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Histamine H2 Receptor Polymorphisms, Myocardial Transcripts, and Heart Failure (from the Multi-Ethnic Study of Atherosclerosis and Beta-Blocker Effect on Remodeling and Gene Expression Trial)

Leary, Peter J. ; Kronmal, Richard A. ; Bluemke, David A. ; [et al.]

Elsevier BV ; 2018

In: The American Journal of Cardiology Vol. 121, No. 2 ( 2018-01), p. 256-261

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In: The American Journal of Cardiology, Elsevier BV, Vol. 121, No. 2 ( 2018-01), p. 256-261

Type of Medium: Online Resource

ISSN: 0002-9149

URL: Article

DOI: 10.1016/j.amjcard.2017.10.016

RVK:

XA 18500

Language: English

Publisher: Elsevier BV

Publication Date: 2018

detail.hit.zdb_id: 2019595-3

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Hypoxia-associated Induction of Early Growth Response-1 Gene Expression

Yan, Shi-Fang ; Lu, Jiesheng ; Zou, Yu Shan ; [et al.]

Elsevier BV ; 1999

In: Journal of Biological Chemistry Vol. 274, No. 21 ( 1999-05), p. 15030-15040

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In: Journal of Biological Chemistry, Elsevier BV, Vol. 274, No. 21 ( 1999-05), p. 15030-15040

Type of Medium: Online Resource

ISSN: 0021-9258

URL: Article

DOI: 10.1074/jbc.274.21.15030

Language: English

Publisher: Elsevier BV

Publication Date: 1999

detail.hit.zdb_id: 2141744-1

detail.hit.zdb_id: 1474604-9

SSG: 12

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Selective Class I Histone Deacetylase Inhibition Suppresses Hypoxia-Induced Cardiopulmonary Remodeling Through an Antiproliferative Mechanism

Cavasin, Maria A. ; Demos-Davies, Kim ; Horn, Todd R. ; [et al.]

Ovid Technologies (Wolters Kluwer Health) ; 2012

In: Circulation Research Vol. 110, No. 5 ( 2012-03-02), p. 739-748

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In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 110, No. 5 ( 2012-03-02), p. 739-748

Abstract: Histone deacetylase (HDAC) inhibitors are efficacious in models of hypertension-induced left ventricular heart failure. The consequences of HDAC inhibition in the context of pulmonary hypertension with associated right ventricular cardiac remodeling are poorly understood. Objective: This study was performed to assess the utility of selective small-molecule inhibitors of class I HDACs in a preclinical model of pulmonary hypertension. Methods and Results: Rats were exposed to hypobaric hypoxia for 3 weeks in the absence or presence of a benzamide HDAC inhibitor, MGCD0103, which selectively inhibits class I HDACs 1, 2, and 3. The compound reduced pulmonary arterial pressure more dramatically than tadalafil, a standard-of-care therapy for human pulmonary hypertension that functions as a vasodilator. MGCD0103 improved pulmonary artery acceleration time and reduced systolic notching of the pulmonary artery flow envelope, which suggests a positive impact of the HDAC inhibitor on pulmonary vascular remodeling and stiffening. Similar results were obtained with an independent class I HDAC-selective inhibitor, MS-275. Reduced pulmonary arterial pressure in MGCD0103-treated animals was associated with blunted pulmonary arterial wall thickening because of suppression of smooth muscle cell proliferation. Right ventricular function was maintained in MGCD0103-treated animals. Although the class I HDAC inhibitor only modestly reduced right ventricular hypertrophy, it had multiple beneficial effects on the right ventricle, which included suppression of pathological gene expression, inhibition of proapoptotic caspase activity, and repression of proinflammatory protein expression. Conclusions: By targeting distinct pathogenic mechanisms, isoform-selective HDAC inhibitors have potential as novel therapeutics for pulmonary hypertension that will complement vasodilator standards of care.

Type of Medium: Online Resource

ISSN: 0009-7330 , 1524-4571

URL: Article

DOI: 10.1161/CIRCRESAHA.111.258426

RVK:

XA 10000

Language: English

Publisher: Ovid Technologies (Wolters Kluwer Health)

Publication Date: 2012

detail.hit.zdb_id: 1467838-X

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Correction: Sequential analysis of myocardial gene expression with phenotypic change: Use of cross-platform concordance to strengthen biologic relevance

Toni, Lee S. ; Carroll, Ian A. ; Jones, Kenneth L. ; [et al.]

