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  • 1
    Online Resource
    Online Resource
    Abstract 307: Regulator of G-protein Signaling 2 (RGS2) Suppresses Pathologic but not Physiologic Cardiac Hypertrophy
    Ovid Technologies (Wolters Kluwer Health) ; 2008
    In:  Circulation Vol. 118, No. suppl_18 ( 2008-10-28)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 118, No. suppl_18 ( 2008-10-28)
    Abstract: Regulator of G-protein signaling 2 (RGS2) is a GTPase activating protein thought to negatively regulate Gα q/11 -protein coupled signaling. In vitro RGS2 over-expression blunts Gα q/11 -stimulated hypertrophy, whereas its knockdown worsens it. Here we tested the impact of pathologic (aortic banding, AB) versus physiologic (swimming, SWM) cardiac stimulation on RGS2-cardiac regulation. Mice lacking RGS2 (RGS2 −/− ) develop modest hypertension but no baseline cardiac phenotype. RGS2 −/− subjected to AB developed accelerated hypertrophy (93% vs 47% increase in heart weight/tibial length at 1 wk, p 〈 0.05) and failure, and early mortality (40% vs. 0% mortality at 1 wk, p=0.012). Their hearts have enhanced activation of Gα q/11 -coupled hypertrophic mediators such as calcineurin (Cn), extracellular response kinase 1/2 (ERK1/2), and calmodulin-dependent protein kinase II (CaMK II) compared to controls. In sharp contrast, after 6 weeks of exercise swimming, control and RGS2 −/− mice developed similar increases in LV mass (17% and 15% increases in heart weight/tibial length; p 〈 0.001 compared to sedentary controls, NS between genotypes). Both groups also had similar increases in relative wall thickness and LV mass by echocardiography. Invasive pressure-volume loop analysis revealed enhanced cardiac output in swimming mice but no differences between genotypes. The only disparities were that heart rate declined slightly (5%) in controls but was unchanged in RGS2 −/− , and RGS2 −/− mice swam more slowly (mean velocity 5.0±0.3cm/s vs 6.7±0.3cm/s, by video tracking). Control and RGS2 −/− mice ± exercise had negligible changes in the Gα q/11 mediators Cn, ERK1/2, and CaMK II. Thus, RGS2 plays a central role in blunting cardiac hypertrophic signaling and mortality in response to pathological stress, but not to physiological stimulation. This highlights its in vivo specificity to the regulation of Gα q/11 signaling as opposed to the signaling of physiologic hypertrophy. Changes in Heart Weight/Tibial Length in response to Aortic Banding (AB) vs Swimming (SWM)
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.118.suppl_18.S_281-d
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2008
    detail.hit.zdb_id: 1466401-X
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  • 2
    Online Resource
    Online Resource
    Abstract 334: Cyclic GMP-dependent Protein Kinase Iα Dependent Regulator of G-protein Signaling 2 Activation Is Required for Early Cardiac Compensation to Pressure-overload
    Ovid Technologies (Wolters Kluwer Health) ; 2007
    In:  Circulation Vol. 116, No. suppl_16 ( 2007-10-16)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 116, No. suppl_16 ( 2007-10-16)
    Abstract: In response to pressure-overload, the heart initially develops adaptive hypertrophy with enhanced contractility, but later decompensates with chamber dilation. Such maladaptation can be induced by activation of G αq -coupled signaling, whereas enhancing cyclic GMP-dependent protein kinase I-α (PKGI-α) by phosphodiesterase 5A inhibition (PDE5A-I) ameliorates pressure-overload pathobiology. A potential coupler of both pathways is RGS2 (regulator of G-protein signaling 2), which is activated by PKGI-α to suppress G αq -stimulation in vascular smooth muscle cells. Here we tested this signaling in hearts exposed to pressure-overload by transverse aortic constriction (TAC). RGS2 is up-regulated in the particulate fraction of control heart lysate within 48 hours of TAC. Unlike controls, RGS2 −/− hearts display no early compensation to TAC, developing accelerated dilation and severe hypertrophy within 1week, with high mortality (Table ). Downstream signaling of G αq stimulation including ERK1/2, CaM kinase II and calcineurin is markedly activated or up-regulated in RGS2 −/− -TAC versus RGS2 +/+ -TAC. In normal myocytes, RGS2 displays weak diffuse subcellular localization by confocal immunofluorescent histochemistry, whereas