Western blot and the bar graph represents the ratios of PDE2A over vinculin quantified expressed as mean±SEM in NaCl-LUC, isoproterenol-LUC and isoproterenol-PDE2A groups. C, Heart weight and lung weight over tibia length ratio expressed as mean±SEM. D, Time course of the normalized ratio of calculated left ventricular weight over body weight and normalized ejection fraction in NaCl-LUC, isoproterenol-LUC and isoproterenol-PDE2A mice. Number of mice is indicated in the brackets. E, Panel on the left, representative images of Masson’s trichrome staining (scale bar 100 μm), bar graph on the left represents quantifications of interstitial fibrosis as mean±SEM in NaCl-LUC (n=9), isoproterenol-LUC (n=9), and isoproterenol+PDE2A (n=9) groups. Statistical significance is indicated by the P value (* vs NaCl-LUC and † vs isoproterenol-LUC) determined using Welch’s t test (B), Kruskal– Wallis followed by a Dunn’s test (C panel bottom and E), 2-way ANOVA followed by a Tukey’s test (D), 1-way ANOVA followed by a Tukey’s test (C panel top). AAV9 indicates serotype 9 adeno-associated viruses; BW, body weight; HW, heart weight; Iso-LUC, isoproterenol-luciferase; Iso-PDE2A, isoproterenol-phosphodiesterase 2A; LUC, luciferase; LVW, left ventricular weight; LW, lung weight; PDE2A, phosphodiesterase 2A; and TL, tibia length.
    Rabbit Polyclonal Anti Pde2a Pd2a 101ap, supplied by FabGennix, 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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    Figure 2. Gene therapy with PDE2A prevents cardiac remodeling and dysfunction induced by chronic isoproterenol infusion. A, Schematic representation of the experimental protocol. Mice were injected in the tail vein with 1012 viral particles of a serotype 9 adeno-associated viruses encoding for luciferase or phosphodiesterase 2A3. Fourteen days later, mice injected with AAV9-LUC were implanted subcutaneously with osmotic pumps diffusing either NaCl (NaCl-LUC) or isoproterenol at 60 mg/kg per day (isoproterenol- LUC) and animals injected with AAV9-PDE2A were implanted with pumps delivering isoproterenol at 60 mg/kg per day (isoproterenol- PDE2A). Treatment duration was 14 days (hatched bars). Minipumps were then removed and mice were kept for 2 additional weeks before euthanasia. Cardiac function was evaluated by serial echocardiography before injection of the virus as well as at 14, 28, 35, and 42 days. B, Left panel shows representative blots of PDE2A and vinculin. PDE2A protein expression in heart tissues extracts measured by Western blot and the bar graph represents the ratios of PDE2A over vinculin quantified expressed as mean±SEM in NaCl-LUC, isoproterenol-LUC and isoproterenol-PDE2A groups. C, Heart weight and lung weight over tibia length ratio expressed as mean±SEM. D, Time course of the normalized ratio of calculated left ventricular weight over body weight and normalized ejection fraction in NaCl-LUC, isoproterenol-LUC and isoproterenol-PDE2A mice. Number of mice is indicated in the brackets. E, Panel on the left, representative images of Masson’s trichrome staining (scale bar 100 μm), bar graph on the left represents quantifications of interstitial fibrosis as mean±SEM in NaCl-LUC (n=9), isoproterenol-LUC (n=9), and isoproterenol+PDE2A (n=9) groups. Statistical significance is indicated by the P value (* vs NaCl-LUC and † vs isoproterenol-LUC) determined using Welch’s t test (B), Kruskal– Wallis followed by a Dunn’s test (C panel bottom and E), 2-way ANOVA followed by a Tukey’s test (D), 1-way ANOVA followed by a Tukey’s test (C panel top). AAV9 indicates serotype 9 adeno-associated viruses; BW, body weight; HW, heart weight; Iso-LUC, isoproterenol-luciferase; Iso-PDE2A, isoproterenol-phosphodiesterase 2A; LUC, luciferase; LVW, left ventricular weight; LW, lung weight; PDE2A, phosphodiesterase 2A; and TL, tibia length.

