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  • 1
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    eLife Sciences Publications, Ltd ; 2018
    In:  eLife Vol. 7 ( 2018-10-03)
    Details
    In: eLife, eLife Sciences Publications, Ltd, Vol. 7 ( 2018-10-03)
    Abstract: Cells contain specialized structures called mitochondria, which help to convert fuel into energy. These tiny energy factories have a unique double membrane, with a smooth outer and a folded inner lining. The folds, called cristae, provide a scaffold for the molecular machinery that produces chemical energy that the cell can use. The cristae are dynamic, and can change shape, condensing to increase energy output. Mitochondria also play a role in cell death. In certain situations, cristae can widen and release the proteins held within their folds. This can trigger a program of self-destruction in the cell. A family of proteins called Bcl-2 control such a ‘programmed cell death’ through the release of mitochondrial proteins. Some family members, including a protein called Bid, can reorganize cristae to regulate this cell-death program. When cells die, Bid proteins that had been split move to the mitochondria. But, even when cells are healthy, Bid molecules that are intact are always there, suggesting that this form of the protein may have another purpose. To investigate this further, Salisbury-Ruf, Bertram et al. used mice with Bid, and mice that lacked the protein. Without Bid, cells – including heart cells – struggled to work properly and used less oxygen than their normal counterparts. A closer look using electron microscopy revealed abnormalities in the cristae. However, adding ‘intact’ Bid proteins back in to the deficient cells restored them to normal. Moreover, without Bid, the mice hearts were less able to respond to an increased demand for energy. This decreased their performance and caused the formation of scars in the heart muscle called fibrosis, similar to a pattern observed in human patients following a heart attack. DNA data from an electronic health record database revealed a link between low levels of Bid genes and heart attack in humans, which was confirmed in further studies. In addition, a specific mutation in the Bid gene was found to affect its ability to regulate the formation of proper cristae. Combining evidence from mice with human genetics revealed new information about heart diseases. Mitochondrial health may be affected by a combination of specific variations in genes and changes in the Bid protein, which could affect heart attack risk. Understanding more about this association could help to identify and potentially reduce certain risk factors for heart attack.
    Type of Medium: Online Resource
    ISSN: 2050-084X
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    DOI: 10.7554/eLife.40907
    DOI: 10.7554/eLife.40907.001
    DOI: 10.7554/eLife.40907.002
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    DOI: 10.7554/eLife.40907.004
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    DOI: 10.7554/eLife.40907.005
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    DOI: 10.7554/eLife.40907.014
    DOI: 10.7554/eLife.40907.017
    DOI: 10.7554/eLife.40907.015
    DOI: 10.7554/eLife.40907.016
    DOI: 10.7554/eLife.40907.018
    DOI: 10.7554/eLife.40907.019
    DOI: 10.7554/eLife.40907.020
    DOI: 10.7554/eLife.40907.021
    DOI: 10.7554/eLife.40907.022
    DOI: 10.7554/eLife.40907.024
    DOI: 10.7554/eLife.40907.023
    DOI: 10.7554/eLife.40907.025
    DOI: 10.7554/eLife.40907.026
    DOI: 10.7554/eLife.40907.027
    DOI: 10.7554/eLife.40907.028
    DOI: 10.7554/eLife.40907.042
    DOI: 10.7554/eLife.40907.043
    Language: English
    Publisher: eLife Sciences Publications, Ltd
    Publication Date: 2018
    detail.hit.zdb_id: 2687154-3
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  • 2
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    Transpulmonary generation of cell‐free hemoglobin contributes to vascular dysfunction in pulmonary arterial hypertension via dysregulated clearance mechanisms
    Wiley ; 2023
    In:  Pulmonary Circulation Vol. 13, No. 1 ( 2023-01)
    Details
    In: Pulmonary Circulation, Wiley, Vol. 13, No. 1 ( 2023-01)