PKGI-α has a striated banding pattern. Stimulation of G αq (angiotensin II, 1μM; endothelin 1, 0.5μM) induces translocation of both RGS2 and PKGI-α to the sarcolemmal membrane, which is dependent on PKG activation. Similar translocation is observed in 48hours-TAC myocytes, but it declines by 1 week. Concomitant PDE5A-I (oral sildenafil; 200mg/kg/day) sustains PKGI-α and RGS2 at the membrane in RGS2 +/+ -TAC 1week, ameliorating hypertrophy, whereas PDE5A-I has no effect on RGS2 −/− -TAC 1week (Table ). Thus RGS2 is an essential regulator of early compensation to pressure-overload, is regulated by PKGI-α activation, and also plays a key mechanistic role in the anti-hypertrophic effects from PDE5A inhibitors. Results TAC 1 week (n = 4–6 for hemodynamics in each group)
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.116.suppl_16.II_49-a
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2007
    detail.hit.zdb_id: 1466401-X
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  • 3
    Online Resource
    Online Resource
    Abstract 1831: Phosphodiesterase-5 Inhibition Prevents Cardiac Hypertrophy, Independently of the Calcineurin Pathway
    Ovid Technologies (Wolters Kluwer Health) ; 2008
    In:  Circulation Vol. 118, No. suppl_18 ( 2008-10-28)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 118, No. suppl_18 ( 2008-10-28)
    Abstract: Cyclic GMP and its downstream kinase protein kinase G (PKG) negatively regulate cardiac hypertrophy. To date the only documented target of this cascade is the serine-threonine phosphatase calcineurin (Cn), whose activation is central to the development of pathologic cardiac hypertrophy. Recently, we reported that phosphodiesterase 5 (PDE5) inhibition (sildenafil, SIL) activates myocardial PKG and prevents pressure-overload induced hypertrophy by suppressing multiple cascades including Cn. To test the centrality of Cn signaling to the in vivo anti-hypertrophic effects of SIL, we subjected mice deficient in the Cn-A β subunit (CnA β −/− ) to severe trans-aortic constriction (TAC) with or without SIL (100mg/kg/day, p.o.) for 3-wks. TAC induced less hypertrophy that was more concentric in CnA β −/− vs WT-controls (50% vs 100% increase in heart mass/tibia length, p 〈 0.03). SIL completely blocked the hypertrophic response and fully normalized fetal gene re-expression (e.g ANP, BNP and β MHC) in CnA β −/− TAC hearts, while it inhibited LVH by 60% and suppressed ANP and β MHC in WT-TAC hearts. SIL improved cardiac systolic and diastolic function (pressure-volume analysis) in CnA β −/− TAC hearts much as in WT-TAC hearts. In CnA β −/− TAC hearts, phosphorylated calcium calmodulin kinase II (CaMK II) increased 10-fold versus only a 2-fold rise in WT-TAC, whereas Akt and glycogen synthase kinase 3 β (GSK3 β ) activation were comparable between groups. Extracellular response kinase (ERK) 1/2 was activated with TAC in WT hearts only. Importantly, SIL stimulated myocardial PKG and markedly inhibited the activation of CaMKII, Akt and GSK3 β similarly in both groups exposed to TAC. Thus, Cn is not required for the anti-hypertrophic effects of SIL. Though TAC-induced hypertrophy is less in CnA β −/− mice, SIL remains effective in suppressing the residual response by targeting alternative cascades such as CaMK II. These findings suggest that SIL acts either on multiple pathways concurrently, or at a node proximal to these pathways likely at or near the sarcolemmal membrane.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.118.suppl_18.S_393-d
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2008
    detail.hit.zdb_id: 1466401-X
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  • 4
    Online Resource
    Online Resource
    Abstract 15554: Heart Failure-Related Hyperphosphorylation of Ser199 on Cardiac Troponin I Causes Divergent Effects on Cardiac Function at Baseline and During Ischemia-Reperfusion
    Ovid Technologies (Wolters Kluwer Health) ; 2015
    In:  Circulation Vol. 132, No. suppl_3 ( 2015-11-10)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 132, No. suppl_3 ( 2015-11-10)