    Journal: Journal of the American Heart Association

    Article Title: Cardiac Gene Therapy With Phosphodiesterase 2A Limits Remodeling and Arrhythmias in Mouse Models of Heart Failure

    doi: 10.1161/jaha.124.037343

    Figure Lengend Snippet: Figure 2. Gene therapy with PDE2A prevents cardiac remodeling and dysfunction induced by chronic isoproterenol infusion. A, Schematic representation of the experimental protocol. Mice were injected in the tail vein with 1012 viral particles of a serotype 9 adeno-associated viruses encoding for luciferase or phosphodiesterase 2A3. Fourteen days later, mice injected with AAV9-LUC were implanted subcutaneously with osmotic pumps diffusing either NaCl (NaCl-LUC) or isoproterenol at 60 mg/kg per day (isoproterenol- LUC) and animals injected with AAV9-PDE2A were implanted with pumps delivering isoproterenol at 60 mg/kg per day (isoproterenol- PDE2A). Treatment duration was 14 days (hatched bars). Minipumps were then removed and mice were kept for 2 additional weeks before euthanasia. Cardiac function was evaluated by serial echocardiography before injection of the virus as well as at 14, 28, 35, and 42 days. B, Left panel shows representative blots of PDE2A and vinculin. PDE2A protein expression in heart tissues extracts measured by Western blot and the bar graph represents the ratios of PDE2A over vinculin quantified expressed as mean±SEM in NaCl-LUC, isoproterenol-LUC and isoproterenol-PDE2A groups. C, Heart weight and lung weight over tibia length ratio expressed as mean±SEM. D, Time course of the normalized ratio of calculated left ventricular weight over body weight and normalized ejection fraction in NaCl-LUC, isoproterenol-LUC and isoproterenol-PDE2A mice. Number of mice is indicated in the brackets. E, Panel on the left, representative images of Masson’s trichrome staining (scale bar 100 μm), bar graph on the left represents quantifications of interstitial fibrosis as mean±SEM in NaCl-LUC (n=9), isoproterenol-LUC (n=9), and isoproterenol+PDE2A (n=9) groups. Statistical significance is indicated by the P value (* vs NaCl-LUC and † vs isoproterenol-LUC) determined using Welch’s t test (B), Kruskal– Wallis followed by a Dunn’s test (C panel bottom and E), 2-way ANOVA followed by a Tukey’s test (D), 1-way ANOVA followed by a Tukey’s test (C panel top). AAV9 indicates serotype 9 adeno-associated viruses; BW, body weight; HW, heart weight; Iso-LUC, isoproterenol-luciferase; Iso-PDE2A, isoproterenol-phosphodiesterase 2A; LUC, luciferase; LVW, left ventricular weight; LW, lung weight; PDE2A, phosphodiesterase 2A; and TL, tibia length.

    Article Snippet: The primary antibodies used were as follows: (1) Figure 1: rabbit anti- PDE2A, Fabgennix; PDE2A- 101AP diluted at 1/1000; rabbit anti- GAPDH, Cell Signaling, 2118 diluted at 1/1000; (2) Figure 2: goat antiPDE2A, Santa Cruz, SC- 17228 diluted at 1/1000; mouse anti- vinculin, V9131 Sigma- Aldrich diluted at 1/1000; (3) Figure 3: rabbit anti- PDE2A, Fabgennix, PDE2A- 101AP diluted at 1/1000; rabbit anti- GAPDH, Cell Signaling, 2118 diluted at 1/1000; (4) Figure S1: rabbit anti- flag L5, Novus Biologicals, NBP1- 06712 diluted at 1/500; rabbit anti- GAPDH, Cell Signaling, 2118 diluted at 1/1000; rabbit anti- PDE2A, Proteintech, 55 306- 1- AP diluted at 1/1000; rabbit anti- flag L5, Novus Biologicals, NBP1- 06712 diluted at 1/500; rabbit anti- GAPDH, Cell Signaling, 2118 diluted at 1/1000; (5) Figure S2B: rabbit anti- PDE2A, Proteintech, 55 306- 1- AP diluted at 1/1000; (6) Figure S3: rabbit antiPDE2A, Proteintech, 55 306- 1- AP diluted at 1/1000; and (7) Figure S4: rabbit anti- PDE4A AC55 (gift from Dr. Marco Conti, University of California San Francisco, San Francisco, CA) diluted at 1/1000; rabbit anti- PDE4B (gift from Dr. Marco Conti) diluted at 1/10000; mouse antiPDE4D (gift from Dr Marco Conti) diluted at 1/1000 and rabbit anti- PDE3A (gift from Dr Chen Yan, University of Rochester, Rochester, NY) diluted at 1/10000.

