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  • 1
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    186 Partial loss of AKAP1 promotes cardiac dysfunction, gut barrier abnormalities, and alteration of gut microbiota composition during ageing
    Oxford University Press (OUP) ; 2021
    In:  European Heart Journal Supplements Vol. 23, No. Supplement_G ( 2021-12-08)
    Details
    In: European Heart Journal Supplements, Oxford University Press (OUP), Vol. 23, No. Supplement_G ( 2021-12-08)
    Abstract: Mitochondrial A-kinase anchoring proteins (mitoAKAP) encoded by the Akap1 gene promote Protein Kinase A mitochondrial targeting, regulating mitochondrial structure and function, reactive oxygen species production, and cardiomyocyte survival. Whether mitoAKAP levels play a role in cardiac ageing, gut barrier integrity and gut microbiota composition is currently unknown. The aim of this study was to highlight the complex interplay between cardiac dysfunction, gut barrier integrity, gut microbiota composition and ageing in young (6-month-old, 6 m) and old (24-month-old, 24 m) wild type (wt) and Akap1 heterozygous mice (Akap1+/−). Methods and results Cardiac function was noninvasively analysed by echocardiography in 6 m and 24 m wt and Akap1+/− mice. Gut microbial DNA was extracted and gut microbiota composition was analysed by Illumina Mi-Seq analysis. Bioinformatics analysis was carried out to identify major intestinal populations. Alpha diversity within each sample was determined, and then analysed according to genotype and age; then, inter-sample diversity was determined. For each dataset, we used UniFrac to calculate the differences between microbial communities based on phylogenetic distance between taxa sets in a phylogenetic tree. Bioinformatics analyses were performed using the analysis of similarities (ANOSIM). To evaluate the role of mitoAKAPs in intestinal permeability, we analysed intestinal junction proteins expression levels in colon samples of all groups. Variance analysis was performed to determine significance among the groups. Partial loss of Akap1 accelerated the progression of cardiac dysfunction in 24 m mice, as demonstrated by a significantly lower % fractional shortening (%FS) compared to 24 m wt mice (%FS, wt 6 m: 60 ± 3; Akap1−/+ 6 m: 58 ± 5; wt 24 m: 49 ± 6*; Akap1−/+ 24 m: 39 ± 12*§; *P  & lt; 0.05 vs. wt 6 m; §P  & lt; 0.05 vs. wt 24 m). In 24 m Akap1+/− mice, ageing was associated to enhanced colon permeability, as shown by reduced levels of Ocln and Tjp1 mRNA expression. A principal Co-ordinate analysis of faecal samples based on their unweighted UniFrac distances revealed that samples from Akap1+/− 24 m mice cluster apart from wt 24 m samples, suggesting that Akap1+/− 24 m mice exhibit a different assortment of microbial communities. This observation was supported by ANOSIM R statistic that revealed significant differences in gut microbiota composition between wt and Akap1+/− 24 m mice (ANOSIM R = 0.475, P = 0.023), while no significant differences in bacterial assortment were identified between wt and Akap1+/− 6 m mice. We analysed the differences in abundance of all 2042 Operational Taxonomic Units (OTUs) between age-matched wt and Akap1+/−. We identified 10 OTUs differently represented in wt and Akap1+/− 6 m mice, while a bigger set of bacterial OTUs (19) were different between wt and Akap1+/− 24 m mice. Consistent with previous results in patients with heart failure, we identified Clostridiales, Blautia producta, and R. Torques among differently regulated species. These results are in accordance with previous data on patients with heart failure (HF). Conclusions Partial Akap1 deletion plays an important role in the progression towards HF and modulates colon permeability and gut microbiota composition during ageing. This work highlights the complex interplay between gut microbiota and development of cardiac dysfunction, and characterization of these processes might lead to the development of new diagnostic and therapeutic approaches for cardiac dysfunction.