    Abstract: Circulating cell‐free hemoglobin (CFH) is elevated in pulmonary arterial hypertension (PAH) and associated with poor outcomes but the mechanisms are unknown. We hypothesized that CFH is generated from the pulmonary circulation and inadequately cleared in PAH. Transpulmonary CFH (difference between wedge and pulmonary artery positions) and lung hemoglobin α were analyzed in patients with PAH and healthy controls. Haptoglobin genotype and plasma hemoglobin processing proteins were analyzed in patients with PAH, unaffected bone morphogenetic protein receptor type II mutation carriers (UMCs), and control subjects. Transpulmonary CFH was increased in patients with PAH ( p  = 0.04) and correlated with pulmonary vascular resistanc (PVR) ( r s  = 0.75, p  = 0.02) and mean pulmonary arterial pressure (mPAP) ( r s  = 0.78, p  = 0.02). Pulmonary vascular hemoglobin α protein was increased in patients with PAH ( p  = 0.006), especially in occluded vessels ( p  = 0.04). Haptoglobin genotype did not differ between groups. Plasma haptoglobin was higher in UMCs compared with both control subjects ( p  = 0.03) and patients with HPAH ( p   〈  0.0001); patients with IPAH had higher circulating haptoglobin levels than patients with HPAH ( p  = 0.006). Notably, circulating CFH to haptoglobin ratio was elevated in patients with HPAH compared to control subjects ( p  = 0.02) and UMCs ( p  = 0.006). Moreover, in patients with PAH, CFH: haptoglobin correlated with PVR ( r s  = 0.37, p  = 0.0004) and mPAP ( r s  = 0.25, p  = 0.02). Broad alterations in other plasma hemoglobin processing proteins (hemopexin, heme oxygenase‐1, and sCD163) were observed. In conclusion, pulmonary vascular CFH is associated with increased PVR and mPAP in PAH and dysregulated CFH clearance may contribute to PAH pathology. Further study is needed to determine whether targeting CFH is a viable therapeutic for pulmonary vascular dysfunction in PAH.
    Type of Medium: Online Resource
    ISSN: 2045-8940 , 2045-8940
    URL: Issue
    URL: Article
    DOI: 10.1002/pul2.v13.1
    DOI: 10.1002/pul2.12185
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 2638089-4
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  • 3
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    Immune profiling of murine cardiac leukocytes identifies triggering receptor expressed on myeloid cells 2 as a novel mediator of hypertensive heart failure
    Oxford University Press (OUP) ; 2023
    In:  Cardiovascular Research ( 2023-06-14)
    Details
    In: Cardiovascular Research, Oxford University Press (OUP), ( 2023-06-14)
    Abstract: Heart failure with preserved ejection fraction (HFpEF) is characterized by diastolic dysfunction, microvascular dysfunction, and myocardial fibrosis with recent evidence implicating the immune system in orchestrating cardiac remodelling. Methods and results Here, we show the mouse model of deoxycorticosterone acetate (DOCA)-salt hypertension induces key elements of HFpEF, including diastolic dysfunction, exercise intolerance, and pulmonary congestion in the setting of preserved ejection fraction. A modified single-cell sequencing approach, cellular indexing of transcriptomes and epitopes by sequencing, of cardiac immune cells reveals an altered abundance and transcriptional signature in multiple cell types, most notably cardiac macrophages. The DOCA-salt model results in differential expression of several known and novel genes in cardiac macrophages, including up-regulation of Trem2, which has been recently implicated in obesity and atherosclerosis. The role of Trem2 in hypertensive heart failure, however, is unknown. We found that mice with genetic deletion of Trem2 exhibit increased cardiac hypertrophy, diastolic dysfunction, renal injury, and decreased cardiac capillary density after DOCA-salt treatment compared to wild-type controls. Moreover, Trem2-deficient macrophages have impaired expression of pro-angiogenic gene programmes and increased expression of pro-inflammatory cytokines. Furthermore, we found that plasma levels of soluble TREM2 are elevated in DOCA-salt treated mice and humans with heart failure. Conclusions Together, our data provide an atlas of immunological alterations that can lead to improved diagnostic and therapeutic strategies for HFpEF. We provide our dataset in an easy to explore and freely accessible web application making it a useful resource for the community. Finally, our results suggest a novel cardioprotective role for Trem2 in hypertensive heart failure.