    Techniques: Injection, Luciferase, Virus, Expressing, Western Blot, Staining

    Figure 3. PDE2A overexpression limits maladaptive remodeling and cardiac dysfunction induced by chronic isoproterenol and phenylephrine infusion. A, Schematic representation of the experimental protocol. Mice were injected with 1012 viral particles of serotype 9 adeno-associated viruses encoding for Luciferase or phosphodiesterase 2A3. Fourteen days later, mice were implanted with osmotic minipumps diffusing either NaCl (NaCl-LUC) or isoproterenol+phenylephrine at 30 mg/kg per day each (isoproterenol+phenylephrine-LUC and isoproterenol + phenylephrine-PDE2A). Minipumps were removed 2 weeks later and mice were euthanized. Cardiac function was assessed throughout the protocol using echocardiography before the injection of the virus and at 2, 3, 4, and 6 weeks. B, Representative blots of PDE2A and GAPDH on the left panel are shown and the bar graph represents ratios of PDE2A over GAPDH quantifications expressed as mean±SEM in a subset of the animals treated with NaCl-LUC, isoproterenol+phenylephrine-LUC, and isoproterenol+phenylephrine-PDE2A. C, Heart weight and lung weight over tibia length ratios expressed as mean±SEM. D, Time course of the normalized ratios of calculated left ventricular weight (over body weight and normalized ejection fraction in NaCl-LUC, isoproterenol+phenylephrine-LUC, and isoproterenol+phenylephrine-PDE2A mice). Number of mice is indicated in the brackets. E, Top panel shows representative images of Masson’s trichrome staining (scale bar 200 μm), the middle panel depicts representative images of terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay (scale bar 100 μm) detecting apoptotic nuclei in green costained with the glycocalix marker wheat germ agglutinin in red and nuclei in blue colored with Hoechst. Bar graphs representing mean±SEM quantifications of interstitial fibrosis and apoptotic nuclei in NaCl-LUC (10), isoproterenol+phenylephrine- LUC (9) and isoproterenol+phenylephrine-PDE2A (9) mice are depicted. Statistical significance indicated by the P value (* vs NaCl- LUC and † vs isoproterenol+phenylephrine-LUC) was determined using Welch’s t test (B), Kruskal–Wallis followed by a Dunn’s test (C), 2-way ANOVA followed by a Tukey’s test (D), Welch’s 1-way ANOVA followed by a Dunnett’s test (E). AAV9 indicates serotype 9 adeno-associated viruses; BW, body weight; HW, heart weight; Iso-Phe-LUC, isoproterenol-phenylephrine-luciferase; Iso-Phe- PDE2A, isoproterenol-phenylephrine-phosphodiesterase 2A; LUC, luciferase; LVW, left ventricular weight; LW, lung weight; ns, not significant; PDE2A, phosphodiesterase 2A; and TL, tibia length.