    Abstract: Background: Phosphorylation of cardiac troponin I (cTnI) on Ser199 is significantly increased in human heart failure (HF), however its cardiac impact in vivo remains unknown. In addition, selective proteolysis of cTnI is a marker of myocardial injury and contributes to cardiac dysfunction in ischemia/reperfusion (I/R), and Ser199 phosphorylation affects cTnI proteolysis in vitro, thus whether Ser199 phosphorylation affects cardiac performance during I/R is of great interest. Methods and Results: We generated transgenic mice (TgS200D) carrying cTnI S200D mutation to mimic the site-specific hyperphosphorylation of murine Ser200 (equivalent to human Ser199). Cardiac function was first assessed in vivo using echocardiography. TgS200D mice demonstrated unaltered ejection fraction (EF), significantly prolonged isovolumic relaxation time, and normal left ventricular (LV) chamber size and wall thickness (n=10). LV pressure-volume studies showed preserved dp/dtmax, significantly decreased -dp/dtmin and increased relaxation time constant in TgS200D when compared to non-transgenic (NTg) control group at baseline (n=10). With increasing heart rates, the two groups showed similar enhancement in both systolic and diastolic function, suggesting the positive force-frequency relation is preserved in TgS200D (n=5). After isoproterenol injection (i.v. 40ng/min/kg), although a comparable increase in dp/dtmax was observed in both groups, there was no enhancement of -dp/dtmin in TgS200D in contrast to 15% of increase in NTg (n=5, p=0.019). After ischemia (30 min)/reperfusion (60 min), LV developed pressure was recovered by ~90% in isolated TgS200D hearts but only ~40% in NTg (n=5, p=0.003). Immunoblotting detected cTnI cleavage only in NTg hearts. Conclusions: Our results indicate that hyperphosphorylation of cTnI Ser199 1) impairs basal diastolic function but preserves systolic function, without LV hypertrophy or dilation; 2) blunts cardiac lusitropic response to β-adrenergic stimulation with isoproterenol; 3) protects heart against I/R injury, likely via preventing cTnI degradation. We propose a dual role of cTnI Ser199 hyperphosphorylaiton: contributing to HF with preserved EF but protecting heart during I/R.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.132.suppl_3.15554
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2015
    detail.hit.zdb_id: 1466401-X
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  • 5
    Online Resource
    Online Resource
    Pathological Cardiac Hypertrophy Alters Intracellular Targeting of Phosphodiesterase Type 5 From Nitric Oxide Synthase-3 to Natriuretic Peptide Signaling
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Circulation Vol. 126, No. 8 ( 2012-08-21), p. 942-951
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 126, No. 8 ( 2012-08-21), p. 942-951
    Abstract: In the normal heart, phosphodiesterase type 5 (PDE5) hydrolyzes cGMP coupled to nitric oxide– (specifically from nitric oxide synthase 3) but not natriuretic peptide (NP)–stimulated guanylyl cyclase. PDE5 is upregulated in hypertrophied and failing hearts and is thought to contribute to their pathophysiology. Because nitric oxide signaling declines whereas NP-derived cGMP rises in such diseases, we hypothesized that PDE5 substrate selectivity is retargeted to blunt NP-derived signaling. Methods and Results Mice with cardiac myocyte inducible PDE5 overexpression (P5 + ) were crossed to those lacking nitric oxide synthase 3 (N3 − ), and each model, the double cross, and controls were subjected to transaortic constriction. P5 + mice developed worse dysfunction and hypertrophy and enhanced NP stimulation, whereas N3 − mice were protected. However, P5 + /N3 − mice behaved similarly to P5 + mice despite the lack of nitric oxide synthase 3–coupled cGMP generation, with protein kinase G activity suppressed in both models. PDE5 inhibition did not alter atrial natriuretic peptide–stimulated cGMP in the resting heart but augmented it in the transaortic constriction heart. This functional retargeting was associated with PDE5 translocation from sarcomeres to a dispersed distribution. P5 + hearts exhibited higher oxidative stress, whereas P5 + /N3 − hearts had low levels (likely owing to the absence of nitric oxide synthase 3 uncoupling). This highlights the importance of myocyte protein kinase G activity as a protection for pathological remodeling. Conclusions These data provide the first evidence for functional retargeting of PDE5 from one compartment to another, revealing a role for natriuretic peptide–derived cGMP hydrolysis by this esterase in diseased heart myocardium. Retargeting likely affects the pathophysiological consequence and the therapeutic impact of PDE5 modulation in heart disease.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/CIRCULATIONAHA.112.090977