    Type of Medium: Online Resource
    ISSN: 0008-6363 , 1755-3245
    URL: Article
    DOI: 10.1093/cvr/cvad093
    RVK:
    WA 15000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2023
    detail.hit.zdb_id: 1499917-1
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  • 4
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    BMPR2 dysfunction impairs insulin signaling and glucose homeostasis in cardiomyocytes
    American Physiological Society ; 2020
    In:  American Journal of Physiology-Lung Cellular and Molecular Physiology Vol. 318, No. 2 ( 2020-02-01), p. L429-L441
    Details
    In: American Journal of Physiology-Lung Cellular and Molecular Physiology, American Physiological Society, Vol. 318, No. 2 ( 2020-02-01), p. L429-L441
    Abstract: Insulin resistance and right ventricular (RV) dysfunction are associated with lipotoxicity in heritable forms of pulmonary arterial hypertension (PAH), commonly due to mutations in bone morphogenetic protein receptor type 2 (BMPR2). How BMPR2 dysfunction in cardiomyocytes alters glucose metabolism and the response of these cells to insulin are unknown. We hypothesized that BMPR2 mutation in cardiomyocytes alters glucose-supported mitochondrial respiration and impairs cellular responses to insulin, including glucose and lipid uptake. We performed metabolic assays, immunofluorescence and Western analysis, RNA profiling, and radioactive isotope uptake studies in H9c2 cardiomyocyte cell lines with and without patient-derived BMPR2 mutations (mutant cells), with and without insulin. Unlike control cells, BMPR2 mutant cardiomyocytes have reduced metabolic plasticity as indicated by reduced mitochondrial respiration with increased mitochondrial superoxide production. These mutant cells show enhanced baseline phosphorylation of insulin-signaling protein as indicated by increased Akt, AMPK, and acetyl-CoA carboxylase phosphorylation that may negatively influence fatty acid oxidation and enhance lipid uptake, and are insulin insensitive. Furthermore, mutant cells demonstrate an increase in milk fat globule-EGF factor-8 protein (MFGE8), which influences the insulin-signaling pathway by phosphorylating Akt Ser473 via phosphatidylinositol 3-kinase and mammalian target of rapamycin. In conclusion, BMPR2 mutant cardiomyocytes have reduced metabolic plasticity and fail to respond to glucose. These cells have enhanced baseline insulin-signaling pattern favoring insulin resistance with failure to augment this pattern in response to insulin. BMPR2 mutation possibly blunts glucose uptake and enhances lipid uptake in these cardiomyocytes. The MFGE8-driven signaling pathway may suggest a new mechanism underlying RV lipotoxicity in PAH.