    Journal: Journal of the American Heart Association

    Article Title: Cardiac Gene Therapy With Phosphodiesterase 2A Limits Remodeling and Arrhythmias in Mouse Models of Heart Failure

    doi: 10.1161/jaha.124.037343

    Figure Lengend Snippet: Figure 3. PDE2A overexpression limits maladaptive remodeling and cardiac dysfunction induced by chronic isoproterenol and phenylephrine infusion. A, Schematic representation of the experimental protocol. Mice were injected with 1012 viral particles of serotype 9 adeno-associated viruses encoding for Luciferase or phosphodiesterase 2A3. Fourteen days later, mice were implanted with osmotic minipumps diffusing either NaCl (NaCl-LUC) or isoproterenol+phenylephrine at 30 mg/kg per day each (isoproterenol+phenylephrine-LUC and isoproterenol + phenylephrine-PDE2A). Minipumps were removed 2 weeks later and mice were euthanized. Cardiac function was assessed throughout the protocol using echocardiography before the injection of the virus and at 2, 3, 4, and 6 weeks. B, Representative blots of PDE2A and GAPDH on the left panel are shown and the bar graph represents ratios of PDE2A over GAPDH quantifications expressed as mean±SEM in a subset of the animals treated with NaCl-LUC, isoproterenol+phenylephrine-LUC, and isoproterenol+phenylephrine-PDE2A. C, Heart weight and lung weight over tibia length ratios expressed as mean±SEM. D, Time course of the normalized ratios of calculated left ventricular weight (over body weight and normalized ejection fraction in NaCl-LUC, isoproterenol+phenylephrine-LUC, and isoproterenol+phenylephrine-PDE2A mice). Number of mice is indicated in the brackets. E, Top panel shows representative images of Masson’s trichrome staining (scale bar 200 μm), the middle panel depicts representative images of terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay (scale bar 100 μm) detecting apoptotic nuclei in green costained with the glycocalix marker wheat germ agglutinin in red and nuclei in blue colored with Hoechst. Bar graphs representing mean±SEM quantifications of interstitial fibrosis and apoptotic nuclei in NaCl-LUC (10), isoproterenol+phenylephrine- LUC (9) and isoproterenol+phenylephrine-PDE2A (9) mice are depicted. Statistical significance indicated by the P value (* vs NaCl- LUC and † vs isoproterenol+phenylephrine-LUC) was determined using Welch’s t test (B), Kruskal–Wallis followed by a Dunn’s test (C), 2-way ANOVA followed by a Tukey’s test (D), Welch’s 1-way ANOVA followed by a Dunnett’s test (E). AAV9 indicates serotype 9 adeno-associated viruses; BW, body weight; HW, heart weight; Iso-Phe-LUC, isoproterenol-phenylephrine-luciferase; Iso-Phe- PDE2A, isoproterenol-phenylephrine-phosphodiesterase 2A; LUC, luciferase; LVW, left ventricular weight; LW, lung weight; ns, not significant; PDE2A, phosphodiesterase 2A; and TL, tibia length.

    Article Snippet: The primary antibodies used were as follows: (1) Figure 1: rabbit anti- PDE2A, Fabgennix; PDE2A- 101AP diluted at 1/1000; rabbit anti- GAPDH, Cell Signaling, 2118 diluted at 1/1000; (2) Figure 2: goat antiPDE2A, Santa Cruz, SC- 17228 diluted at 1/1000; mouse anti- vinculin, V9131 Sigma- Aldrich diluted at 1/1000; (3) Figure 3: rabbit anti- PDE2A, Fabgennix, PDE2A- 101AP diluted at 1/1000; rabbit anti- GAPDH, Cell Signaling, 2118 diluted at 1/1000; (4) Figure S1: rabbit anti- flag L5, Novus Biologicals, NBP1- 06712 diluted at 1/500; rabbit anti- GAPDH, Cell Signaling, 2118 diluted at 1/1000; rabbit anti- PDE2A, Proteintech, 55 306- 1- AP diluted at 1/1000; rabbit anti- flag L5, Novus Biologicals, NBP1- 06712 diluted at 1/500; rabbit anti- GAPDH, Cell Signaling, 2118 diluted at 1/1000; (5) Figure S2B: rabbit anti- PDE2A, Proteintech, 55 306- 1- AP diluted at 1/1000; (6) Figure S3: rabbit antiPDE2A, Proteintech, 55 306- 1- AP diluted at 1/1000; and (7) Figure S4: rabbit anti- PDE4A AC55 (gift from Dr. Marco Conti, University of California San Francisco, San Francisco, CA) diluted at 1/1000; rabbit anti- PDE4B (gift from Dr. Marco Conti) diluted at 1/10000; mouse antiPDE4D (gift from Dr Marco Conti) diluted at 1/1000 and rabbit anti- PDE3A (gift from Dr Chen Yan, University of Rochester, Rochester, NY) diluted at 1/10000.