    Type of Medium: Online Resource
    ISSN: 1520-765X , 1554-2815
    URL: Article
    DOI: 10.1093/eurheartj/suab139.010
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2021
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  • 2
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    527 CIRCULATING SMALL NUCLEOLAR RNA SNORD3A AS A NOVEL PREDICTIVE BIOMARKERS OF HEART FAILURE
    Oxford University Press (OUP) ; 2022
    In:  European Heart Journal Supplements Vol. 24, No. Supplement_K ( 2022-12-15)
    Details
    In: European Heart Journal Supplements, Oxford University Press (OUP), Vol. 24, No. Supplement_K ( 2022-12-15)
    Abstract: Despite optimal therapy, heart failure (HF) remains a relentless and deadly disease. Given the relative inaccessibility of myocardial human tissues, identification of circulating biomarkers mirroring myocardial pathological signaling pathways, especially in peripheral blood mononuclear cells (PBMC) is expected to be extremely relevant. Small Nucleolar RNAs (snoRNAs) have been shown to play important roles in various cellular physiological processes. However, the connection between snoRNAs and pathological dysfunction in the heart or peripheral blood mononuclear cells (PBMC) is still poorly understood. Purpose To identify novel circulating PBMC biomarkers linked to myocardial dysfunction and HF. Methods : Myocardial left ventricle (LV) samples and PBMC were obtained from patients affected by ischemic HF (HF, n =13) undergoing heart transplantation and control donors (CD, n=7) and analyzed by RNA sequencing analysis (RNASeq). SNORD3A expression levels in the different groups were evaluated by quantitative real-time PCR. HF was induced in 8-week-old wild type C57BL/6 mice by transverse aortic constriction (TAC). Sham-operated mice (sham) were used as controls. After twelve-week-TAC (12w) or sham operation, mice were anesthetized, cardiac function was analyzed by echocardiography, and cardiac/PBMC samples were collected after sacrifice. In order to test the role of SNORD3A in cardiomyocyte hypoxia, H9C2 cardiomyoblasts were transfected with SNORD3A-targeted antisense oligonucleotides (ASO) and cell survival was analyzed. Results RnaSeq analysis identified a small set of genes differentially expressed in the heart and PBMC from HF patients. Among these, SNORD3A was up-regulated in cardiac and PBMC samples from HF patients compared to CD (Figure 1A). Similarly, in murine HF induced by 12w TAC, SNORD3A levels were increased by rtPCR, both in the heart and PBMC (Figure 1B). SNORD3A expression levels were also significantly increased in H9C2 cells exposed to in vitro hypoxia (Figure 1C). Interestingly, H9C2 transfection with SNORD3A-specific ASO significantly reduced hypoxia-induced SNORD3A upregulation and reduced hypoxia-induced cell death (Figure 1D). Conclusions In this study, we identify SNORD3A as a novel possible biomarker in human HF, similarly up-regulated in the heart and PBMC, induced by hypoxia in vitro and modulating cell survival.