    Type of Medium: Online Resource
    ISSN: 1040-0605 , 1522-1504
    URL: Article
    DOI: 10.1152/ajplung.00555.2018
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2020
    detail.hit.zdb_id: 1477300-4
    SSG: 12
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  • 5
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    Pulmonary vascular effect of insulin in a rodent model of pulmonary arterial hypertension
    Wiley ; 2017
    In:  Pulmonary Circulation Vol. 7, No. 3 ( 2017-07), p. 624-634
    Details
    In: Pulmonary Circulation, Wiley, Vol. 7, No. 3 ( 2017-07), p. 624-634
    Abstract: Pulmonary arterial hypertension (PAH) is associated with metabolic derangements including insulin resistance, although their effects on the cardiopulmonary disease are unclear. We hypothesized that insulin resistance promotes pulmonary hypertension (PH) development and mutations in type 2 bone morphogenetic protein receptor (BMPR2) cause cellular insulin resistance. Using a BMPR2 transgenic murine model of PAH and two models of inducible diabetes mellitus, we explored the impact of hyperglycemia and/or hyperinsulinemia on development and severity of PH. We assessed insulin signaling and insulin‐mediated glucose uptake in human endothelial cells with and without mutations in BMPR2. PH developed in control mice fed a Western diet and PH in BMPR2 mutant mice was increased by Western diet. Pulmonary artery pressure correlated strongly with fasting plasma insulin but not glucose. Reactive oxygen species were increased in lungs of insulin‐resistant animals. BMPR2 mutation impaired insulin‐mediated endothelial glucose uptake via reduced glucose transporter translocation despite intact insulin signaling. Experimental hyperinsulinemia is strongly associated with PH in both control and BMPR2‐mutant mice, though to a greater degree in those with BMPR2 mutation. Human pulmonary endothelial cells with BMPR2 mutation have evidence of reduced glucose uptake due to impaired glucose transporter translocation. These experiments support a role for hyperinsulinemia in pulmonary vascular disease.
    Type of Medium: Online Resource
    ISSN: 2045-8940 , 2045-8940
    URL: Article
    DOI: 10.1086/689908
    Language: English
    Publisher: Wiley
    Publication Date: 2017
    detail.hit.zdb_id: 2638089-4
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    A multifaceted investigation into molecular associations of chronic thromboembolic pulmonary hypertension pathogenesis
    SAGE Publications ; 2020
    In:  JRSM Cardiovascular Disease Vol. 9 ( 2020-01), p. 204800402090699-
    Details
    In: JRSM Cardiovascular Disease, SAGE Publications, Vol. 9 ( 2020-01), p. 204800402090699-
    Type of Medium: Online Resource
    ISSN: 2048-0040 , 2048-0040
    URL: Article
    DOI: 10.1177/2048004020906994
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2020
    detail.hit.zdb_id: 2663207-X
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  • 7
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    Myeloid Cell Derived IL1β Contributes to Pulmonary Hypertension in HFpEF
    Ovid Technologies (Wolters Kluwer Health) ; 2023
    In:  Circulation Research Vol. 133, No. 11 ( 2023-11-10), p. 885-898
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 133, No. 11 ( 2023-11-10), p. 885-898
    Abstract: Pulmonary hypertension (PH) in heart failure with preserved ejection fraction (HFpEF) is a common and highly morbid syndrome, but mechanisms driving PH-HFpEF are poorly understood. We sought to determine whether a well-accepted murine model of HFpEF also displays features of PH, and we sought to identify pathways that might drive early remodeling of the pulmonary vasculature in HFpEF. METHODS: Eight-week-old male and female C57BL/6J mice received either N γ -nitro-L-arginine methyl ester and high-fat diet or control water and diet for 2, 5, and 12 weeks. The db/db mice were studied as a second model of HFpEF. Early pathways regulating PH were identified by bulk and single-cell RNA sequencing. Findings were confirmed by immunostain in lungs of mice or lung slides from clinically performed autopsies of patients with PH-HFpEF. ELISA was used to verify IL-1β (interleukin-1 beta) in mouse lung, mouse plasma, and also human plasma from patients with PH-HFpEF obtained at the time of right heart catheterization. Clodronate liposomes and an anti–IL-1β antibody were utilized to deplete macrophages and IL-1β, respectively, to assess their impact on pulmonary vascular remodeling in HFpEF in mouse models. RESULTS: N γ -nitro-L-arginine methyl ester/high-fat diet–treated mice developed PH, small vessel muscularization, and right heart dysfunction. Inflammation-related gene ontologies were overrepresented in bulk RNA sequencing analysis of whole lungs, with an increase in CD68 + cells in both murine and human PH-HFpEF lungs. Cytokine profiling showed an increase in IL-1β in mouse and human plasma. Finally, clodronate liposome treatment in mice prevented PH in N γ -nitro-L-arginine methyl ester/high-fat diet–treated mice, and IL-1β depletion also attenuated PH in N γ -nitro-L-arginine methyl ester/high-fat diet–treated mice. CONCLUSIONS: We report a novel model for the study of PH and right heart remodeling in HFpEF, and we identify myeloid cell–derived IL-1β as an important contributor to PH in HFpEF.