    Techniques: Over Expression, Injection, Luciferase, Virus, Staining, TUNEL Assay, Marker

    Figure 2. Gene therapy with PDE2A prevents cardiac remodeling and dysfunction induced by chronic isoproterenol infusion. A, Schematic representation of the experimental protocol. Mice were injected in the tail vein with 1012 viral particles of a serotype 9 adeno-associated viruses encoding for luciferase or phosphodiesterase 2A3. Fourteen days later, mice injected with AAV9-LUC were implanted subcutaneously with osmotic pumps diffusing either NaCl (NaCl-LUC) or isoproterenol at 60 mg/kg per day (isoproterenol- LUC) and animals injected with AAV9-PDE2A were implanted with pumps delivering isoproterenol at 60 mg/kg per day (isoproterenol- PDE2A). Treatment duration was 14 days (hatched bars). Minipumps were then removed and mice were kept for 2 additional weeks before euthanasia. Cardiac function was evaluated by serial echocardiography before injection of the virus as well as at 14, 28, 35, and 42 days. B, Left panel shows representative blots of PDE2A and vinculin. PDE2A protein expression in heart tissues extracts measured by Western blot and the bar graph represents the ratios of PDE2A over vinculin quantified expressed as mean±SEM in NaCl-LUC, isoproterenol-LUC and isoproterenol-PDE2A groups. C, Heart weight and lung weight over tibia length ratio expressed as mean±SEM. D, Time course of the normalized ratio of calculated left ventricular weight over body weight and normalized ejection fraction in NaCl-LUC, isoproterenol-LUC and isoproterenol-PDE2A mice. Number of mice is indicated in the brackets. E, Panel on the left, representative images of Masson’s trichrome staining (scale bar 100 μm), bar graph on the left represents quantifications of interstitial fibrosis as mean±SEM in NaCl-LUC (n=9), isoproterenol-LUC (n=9), and isoproterenol+PDE2A (n=9) groups. Statistical significance is indicated by the P value (* vs NaCl-LUC and † vs isoproterenol-LUC) determined using Welch’s t test (B), Kruskal– Wallis followed by a Dunn’s test (C panel bottom and E), 2-way ANOVA followed by a Tukey’s test (D), 1-way ANOVA followed by a Tukey’s test (C panel top). AAV9 indicates serotype 9 adeno-associated viruses; BW, body weight; HW, heart weight; Iso-LUC, isoproterenol-luciferase; Iso-PDE2A, isoproterenol-phosphodiesterase 2A; LUC, luciferase; LVW, left ventricular weight; LW, lung weight; PDE2A, phosphodiesterase 2A; and TL, tibia length.

    Journal: Journal of the American Heart Association

    Article Title: Cardiac Gene Therapy With Phosphodiesterase 2A Limits Remodeling and Arrhythmias in Mouse Models of Heart Failure