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
    detail.hit.zdb_id: 1466401-X
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  • 6
    Online Resource
    Online Resource
    Inhibition of Glycosphingolipid Synthesis Ameliorates Atherosclerosis and Arterial Stiffness in Apolipoprotein E −/− Mice and Rabbits Fed a High-Fat and -Cholesterol Diet
    Ovid Technologies (Wolters Kluwer Health) ; 2014
    In:  Circulation Vol. 129, No. 23 ( 2014-06-10), p. 2403-2413
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 129, No. 23 ( 2014-06-10), p. 2403-2413
    Abstract: Glycosphingolipids, integral components of the cell membrane, have been shown to serve as messengers, transducing growth factor–initiated phenotypes. Here, we have examined whether inhibition of glycosphingolipid synthesis could ameliorate atherosclerosis and arterial stiffness in transgenic mice and rabbits. Methods and Results— Apolipoprotein E −/− mice (12 weeks of age; n=6) were fed regular chow or a Western diet (1.25% cholesterol, 2% fat). Mice were fed 5 or 10 mg/kg of an inhibitor of glycosphingolipid synthesis, D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (D-PDMP), solubilized in vehicle (5% Tween-80 in PBS); the placebo group received vehicle only. At 20 and 36 weeks of age, serial echocardiography was performed to measure aortic intima-media thickening. Aortic pulse-wave velocity measured vascular stiffness. Feeding mice a Western diet markedly increased aortic pulse-wave velocity, intima-media thickening, oxidized low-density lipoprotein, Ca 2+ deposits, and glucosylceramide and lactosylceramide synthase activity. These were dose-dependently decreased by feeding D-PDMP. In liver, D-PDMP decreased cholesterol and triglyceride levels by raising the expression of SREBP2, low-density lipoprotein receptor, HMGCo-A reductase, and the cholesterol efflux genes (eg, ABCG5 , ABCG8 ). D-PDMP affected very-low-density lipoprotein catabolism by increasing the gene expression for lipoprotein lipase and very-low-density lipoprotein receptor. Rabbits fed a Western diet for 90 days had extensive atherosclerosis accompanied by a 17.5-fold increase in total cholesterol levels and a 3-fold increase in lactosylceramide levels. This was completely prevented by feeding D-PDMP. Conclusions— Inhibition of glycosphingolipid synthesis ameliorates atherosclerosis and arterial stiffness in apolipoprotein E −/− mice and rabbits. Thus, inhibition of glycosphingolipid synthesis may be a novel approach to ameliorate atherosclerosis and arterial stiffness.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/CIRCULATIONAHA.113.007559
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2014
    detail.hit.zdb_id: 1466401-X
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  • 7
    Online Resource
    Online Resource
    Abstract 19439: Melatonin Blunts Pressure-overload Left Ventricular Hypertrophy and Improves Cardiac Performance in Pathologic and PPhysiologic Cardiac Hypertrophy
    Ovid Technologies (Wolters Kluwer Health) ; 2015
    In:  Circulation Vol. 132, No. suppl_3 ( 2015-11-10)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 132, No. suppl_3 ( 2015-11-10)
    Abstract: Introduction: Reactive oxygen species (ROS) has been established as key mediators in cardiac hypertrophy and function through activation of redox-sensitive kinases, by stimulating NADPH oxidase. Melatonin has been described as having potent antioxidant properties in different tissues. Hypothesis: The hormone melatonin, would prevent pressure-overload (pathologic) hypertrophy, Methods: Mice (C57Bl6) were subjected to transverse aortic constriction (TAC), and treated with melatonin (MEL, 10 mg/Kg/day) in water (“TAC+MEL”) or placebo (TAC). A second group underwent intense treadmill exercise for 8 weeks and also received melatonin (EX-MEL) or water (EX). A sham operated group served as control (“sham”). After 7 weeks of TAC and 8 weeks of exercise, cardiac function was assessed by echocardiography and pressure –volumetric analysis. Cardiac ROS activity (TBARS, NRF2, Keap-1) was determined. Results: TAC promoted LVH in mice (LVMI: 6.38±0.38 mg/mm tibia length (sham), 8.11±0.63 (TAC) which was