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/CIRCRESAHA.123.323119
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2023
    detail.hit.zdb_id: 1467838-X
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  • 8
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    l ‐Carnitine therapy improves right heart dysfunction through Cpt1‐dependent fatty acid oxidation
    Wiley ; 2022
    In:  Pulmonary Circulation Vol. 12, No. 3 ( 2022-07)
    Details
    In: Pulmonary Circulation, Wiley, Vol. 12, No. 3 ( 2022-07)
    Abstract: Pulmonary arterial hypertension (PAH) is a fatal vasculopathy that ultimately leads to elevated pulmonary pressure and death by right ventricular (RV) failure, which occurs in part due to decreased fatty acid oxidation and cytotoxic lipid accumulation. In this study, we tested the hypothesis that decreased fatty acid oxidation and increased lipid accumulation in the failing RV is driven, in part, by a relative carnitine deficiency. We then tested whether supplementation of l ‐carnitine can reverse lipotoxic RV failure through augmentation of fatty acid oxidation. In vivo in transgenic mice harboring a human BMPR2 mutation, l ‐carnitine supplementation reversed RV failure by increasing RV cardiac output, improving RV ejection fraction, and decreasing RV lipid accumulation through increased PPARγ expression and augmented fatty acid oxidation of long chain fatty acids. These findings were confirmed in a second model of pulmonary artery banding‐induced RV dysfunction. In vitro, l ‐carnitine supplementation selectively increased fatty acid oxidation in mitochondria and decreased lipid accumulation through a Cpt1‐dependent pathway. l ‐Carnitine supplementation improves right ventricular contractility in the stressed RV through augmentation of fatty acid oxidation and decreases lipid accumulation. Correction of carnitine deficiency through l ‐carnitine supplementation in PAH may reverse RV failure.
    Type of Medium: Online Resource
    ISSN: 2045-8940 , 2045-8940
    URL: Issue
    URL: Article
    DOI: 10.1002/pul2.v12.3
    DOI: 10.1002/pul2.12107
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 2638089-4
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  • 9
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    A potential therapeutic role for angiotensin-converting enzyme 2 in human pulmonary arterial hypertension
    European Respiratory Society (ERS) ; 2018
    In:  European Respiratory Journal Vol. 51, No. 6 ( 2018-06), p. 1702638-
    Details
    In: European Respiratory Journal, European Respiratory Society (ERS), Vol. 51, No. 6 ( 2018-06), p. 1702638-
    Abstract: Pulmonary arterial hypertension (PAH) is a deadly disease with no cure. Alternate conversion of angiotensin II (AngII) to angiotensin-(1–7) (Ang-(1–7)) by angiotensin-converting enzyme 2 (ACE2) resulting in Mas receptor (Mas1) activation improves rodent models of PAH. Effects of recombinant human (rh) ACE2 in human PAH are unknown. Our objective was to determine the effects of rhACE2 in PAH. We defined the molecular effects of Mas1 activation using porcine pulmonary arteries, measured AngII/Ang-(1–7) levels in human PAH and conducted a phase IIa, open-label pilot study of a single infusion of rhACE2 (GSK2586881, 0.2 or 0.4 mg·kg −1 intravenously). Superoxide dismutase 2 (SOD2) and inflammatory gene expression were identified as markers of Mas1 activation. After confirming reduced plasma ACE2 activity in human PAH, five patients were enrolled in the trial. GSK2586881 was well tolerated with significant improvement in cardiac output and pulmonary vascular resistance. GSK2586881 infusion was associated with reduced plasma markers of inflammation within 2–4 h and increased SOD2 plasma protein at 2 weeks. PAH is characterised by reduced ACE2 activity. Augmentation of ACE2 in a pilot study was well tolerated, associated with improved pulmonary haemodynamics and reduced markers of oxidant and inflammatory mediators. Targeting this pathway may be beneficial in human PAH.