    doi: 10.1161/jaha.124.037343

    Figure Lengend Snippet: Figure 2. Gene therapy with PDE2A prevents cardiac remodeling and dysfunction induced by chronic isoproterenol infusion. A, Schematic representation of the experimental protocol. Mice were injected in the tail vein with 1012 viral particles of a serotype 9 adeno-associated viruses encoding for luciferase or phosphodiesterase 2A3. Fourteen days later, mice injected with AAV9-LUC were implanted subcutaneously with osmotic pumps diffusing either NaCl (NaCl-LUC) or isoproterenol at 60 mg/kg per day (isoproterenol- LUC) and animals injected with AAV9-PDE2A were implanted with pumps delivering isoproterenol at 60 mg/kg per day (isoproterenol- PDE2A). Treatment duration was 14 days (hatched bars). Minipumps were then removed and mice were kept for 2 additional weeks before euthanasia. Cardiac function was evaluated by serial echocardiography before injection of the virus as well as at 14, 28, 35, and 42 days. B, Left panel shows representative blots of PDE2A and vinculin. PDE2A protein expression in heart tissues extracts measured by Western blot and the bar graph represents the ratios of PDE2A over vinculin quantified expressed as mean±SEM in NaCl-LUC, isoproterenol-LUC and isoproterenol-PDE2A groups. C, Heart weight and lung weight over tibia length ratio expressed as mean±SEM. D, Time course of the normalized ratio of calculated left ventricular weight over body weight and normalized ejection fraction in NaCl-LUC, isoproterenol-LUC and isoproterenol-PDE2A mice. Number of mice is indicated in the brackets. E, Panel on the left, representative images of Masson’s trichrome staining (scale bar 100 μm), bar graph on the left represents quantifications of interstitial fibrosis as mean±SEM in NaCl-LUC (n=9), isoproterenol-LUC (n=9), and isoproterenol+PDE2A (n=9) groups. Statistical significance is indicated by the P value (* vs NaCl-LUC and † vs isoproterenol-LUC) determined using Welch’s t test (B), Kruskal– Wallis followed by a Dunn’s test (C panel bottom and E), 2-way ANOVA followed by a Tukey’s test (D), 1-way ANOVA followed by a Tukey’s test (C panel top). AAV9 indicates serotype 9 adeno-associated viruses; BW, body weight; HW, heart weight; Iso-LUC, isoproterenol-luciferase; Iso-PDE2A, isoproterenol-phosphodiesterase 2A; LUC, luciferase; LVW, left ventricular weight; LW, lung weight; PDE2A, phosphodiesterase 2A; and TL, tibia length.

    Article Snippet: The primary antibodies used were as follows: (1) Figure 1: rabbit anti- PDE2A, Fabgennix; PDE2A- 101AP diluted at 1/1000; rabbit anti- GAPDH, Cell Signaling, 2118 diluted at 1/1000; (2) Figure 2: goat antiPDE2A, Santa Cruz, SC- 17228 diluted at 1/1000; mouse anti- vinculin, V9131 Sigma- Aldrich diluted at 1/1000; (3) Figure 3: rabbit anti- PDE2A, Fabgennix, PDE2A- 101AP diluted at 1/1000; rabbit anti- GAPDH, Cell Signaling, 2118 diluted at 1/1000; (4) Figure S1: rabbit anti- flag L5, Novus Biologicals, NBP1- 06712 diluted at 1/500; rabbit anti- GAPDH, Cell Signaling, 2118 diluted at 1/1000; rabbit anti- PDE2A, Proteintech, 55 306- 1- AP diluted at 1/1000; rabbit anti- flag L5, Novus Biologicals, NBP1- 06712 diluted at 1/500; rabbit anti- GAPDH, Cell Signaling, 2118 diluted at 1/1000; (5) Figure S2B: rabbit anti- PDE2A, Proteintech, 55 306- 1- AP diluted at 1/1000; (6) Figure S3: rabbit antiPDE2A, Proteintech, 55 306- 1- AP diluted at 1/1000; and (7) Figure S4: rabbit anti- PDE4A AC55 (gift from Dr. Marco Conti, University of California San Francisco, San Francisco, CA) diluted at 1/1000; rabbit anti- PDE4B (gift from Dr. Marco Conti) diluted at 1/10000; mouse antiPDE4D (gift from Dr Marco Conti) diluted at 1/1000 and rabbit anti- PDE3A (gift from Dr Chen Yan, University of Rochester, Rochester, NY) diluted at 1/10000.

