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Journal articles on the topic 'GATA4 Hypertrophie Herz'

Author: Grafiati

Published: 4 June 2021

Last updated: 10 February 2022

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1

Liang, Qiangrong, Russell J. Wiese, Orlando F. Bueno, Yan-Shan Dai, Bruce E. Markham, and Jeffery D. Molkentin. "The Transcription Factor GATA4 Is Activated by Extracellular Signal-Regulated Kinase 1- and 2-Mediated Phosphorylation of Serine 105 in Cardiomyocytes." Molecular and Cellular Biology 21, no. 21 (2001): 7460–69. http://dx.doi.org/10.1128/mcb.21.21.7460-7469.2001.

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ABSTRACT The zinc finger-containing transcription factor GATA4 has been implicated as a critical regulator of multiple cardiac-expressed genes as well as a regulator of inducible gene expression in response to hypertrophic stimulation. Here we demonstrate that GATA4 is itself regulated by the mitogen-activated protein kinase signaling cascade through direct phosphorylation. Site-directed mutagenesis and phospho-specific GATA4 antiserum revealed serine 105 as the primary site involved in agonist-induced phosphorylation of GATA4. Infection of cultured cardiomyocytes with an activated MEK1-expres

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2

Ahmadvand, Shiva, Ali Osia, Anna Meyfour, and Sara Pahlavan. "Gender-specific characteristics of hypertrophic response in cardiomyocytes derived from human embryonic stem cells." Journal of Cardiovascular and Thoracic Research 13, no. 2 (2021): 146–55. http://dx.doi.org/10.34172/jcvtr.2021.32.

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Introduction: Gender-specific phenotypes of the heart were reported with respect to both physiology and pathology. While most differences were associated with the sex hormones, differential expression of genes received special attention, particularly X-Y chromosomes’ genes. Methods: Here, we compared cardiogenesis by gene expression analysis of lineage specific markers and X-Y chromosomes’ genes, during in vitro differentiation of XY and XX human embryonic stem cells (hESC), in a hormone-free setup. Results: Downregulation of pluripotency marker (NANOG) and upregulation of cardiac mesoderm and

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3

Lu, Chieh-Hsiang, Chia-Yao Shen, Dennis Jine-Yuan Hsieh, et al. "Deep ocean minerals inhibit IL-6 and IGFIIR hypertrophic signaling pathways to attenuate diabetes-induced hypertrophy in rat hearts." Journal of Applied Physiology 127, no. 2 (2019): 356–64. http://dx.doi.org/10.1152/japplphysiol.00184.2019.

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We previously reported that deep sea water (DSW) prolongs the life span of streptozotocin (STZ)-induced diabetic rats by the compensatory augmentation of the insulin like growth factor (IGF)-I survival signaling and inhibition of apoptosis. Here, we investigated the effects of DSW on cardiac hypertrophy in diabetic rats. Cardiac hypertrophy was induced in rats by using STZ (65 mg/kg) administered via IP injection. DSW was prepared by mixing DSW mineral extracts and desalinated water. Different dosages of DSW-1X (equivalent to 37 mg Mg2+·kg−1·day−1), 2X (equivalent to 74 mg Mg2+·kg−1·day−1) and

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4

Harrison, Brooke C., Charles R. Roberts, David B. Hood, et al. "The CRM1 Nuclear Export Receptor Controls Pathological Cardiac Gene Expression." Molecular and Cellular Biology 24, no. 24 (2004): 10636–49. http://dx.doi.org/10.1128/mcb.24.24.10636-10649.2004.