    Type of Medium: Online Resource
    ISSN: 0903-1936 , 1399-3003
    URL: Article
    URL: Article
    DOI: 10.1183/13993003.02638-2017
    DOI: 10.1183/13993003.02638-2017.Supp1
    Language: English
    Publisher: European Respiratory Society (ERS)
    Publication Date: 2018
    detail.hit.zdb_id: 2834928-3
    detail.hit.zdb_id: 1499101-9
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  • 10
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    Frontiers Media SA ; 2023
    In:  Frontiers in Medicine Vol. 10 ( 2023-10-5)
    Details
    In: Frontiers in Medicine, Frontiers Media SA, Vol. 10 ( 2023-10-5)
    Abstract: Pulmonary arterial hypertension is a fatal cardiopulmonary disease. Leptin, a neuroendocrine hormone released by adipose tissue, has a complex relationship with cardiovascular diseases, including PAH. Leptin is thought to be an important factor linking metabolic syndrome and cardiovascular disorders. Given the published association between metabolic syndrome and RV dysfunction in PAH, we sought to determine the association between leptin and RV dysfunction. We hypothesized that in PAH-RV, leptin influences metabolic changes via leptin receptors, which can be manipulated by metformin. Methods Plasma leptin was measured in PAH patients and healthy controls from a published trial of metformin in PAH. Leptin receptor localization was detected in RV from PAH patients, healthy controls, animal models of PH with RV dysfunction before and after metformin treatment, and cultured cardiomyocytes with two different BMPR2 mutants by performing immunohistochemical and cell fractionation studies. Functional studies were conducted in cultured cardiomyocytes to examine the role of leptin and metformin in lipid-driven mitochondrial respiration. Results In human studies, we found that plasma leptin levels were higher in PAH patients and moderately correlated with higher BMI, but not in healthy controls. Circulating leptin levels were reduced by metformin treatment, and these findings were confirmed in an animal model of RV dysfunction. Leptin receptor expression was increased in PAH-RV cardiomyocytes. In animal models of RV dysfunction and cultured cardiomyocytes with BMPR2 mutation, we found increased expression and membrane localization of the leptin receptor. In cultured cardiomyocytes with BMPR2 mutation, leptin moderately influences palmitate uptake, possibly via CD36, in a mutation-specific manner. Furthermore, in cultured cardiomyocytes, the Seahorse XFe96 Extracellular Flux Analyzer and gene expression data indicate that leptin may not directly influence lipid-driven mitochondrial respiration in BMPR2 mutant cardiomyocytes. However, metformin alone or when supplemented with leptin can improve lipid-driven mitochondrial respiration in BMPR2 mutant cardiomyocytes. The effect of metformin on lipid-driven mitochondrial respiration in cardiomyocytes is BMPR2 mutation-specific. Conclusion In PAH, increased circulating leptin can influence metabolic signaling in RV cardiomyocytes via the leptin receptor; in particular, it may alter lipid-dependent RV metabolism in combination with metformin in a mutation-specific manner and warrants further investigation.
    Type of Medium: Online Resource
    ISSN: 2296-858X
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.3389/fmed.2023.1276422
    DOI: 10.3389/fmed.2023.1276422.s001
    DOI: 10.3389/fmed.2023.1276422.s002
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2023
    detail.hit.zdb_id: 2775999-4
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