    Techniques: Injection, Luciferase, Virus, Expressing, Western Blot, Staining

    Figure 3. PDE2A overexpression limits maladaptive remodeling and cardiac dysfunction induced by chronic isoproterenol and phenylephrine infusion. A, Schematic representation of the experimental protocol. Mice were injected with 1012 viral particles of serotype 9 adeno-associated viruses encoding for Luciferase or phosphodiesterase 2A3. Fourteen days later, mice were implanted with osmotic minipumps diffusing either NaCl (NaCl-LUC) or isoproterenol+phenylephrine at 30 mg/kg per day each (isoproterenol+phenylephrine-LUC and isoproterenol + phenylephrine-PDE2A). Minipumps were removed 2 weeks later and mice were euthanized. Cardiac function was assessed throughout the protocol using echocardiography before the injection of the virus and at 2, 3, 4, and 6 weeks. B, Representative blots of PDE2A and GAPDH on the left panel are shown and the bar graph represents ratios of PDE2A over GAPDH quantifications expressed as mean±SEM in a subset of the animals treated with NaCl-LUC, isoproterenol+phenylephrine-LUC, and isoproterenol+phenylephrine-PDE2A. C, Heart weight and lung weight over tibia length ratios expressed as mean±SEM. D, Time course of the normalized ratios of calculated left ventricular weight (over body weight and normalized ejection fraction in NaCl-LUC, isoproterenol+phenylephrine-LUC, and isoproterenol+phenylephrine-PDE2A mice). Number of mice is indicated in the brackets. E, Top panel shows representative images of Masson’s trichrome staining (scale bar 200 μm), the middle panel depicts representative images of terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay (scale bar 100 μm) detecting apoptotic nuclei in green costained with the glycocalix marker wheat germ agglutinin in red and nuclei in blue colored with Hoechst. Bar graphs representing mean±SEM quantifications of interstitial fibrosis and apoptotic nuclei in NaCl-LUC (10), isoproterenol+phenylephrine- LUC (9) and isoproterenol+phenylephrine-PDE2A (9) mice are depicted. Statistical significance indicated by the P value (* vs NaCl- LUC and † vs isoproterenol+phenylephrine-LUC) was determined using Welch’s t test (B), Kruskal–Wallis followed by a Dunn’s test (C), 2-way ANOVA followed by a Tukey’s test (D), Welch’s 1-way ANOVA followed by a Dunnett’s test (E). AAV9 indicates serotype 9 adeno-associated viruses; BW, body weight; HW, heart weight; Iso-Phe-LUC, isoproterenol-phenylephrine-luciferase; Iso-Phe- PDE2A, isoproterenol-phenylephrine-phosphodiesterase 2A; LUC, luciferase; LVW, left ventricular weight; LW, lung weight; ns, not significant; PDE2A, phosphodiesterase 2A; and TL, tibia length.

    Journal: Journal of the American Heart Association

    Article Title: Cardiac Gene Therapy With Phosphodiesterase 2A Limits Remodeling and Arrhythmias in Mouse Models of Heart Failure