Public Library of Science (PLoS) ; 2019

In: PLOS ONE Vol. 14, No. 10 ( 2019-10-22), p. e0224389-

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In: PLOS ONE, Public Library of Science (PLoS), Vol. 14, No. 10 ( 2019-10-22), p. e0224389-

Type of Medium: Online Resource

ISSN: 1932-6203

URL: Article

DOI: 10.1371/journal.pone.0224389

DOI: 10.1371/journal.pone.0224389.g001

DOI: 10.1371/journal.pone.0224389.s001

DOI: 10.1371/journal.pone.0224389.s002

DOI: 10.1371/journal.pone.0224389.s003

DOI: 10.1371/journal.pone.0224389.s004

Language: English

Publisher: Public Library of Science (PLoS)

Publication Date: 2019

detail.hit.zdb_id: 2267670-3

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Dynamic Regulation of SARS-Cov-2 Binding and Cell Entry Mechanisms in Remodeled Human Ventricular Myocardium

Bristow, Michael R. ; Zisman, Lawrence S. ; Altman, Natasha L. ; [et al.]

Elsevier BV ; 2020

In: JACC: Basic to Translational Science Vol. 5, No. 9 ( 2020-09), p. 871-883

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In: JACC: Basic to Translational Science, Elsevier BV, Vol. 5, No. 9 ( 2020-09), p. 871-883

Type of Medium: Online Resource

ISSN: 2452-302X

URL: Article

DOI: 10.1016/j.jacbts.2020.06.007

Language: English

Publisher: Elsevier BV

Publication Date: 2020

detail.hit.zdb_id: 2865010-4

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Increased contractility and altered Ca 2+ transients of mouse heart myocytes conditionally expressing PKCβ

Huang, Lin ; Wolska, Beata M. ; Montgomery, David E. ; [et al.]

American Physiological Society ; 2001

In: American Journal of Physiology-Cell Physiology Vol. 280, No. 5 ( 2001-05-01), p. C1114-C1120

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In: American Journal of Physiology-Cell Physiology, American Physiological Society, Vol. 280, No. 5 ( 2001-05-01), p. C1114-C1120

Abstract: Activation of protein kinase C (PKC) in heart muscle signals hypertrophy and may also directly affect contractile function. We tested this idea using a transgenic (TG) mouse model in which conditionally expressed PKCβ was turned on at 10 wk of age and remained on for either 6 or 10 mo. Compared with controls, TG cardiac myocytes demonstrated an increase in the peak amplitude of the Ca 2+ transient, an increase in the extent and rate of shortening, and an increase in the rate of relengthening at both 6 and 10 mo of age. Phospholamban phosphorylation and Ca 2+ -uptake rates of sarcoplasmic reticulum vesicles were the same in TG and control heart preparations. At 10 mo, TG skinned fiber bundles demonstrated the same sensitivity to Ca 2+ as controls, but maximum tension was depressed and there was increased myofilament protein phosphorylation. Our results differ from studies in which PKCβ was constitutively overexpressed in the heart and in studies that reported a depression of myocyte contraction with no change in the Ca 2+ transient.

Type of Medium: Online Resource

ISSN: 0363-6143 , 1522-1563

URL: Article

DOI: 10.1152/ajpcell.2001.280.5.C1114

Language: English

Publisher: American Physiological Society

Publication Date: 2001

detail.hit.zdb_id: 1477334-X

SSG: 12

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LAMP-2B regulates human cardiomyocyte function by mediating autophagosome–lysosome fusion

Chi, Congwu ; Leonard, Andrea ; Knight, Walter E. ; [et al.]

Proceedings of the National Academy of Sciences ; 2019

In: Proceedings of the National Academy of Sciences Vol. 116, No. 2 ( 2019-01-08), p. 556-565

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In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 116, No. 2 ( 2019-01-08), p. 556-565