    Type of Medium: Online Resource
    ISSN: 1520-765X , 1554-2815
    URL: Article
    DOI: 10.1093/eurheartjsupp/suac121.415
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
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  • 3
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    183 Small nucleolar RNA SNORD3A: a potential new biomarker and molecular player in heart failure
    Oxford University Press (OUP) ; 2021
    In:  European Heart Journal Supplements Vol. 23, No. Supplement_G ( 2021-12-08)
    Details
    In: European Heart Journal Supplements, Oxford University Press (OUP), Vol. 23, No. Supplement_G ( 2021-12-08)
    Abstract: Despite optimal therapy, heart failure (HF) remains a relentless and deadly disease. Given the relative inaccessibility of myocardial human tissues, identification of circulating biomarkers mirroring myocardial pathological signalling pathways, especially in peripheral blood mononuclear cells (PBMC) is expected to be extremely relevant. Small Nucleolar RNAs (snoRNAs) have been shown to play important roles in various cellular physiological processes. However, the connection between snoRNAs and pathological dysfunction in the heart or peripheral blood mononuclear cells (PBMC) is still poorly understood. To identify novel circulating PBMC biomarkers linked to myocardial dysfunction and HF. Methods Myocardial left ventricle (LV) samples and PBMC were obtained from patients affected by ischaemic HF (HF, n = 13) undergoing heart transplantation and control donors (CD, n = 7) and analysed by RNA sequencing analysis (RNASeq). SNORD3A expression levels in the different groups were evaluated by quantitative real-time PCR. HF was induced in 8-week-old wild type C57BL/6 mice by transverse aortic constriction (TAC). Sham-operated mice (sham) were used as controls. After 12-week-TAC (12w) or sham operation, mice were anesthetized, cardiac function was analysed by echocardiography, and cardiac/PBMC samples were collected after sacrifice. In order to test the role of SNORD3A in cardiomyocyte hypoxia, H9C2 cardiomyoblasts were transfected with SNORD3A-targeted antisense oligonucleotides (ASO) and cell survival was analysed. Results RNASeq analysis identified a small set of genes differentially expressed in the heart and PBMC from HF patients. Among these, SNORD3A was up-regulated in cardiac and PBMC samples from HF patients compared to CD (Figure 1A). Similarly, in murine HF induced by 12w TAC, SNORD3A levels were increased by rtPCR, both in the heart and PBMC (Figure 1B). SNORD3A expression levels were also significantly increased in H9C2 cells exposed to in vitro hypoxia (Figure 1C). Interestingly, H9C2 transfection with SNORD3A-specific ASO significantly reduced hypoxia-induced SNORD3A up-regulation and reduced hypoxia-induced cell death (Figure 1D). Conclusions In this study, we identify SNORD3A as a novel possible biomarker in human HF, similarly up-regulated in the heart and PBMC, induced by hypoxia in vitro and modulating cell survival.
    Type of Medium: Online Resource
    ISSN: 1520-765X , 1554-2815
    URL: Article
    DOI: 10.1093/eurheartj/suab138.005
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2021
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  • 4
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    514 ATAXIA TELANGIECTASIA MUTATED PROTEIN MODULATES GLUCOSE AND LIPID METABOLISM IN THE HEART
    Oxford University Press (OUP) ; 2022
    In:  European Heart Journal Supplements Vol. 24, No. Supplement_K ( 2022-12-15)
    Details
    In: European Heart Journal Supplements, Oxford University Press (OUP), Vol. 24, No. Supplement_K ( 2022-12-15)
    Abstract: Ataxia Telangiectasia Mutated (ATM) protein kinase is the major sensor of DNA damage response (DDR) and oxidative stress, variously implicated in cellular metabolism. Previous studies on ATM functions in the heart have produced conflicting results. Here we hypothesized that ATM might regulate cardiomyocyte metabolic homeostasis and function. Methods Atm-mutated mice (Atm-/-) and their wild-type littermates (Atm+/+) were used to assess the effects of ATM inactivation on cardiomyocyte hypertrophy, cardiac structure, function, DDR and metabolism under sham conditions or after pressure overload by transverse aortic constriction (TAC). Results ATM inactivation induced cardiomyocyte hypertrophy (FIG.1 A), fetal gene expression re-activation and a specific metabolomic signature in the heart, characterized by significant accumulation of pyruvate, branched chain amino-acids, short-medium acyl-carnitines and metabolites of tricarboxylic acid cycle (FIG.1 C, D),. Importantly, pyruvate was trapped in the cytosol because mitochondrial carriers were suppressed and the enzymes that process pyruvate were dysregulated. As a consequence of pyruvate metabolic block, fatty acids oxidation was inefficient and resulted in the accumulation of acyl-carnitines and insulin resistance. Although these metabolic changes were present constitutively in Atm-/- mice, they were amplified by TAC, which rapidly induced heart failure (FIG.1 B) in Atm-/- mice. ATM inactivation also increased basal and TAC-induced genomic stress in cardiomyocytes, as shown by the levels of p-γ-H2AX, 8-oxodG glycosylase (OGG1/2) and apurinic site nuclease (APE1). Cardiac metabolic changes induced by ATM loss (rise of pyruvate, lactate and succinate levels) were also present in Atm-/- brains, although the basal conditions were different. Conclusions ATM rewires the metabolism of cardiac cells by inducing glycolysis and fatty acids oxidation. Combining metabolomic, DNA damage and cardiac phenotypes, we deduce that ATM stimulates glycolysis to repair DNA lesions and protect the heart against stress-induced dysfunction.