    doi: 10.1161/jaha.124.037343

    Figure Lengend Snippet: Figure 3. PDE2A overexpression limits maladaptive remodeling and cardiac dysfunction induced by chronic isoproterenol and phenylephrine infusion. A, Schematic representation of the experimental protocol. Mice were injected with 1012 viral particles of serotype 9 adeno-associated viruses encoding for Luciferase or phosphodiesterase 2A3. Fourteen days later, mice were implanted with osmotic minipumps diffusing either NaCl (NaCl-LUC) or isoproterenol+phenylephrine at 30 mg/kg per day each (isoproterenol+phenylephrine-LUC and isoproterenol + phenylephrine-PDE2A). Minipumps were removed 2 weeks later and mice were euthanized. Cardiac function was assessed throughout the protocol using echocardiography before the injection of the virus and at 2, 3, 4, and 6 weeks. B, Representative blots of PDE2A and GAPDH on the left panel are shown and the bar graph represents ratios of PDE2A over GAPDH quantifications expressed as mean±SEM in a subset of the animals treated with NaCl-LUC, isoproterenol+phenylephrine-LUC, and isoproterenol+phenylephrine-PDE2A. C, Heart weight and lung weight over tibia length ratios expressed as mean±SEM. D, Time course of the normalized ratios of calculated left ventricular weight (over body weight and normalized ejection fraction in NaCl-LUC, isoproterenol+phenylephrine-LUC, and isoproterenol+phenylephrine-PDE2A mice). Number of mice is indicated in the brackets. E, Top panel shows representative images of Masson’s trichrome staining (scale bar 200 μm), the middle panel depicts representative images of terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay (scale bar 100 μm) detecting apoptotic nuclei in green costained with the glycocalix marker wheat germ agglutinin in red and nuclei in blue colored with Hoechst. Bar graphs representing mean±SEM quantifications of interstitial fibrosis and apoptotic nuclei in NaCl-LUC (10), isoproterenol+phenylephrine- LUC (9) and isoproterenol+phenylephrine-PDE2A (9) mice are depicted. Statistical significance indicated by the P value (* vs NaCl- LUC and † vs isoproterenol+phenylephrine-LUC) was determined using Welch’s t test (B), Kruskal–Wallis followed by a Dunn’s test (C), 2-way ANOVA followed by a Tukey’s test (D), Welch’s 1-way ANOVA followed by a Dunnett’s test (E). AAV9 indicates serotype 9 adeno-associated viruses; BW, body weight; HW, heart weight; Iso-Phe-LUC, isoproterenol-phenylephrine-luciferase; Iso-Phe- PDE2A, isoproterenol-phenylephrine-phosphodiesterase 2A; LUC, luciferase; LVW, left ventricular weight; LW, lung weight; ns, not significant; PDE2A, phosphodiesterase 2A; and TL, tibia length.

    Article Snippet: The primary antibodies used were as follows: (1) Figure 1: rabbit anti- PDE2A, Fabgennix; PDE2A- 101AP diluted at 1/1000; rabbit anti- GAPDH, Cell Signaling, 2118 diluted at 1/1000; (2) Figure 2: goat antiPDE2A, Santa Cruz, SC- 17228 diluted at 1/1000; mouse anti- vinculin, V9131 Sigma- Aldrich diluted at 1/1000; (3) Figure 3: rabbit anti- PDE2A, Fabgennix, PDE2A- 101AP diluted at 1/1000; rabbit anti- GAPDH, Cell Signaling, 2118 diluted at 1/1000; (4) Figure S1: rabbit anti- flag L5, Novus Biologicals, NBP1- 06712 diluted at 1/500; rabbit anti- GAPDH, Cell Signaling, 2118 diluted at 1/1000; rabbit anti- PDE2A, Proteintech, 55 306- 1- AP diluted at 1/1000; rabbit anti- flag L5, Novus Biologicals, NBP1- 06712 diluted at 1/500; rabbit anti- GAPDH, Cell Signaling, 2118 diluted at 1/1000; (5) Figure S2B: rabbit anti- PDE2A, Proteintech, 55 306- 1- AP diluted at 1/1000; (6) Figure S3: rabbit antiPDE2A, Proteintech, 55 306- 1- AP diluted at 1/1000; and (7) Figure S4: rabbit anti- PDE4A AC55 (gift from Dr. Marco Conti, University of California San Francisco, San Francisco, CA) diluted at 1/1000; rabbit anti- PDE4B (gift from Dr. Marco Conti) diluted at 1/10000; mouse antiPDE4D (gift from Dr Marco Conti) diluted at 1/1000 and rabbit anti- PDE3A (gift from Dr Chen Yan, University of Rochester, Rochester, NY) diluted at 1/10000.

    Techniques: Over Expression, Injection, Luciferase, Virus, Staining, TUNEL Assay, Marker