Abstract: Mutations in lysosomal-associated membrane protein 2 ( LAMP-2 ) gene are associated with Danon disease, which often leads to cardiomyopathy/heart failure through poorly defined mechanisms. Here, we identify the LAMP-2 isoform B (LAMP-2B) as required for autophagosome–lysosome fusion in human cardiomyocytes (CMs). Remarkably, LAMP-2B functions independently of syntaxin 17 (STX17), a protein that is essential for autophagosome–lysosome fusion in non-CMs. Instead, LAMP-2B interacts with autophagy related 14 (ATG14) and vesicle-associated membrane protein 8 (VAMP8) through its C-terminal coiled coil domain (CCD) to promote autophagic fusion. CMs derived from induced pluripotent stem cells (hiPSC-CMs) from Danon patients exhibit decreased colocalization between ATG14 and VAMP8, profound defects in autophagic fusion, as well as mitochondrial and contractile abnormalities. This phenotype was recapitulated by LAMP-2B knockout in non-Danon hiPSC-CMs. Finally, gene correction of LAMP-2 mutation rescues the Danon phenotype. These findings reveal a STX17-independent autophagic fusion mechanism in human CMs, providing an explanation for cardiomyopathy in Danon patients and a foundation for targeting defective LAMP-2B–mediated autophagy to treat this patient population.

Type of Medium: Online Resource

ISSN: 0027-8424 , 1091-6490

URL: Article

DOI: 10.1073/pnas.1808618116

RVK:

TA 1000

RVK:

WA 15000

Language: English

Publisher: Proceedings of the National Academy of Sciences

Publication Date: 2019

detail.hit.zdb_id: 209104-5

detail.hit.zdb_id: 1461794-8

SSG: 11

SSG: 12

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Dynamic Regulation of SARS-CoV-2 Binding and Cell Entry Mechanisms in Remodeled Human Ventricular Myocardium

Bristow, Michael R. ; Zisman, Lawrence S. ; Altman, Natasha Lipson ; [et al.]

Elsevier BV ; 2020

In: SSRN Electronic Journal

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In: SSRN Electronic Journal, Elsevier BV

Type of Medium: Online Resource

ISSN: 1556-5068

URL: Article

DOI: 10.2139/ssrn.3595038

Language: English

Publisher: Elsevier BV

Publication Date: 2020

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Sequential analysis of myocardial gene expression with phenotypic change: Use of cross-platform concordance to strengthen biologic relevance

Toni, Lee S. ; Carroll, Ian A. ; Jones, Kenneth L. ; [et al.]

Public Library of Science (PLoS) ; 2019

In: PLOS ONE Vol. 14, No. 8 ( 2019-8-30), p. e0221519-

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In: PLOS ONE, Public Library of Science (PLoS), Vol. 14, No. 8 ( 2019-8-30), p. e0221519-

Type of Medium: Online Resource

ISSN: 1932-6203

URL: Article

DOI: 10.1371/journal.pone.0221519

DOI: 10.1371/journal.pone.0221519.g001

DOI: 10.1371/journal.pone.0221519.g002

DOI: 10.1371/journal.pone.0221519.g003

DOI: 10.1371/journal.pone.0221519.g004

DOI: 10.1371/journal.pone.0221519.t001

DOI: 10.1371/journal.pone.0221519.t002

DOI: 10.1371/journal.pone.0221519.t003

DOI: 10.1371/journal.pone.0221519.t004

DOI: 10.1371/journal.pone.0221519.t005

DOI: 10.1371/journal.pone.0221519.s001

DOI: 10.1371/journal.pone.0221519.s002

DOI: 10.1371/journal.pone.0221519.s003

DOI: 10.1371/journal.pone.0221519.s004

DOI: 10.1371/journal.pone.0221519.s005

DOI: 10.1371/journal.pone.0221519.s006

DOI: 10.1371/journal.pone.0221519.s007

DOI: 10.1371/journal.pone.0221519.s008

DOI: 10.1371/journal.pone.0221519.s009

Language: English

Publisher: Public Library of Science (PLoS)

Publication Date: 2019

detail.hit.zdb_id: 2267670-3

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Intense Light-Mediated Circadian Cardioprotection via Transcriptional Reprogramming of the Endothelium

Oyama, Yoshimasa ; Bartman, Colleen M. ; Bonney, Stephanie ; [et al.]

Elsevier BV ; 2019

In: Cell Reports Vol. 28, No. 6 ( 2019-08), p. 1471-1484.e11

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In: Cell Reports, Elsevier BV, Vol. 28, No. 6 ( 2019-08), p. 1471-1484.e11

Type of Medium: Online Resource

ISSN: 2211-1247

URL: Article

DOI: 10.1016/j.celrep.2019.07.020

Language: English

Publisher: Elsevier BV

Publication Date: 2019

detail.hit.zdb_id: 2649101-1

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