    Type of Medium: Online Resource
    ISSN: 1520-765X , 1554-2815
    URL: Article
    DOI: 10.1093/eurheartjsupp/suac121.413
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
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  • 5
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    523 MITOAKAP PLAY A ROLE IN THE PROGRESSION TOWARDS HEART FAILURE MODULATING GUT INTEGRITY AND COMPOSITION DURING AGING
    Oxford University Press (OUP) ; 2022
    In:  European Heart Journal Supplements Vol. 24, No. Supplement_K ( 2022-12-15)
    Details
    In: European Heart Journal Supplements, Oxford University Press (OUP), Vol. 24, No. Supplement_K ( 2022-12-15)
    Abstract: Mitochondrial A-kinase anchoring proteins (mitoAKAP) encoded by the Akap1 gene promote Protein Kinase A mitochondrial targeting, regulating mitochondrial structure and function, reactive oxygen species production and cardiomyocyte survival. Whether mitoAKAP levels play a role in cardiac aging, gut barrier integrity and gut microbiota composition is currently unknown. Purpose The aim of this study was to highlight the complex interplay between cardiac dysfunction, gut barrier integrity, gut microbiota composition and aging in young (6-month-old, 6m) and old (24-month-old, 24m) wild type (wt) and Akap1 heterozygous mice (Akap1+/-). Methods Cardiac function was noninvasively analyzed by echocardiography in 6m and 24m wt and Akap1+/- mice. Gut microbial DNA was extracted and gut microbiota composition was analyzed by Illumina Mi-Seq analysis. Bioinformatics analysis was carried out to identify major intestinal populations. Alpha diversity within each sample was determined, and then analyzed according to genotype and age; then, inter-sample diversity was determined. For each dataset, we used UniFrac to calculate the differences between microbial communities based on phylogenetic distance between taxa sets in a phylogenetic tree. Bioinformatics analyses were performed using the analysis of similarities (ANOSIM). To evaluate the role of mitoAKAPs in intestinal permeability, we analyzed intestinal junction proteins expression levels in colon samples of all groups. Variance analysis was performed to determine significance among the groups. Results Partial loss of Akap1 accelerated the progression of cardiac dysfunction in 24m mice, as demonstrated by a significantly lower % fractional shortening (%FS) compared to 24m wt mice (%FS, wt 6m: 60±3; Akap1-/+ 6m: 58±5; wt 24m: 49±6*; Akap1-/+ 24m: 39±12*§; *p & lt;0.05 vs. wt 6m; §p & lt;0.05 vs. wt 24m). In 24m Akap1+/- mice, aging was associated to enhanced colon permeability, as shown by reduced levels of Ocln and Tjp1 mRNA expression. A principal coordinate analysis of fecal samples based on their unweighted UniFrac distances revealed that samples from Akap1+/- 24m mice cluster apart from wt 24m samples, suggesting that Akap1+/- 24m mice exhibit a different assortment of microbial communities. This observation was supported by ANOSIM R statistic that revealed significant differences in gut microbiota composition between wt and Akap1+/- 24m mice (ANOSIM R=0.475, P=0.023), while no significant differences in bacterial assortment were identified between wt and Akap1+/- 6m mice. We analyzed the differences in abundance of all 2,042 Operational Taxonomic Units (OTUs) between age-matched wt and Akap1+/-. We identified 10 OTUs differently represented in wt and Akap1+/- 6m mice, while a bigger set of bacterial OTUs (19) were different between wt and Akap1+/-24m mice. Consistent with previous results in patients with heart failure, we identified Clostridiales, Blautia producta and R. Torques among differently regulated species. These results are in accordance with previous data on patients with heart failure (HF). Conclusion Partial Akap1 deletion plays an important role in the progression toward HF and modulates colon permeability and gut microbiota composition during aging. This work highlights the complex interplay between gut microbiota and development of cardiac dysfunction, and characterization of these processes might lead to the development of new diagnostic and therapeutic approaches for cardiac dysfunction.