blunted by melatonin (LVMI: 6.34±0.31 (TAC+MEL) mg/mm, P 〈 0.05). Increased LVH was associated with decreased endocardial shortening measured by echocardiography, from 61±2 (sham) to 54±1.8 % (TAC + placebo), P 〈 0.05. This decrease in fractional shortening was less pronounced in the TAC+ MEL group (58±2.9%) as well as in PV loop analysis. The antioxidant action of MEL was evidenced by the decrease in myocardial lipid peroxidation (TBARS) from 0.35±0.02 (TAC) to 0.25±0.02 (TAC+MEL) nmol/mg of protein, P 〈 0.05. Adult mice isolated myocyte studies revealed that Ang 2 (20nM) increased sarcomere shortening and calcium transient, both of which were blunted when cells were pre-incubated with melatonin (p 〈 0.005, Ang2 vs MEL + Ang2). In the exercise group, melatonin had only a small, non-significant reduction in LVMI, but a marked improvement in cardiac performance (PV loop analysis). Conclusion: Melatonin prevents pressure-overload LVH and improves contractility due to its antioxidant action. In physiologic LVH (exercise), melatonin does not affect hypertrophy, but exerts a positive effect on cardiac performance. These effects seem to be, at least in part, mediated through melatonin interfering with the Keap-1- Nrf2 antioxidant pathway.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.132.suppl_3.19439
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2015
    detail.hit.zdb_id: 1466401-X
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  • 8
    Online Resource
    Online Resource
    The protective role of IL‐13 in Experimental Autoimmune Myocarditis
    Wiley ; 2007
    In:  The FASEB Journal Vol. 21, No. 5 ( 2007-04)
    Details
    In: The FASEB Journal, Wiley, Vol. 21, No. 5 ( 2007-04)
    Type of Medium: Online Resource
    ISSN: 0892-6638 , 1530-6860
    URL: Issue
    URL: Article
    DOI: 10.1096/fsb2.v21.5
    DOI: 10.1096/fasebj.21.5.A128-c
    Language: English
    Publisher: Wiley
    Publication Date: 2007
    detail.hit.zdb_id: 1468876-1
    SSG: 12
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  • 9
    Online Resource
    Online Resource
    The mitochondrial regulator PGC1α is induced by cGMP–PKG signaling and mediates the protective effects of phosphodiesterase 5 inhibition in heart failure
    Wiley ; 2022
    In:  FEBS Letters Vol. 596, No. 1 ( 2022-01), p. 17-28
    Details
    In: FEBS Letters, Wiley, Vol. 596, No. 1 ( 2022-01), p. 17-28
    Abstract: Phosphodiesterase 5 inhibition (PDE5i) activates cGMP‐dependent protein kinase (PKG) and ameliorates heart failure; however, its impact on cardiac mitochondrial regulation has not been fully determined. Here, we investigated the role of the mitochondrial regulator peroxisome proliferator‐activated receptor γ co‐activator‐1α (PGC1α) in the PDE5i‐conferred cardioprotection, utilizing PGC1α null mice. In PGC1α +/+ hearts exposed to 7 weeks of pressure overload by transverse aortic constriction, chronic treatment with the PDE5 inhibitor sildenafil improved cardiac function and remodeling, with improved mitochondrial respiration and upregulation of PGC1α mRNA in the myocardium. By contrast, PDE5i‐elicited benefits were abrogated in PGC1α −/− hearts. In cultured cardiomyocytes, PKG overexpression induced PGC1α, while inhibition of the transcription factor CREB abrogated the PGC1α induction. Together, these results suggest that the PKG–PGC1α axis plays a pivotal role in the therapeutic efficacy of PDE5i in heart failure.
    Type of Medium: Online Resource
    ISSN: 0014-5793 , 1873-3468
    URL: Issue
    URL: Article
    DOI: 10.1002/feb2.v596.1
    DOI: 10.1002/1873-3468.14228
    RVK:
    WA 15000
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 1460391-3
    SSG: 12
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  • 10
    Online Resource
    Online Resource
    Evidence for a role of immunoproteasomes in regulating cardiac muscle mass in diabetic mice
    Elsevier BV ; 2010
    In:  Journal of Molecular and Cellular Cardiology Vol. 49, No. 1 ( 2010-07), p. 5-15
    Details
    In: Journal of Molecular and Cellular Cardiology, Elsevier BV, Vol. 49, No. 1 ( 2010-07), p. 5-15
    Type of Medium: Online Resource
    ISSN: 0022-2828
    URL: Article
    DOI: 10.1016/j.yjmcc.2010.02.007
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2010
    detail.hit.zdb_id: 1469767-1
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