    Type of Medium: Online Resource
    ISSN: 1520-765X , 1554-2815
    URL: Article
    DOI: 10.1093/eurheartjsupp/suac121.414
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
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  • 6
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    Presentation_1.PDF
    Frontiers Media SA ; 2018
    In:  Frontiers in Physiology Vol. 9 ( 2018-5-28)
    Details
    In: Frontiers in Physiology, Frontiers Media SA, Vol. 9 ( 2018-5-28)
    Type of Medium: Online Resource
    ISSN: 1664-042X
    URL: Article
    URL: Article
    DOI: 10.3389/fphys.2018.00558
    DOI: 10.3389/fphys.2018.00558.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2018
    detail.hit.zdb_id: 2564217-0
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  • 7
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    Akap1 Deficiency Promotes Mitochondrial Aberrations and Exacerbates Cardiac Injury Following Permanent Coronary Ligation via Enhanced Mitophagy and Apoptosis
    Public Library of Science (PLoS) ; 2016
    In:  PLOS ONE Vol. 11, No. 5 ( 2016-5-2), p. e0154076-
    Details
    In: PLOS ONE, Public Library of Science (PLoS), Vol. 11, No. 5 ( 2016-5-2), p. e0154076-
    Type of Medium: Online Resource
    ISSN: 1932-6203
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.1371/journal.pone.0154076
    DOI: 10.1371/journal.pone.0154076.g001
    DOI: 10.1371/journal.pone.0154076.g002
    DOI: 10.1371/journal.pone.0154076.g003
    DOI: 10.1371/journal.pone.0154076.g004
    DOI: 10.1371/journal.pone.0154076.t001
    DOI: 10.1371/journal.pone.0154076.t002
    DOI: 10.1371/journal.pone.0154076.s001
    DOI: 10.1371/journal.pone.0154076.s002
    Language: English
    Publisher: Public Library of Science (PLoS)
    Publication Date: 2016
    detail.hit.zdb_id: 2267670-3
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  • 8
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    Effects of Carvedilol Versus Metoprolol on Platelet Aggregation in Patients With Acute Coronary Syndrome: The PLATE-BLOCK Study
    Elsevier BV ; 2018
    In:  The American Journal of Cardiology Vol. 122, No. 1 ( 2018-07), p. 6-11
    Details
    In: The American Journal of Cardiology, Elsevier BV, Vol. 122, No. 1 ( 2018-07), p. 6-11
    Type of Medium: Online Resource
    ISSN: 0002-9149
    URL: Article
    DOI: 10.1016/j.amjcard.2018.03.004
    RVK:
    XA 18500
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2018
    detail.hit.zdb_id: 2019595-3
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  • 9
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    Akap1 Regulates Vascular Function and Endothelial Cells Behavior
    Ovid Technologies (Wolters Kluwer Health) ; 2018
    In:  Hypertension Vol. 71, No. 3 ( 2018-03), p. 507-517
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 71, No. 3 ( 2018-03), p. 507-517
    Abstract: MitoAKAPs (mitochondrial A kinase anchoring proteins), encoded by the Akap1 gene, regulate multiple cellular processes governing mitochondrial homeostasis and cell viability. Although mitochondrial alterations have been associated to endothelial dysfunction, the role of mitoAKAPs in the vasculature is currently unknown. To test this, postischemic neovascularization, vascular function, and arterial blood pressure were analyzed in Akap1 knockout mice ( Akap1 −/− ) and their wild-type (wt) littermates. Primary cultures of aortic endothelial cells (ECs) were also obtained from Akap1 −/− and wt mice, and ECs migration, proliferation, survival, and capillary-like network formation were analyzed under different experimental conditions. After femoral artery ligation, Akap1 −/− mice displayed impaired blood flow and functional recovery, reduced skeletal muscle capillary density, and Akt phosphorylation compared with wt mice. In Akap1 −/− ECs, a significant enhancement of hypoxia-induced mitophagy, mitochondrial dysfunction, reactive oxygen species production, and apoptosis were observed. Consistently, capillary-like network formation, migration, proliferation, and AKT phosphorylation were reduced in Akap1 −/− ECs. Alterations in Akap1 −/− ECs behavior were also confirmed in Akap1 −/− mice, which exhibited a selective reduction in acetylcholine-induced vasorelaxation in mesenteric arteries and a mild but significant increase in arterial blood pressure levels compared with wt. Finally, overexpression of a constitutively active Akt mutant restored vascular reactivity and ECs function in Akap1 −/− conditions. These results demonstrate the important role of mitoAKAPs in the modulation of multiple ECs functions in vivo and in vitro, suggesting that mitochondria-dependent regulation of ECs might represent a novel therapeutic approach in cardiovascular diseases characterized by endothelial dysfunction.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/HYPERTENSIONAHA.117.10185
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2018
    detail.hit.zdb_id: 2094210-2
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  • 10
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    Impact of chronic kidney disease on platelet aggregation in patients with acute coronary syndrome
    Ovid Technologies (Wolters Kluwer Health) ; 2020
    In:  Journal of Cardiovascular Medicine Vol. 21, No. 9 ( 2020-09), p. 660-666
    Details
    In: Journal of Cardiovascular Medicine, Ovid Technologies (Wolters Kluwer Health), Vol. 21, No. 9 ( 2020-09), p. 660-666
    Abstract: Chronic kidney disease (CKD) is associated with increased thrombotic events and seems to influence platelet reactivity. Conflicting results have been published on platelet response in CKD patients with stable coronary artery disease. The aim of our study was to investigate the impact of CKD on platelet aggregation in acute coronary syndrome (ACS) patients receiving dual antiplatelet therapy, included the more potent P2Y12 inhibitors. Methods We enrolled 206 patients with ACS, divided in two groups, according to the presence or the absence of moderate/severe CKD. Platelet aggregation was performed with light transmission aggregometry and results are expressed as percentage of maximum platelet aggregation. High residual platelet reactivity (HRPR) was defined as maximum platelet aggregation more than 59%. Results Patients with CKD [estimate glomerular filtration rate (eGFR)  〈  60 ml/min/1.73 m 2 , n  = 28] were prevalent older, diabetic, had previous coronary revascularization. In these patients, platelet aggregation was significantly higher than in those with eGFR ≥ 60 ml/min/1.73 m 2 (ADP 10 μmol/l: 28.46 ± 26.19 vs. 16.64 ± 12.79, P   〈  0.001; ADP 20 μmol/l: 30.07 ± 25.89 vs. 17.46 ± 12.82, P   〈  0.001). HRPR was observed in 4.4% of patients, with higher prevalence in those with eGFR less than 60 ml/min/1.73 m 2 [21.4 vs. 1.7%, P   〈  0.001, odds ratio (OR) [95% confidence interval (CI)] = 15.91 (3.71–68.17), P   〈  0.001]. At multivariate analysis, after correction for baseline confounders, eGFR [adjusted OR (95% CI) = 0.95 (0.91–0.98), P  = 0.007], together with the use of clopidogrel [adjusted OR (95% CI) = 23.59 (4.01–138.82), P   〈  0.001], emerged as determinants of HRPR. Conclusion In patients with ACS receiving dual antiplatelet therapy, CKD is associated with an increasing ADP-induced platelet aggregation and higher prevalence of HRPR, which is mainly correlated to clopidogrel use.
    Type of Medium: Online Resource
    ISSN: 1558-2027 , 1558-2035
    URL: Article
    DOI: 10.2459/JCM.0000000000000981
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2020
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