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ABSTRACT Diverse pathological insults trigger a cardiac remodeling process during which myocytes undergo hypertrophy, with consequent decline in cardiac function and eventual heart failure. Multiple transcriptional regulators of pathological cardiac hypertrophy are controlled at the level of subcellular distribution. For example, prohypertrophic transcription factors belonging to the nuclear factor of activated T cells (NFAT) and GATA families are subject to CRM1-dependent nuclear export but are rapidly relocalized to the nucleus in response to cues for hypertrophic growth. Here, we demonstrat

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5

Kim, Tae-gyun, Junqin Chen, Junich Sadoshima, and Youngsook Lee. "Jumonji Represses Atrial Natriuretic Factor Gene Expression by Inhibiting Transcriptional Activities of Cardiac Transcription Factors." Molecular and Cellular Biology 24, no. 23 (2004): 10151–60. http://dx.doi.org/10.1128/mcb.24.23.10151-10160.2004.

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ABSTRACT Mice with a homozygous knockout of the jumonji (jmj) gene showed abnormal heart development and defective regulation of cardiac-specific genes, including the atrial natriuretic factor (ANF). ANF is one of the earliest markers of cardiac differentiation and a hallmark for cardiac hypertrophy. Here, we show that JMJ represses ANF gene expression by inhibiting transcriptional activities of Nkx2.5 and GATA4. JMJ represses the Nkx2.5- or GATA4-dependent activation of the reporter genes containing the ANF promoter-enhancer or containing the Nkx2.5 or GATA4-binding consensus sequence. JMJ ph

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6

Oka, Toru, Yan-Shan Dai та Jeffery D. Molkentin. "Regulation of Calcineurin through Transcriptional Induction of the calcineurin Aβ Promoter In Vitro and In Vivo". Molecular and Cellular Biology 25, № 15 (2005): 6649–59. http://dx.doi.org/10.1128/mcb.25.15.6649-6659.2005.

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ABSTRACT The calcineurin-nuclear factor of activated T cells (NFAT) signaling pathway has been shown to be of critical importance in regulating the growth response of cardiac myocytes. We have previously demonstrated that calcineurin Aβ (CnAβ) mRNA and protein are increased in response to growth stimulation, although the precise regulatory mechanism underlying CnAβ upregulation is not clear. Here, we isolated the mouse CnAβ promoter and characterized its responsiveness to growth stimuli in vitro and in vivo. A 2.3-kb promoter fragment was strongly activated by phenylephrine and endothelin-1 st

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7

Panguluri, Siva K., Jared Tur, Jutaro Fukumoto, et al. "Hyperoxia-induced hypertrophy and ion channel remodeling in left ventricle." American Journal of Physiology-Heart and Circulatory Physiology 304, no. 12 (2013): H1651—H1661. http://dx.doi.org/10.1152/ajpheart.00474.2012.

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Ventricular arrhythmias account for high mortality in cardiopulmonary patients in intensive care units. Cardiovascular alterations and molecular-level changes in response to the commonly used oxygen treatment remains unknown. In the present study we investigated cardiac hypertrophy and cardiac complications in mice subjected to hyperoxia. Results demonstrate that there is a significant increase in average heart weight to tibia length (22%) in mice subjected to hyperoxia treatment vs. normoxia. Functional assessment was performed in mice subjected to hyperoxic treatment, and results demonstrate

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8

Purcell, Nicole H., Dina Darwis, Orlando F. Bueno, Judith M. Müller, Roland Schüle, and Jeffery D. Molkentin. "Extracellular Signal-Regulated Kinase 2 Interacts with and Is Negatively Regulated by the LIM-Only Protein FHL2 in Cardiomyocytes." Molecular and Cellular Biology 24, no. 3 (2004): 1081–95. http://dx.doi.org/10.1128/mcb.24.3.1081-1095.2004.

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ABSTRACT The mitogen-activated protein kinase (MAPK) signaling pathway regulates diverse biologic functions including cell growth, differentiation, proliferation, and apoptosis. The extracellular signal-regulated kinases (ERKs) constitute one branch of the MAPK pathway that has been implicated in the regulation of cardiac differentiated growth, although the downstream mechanisms whereby ERK signaling affects this process are not well characterized. Here we performed a yeast two-hybrid screen with ERK2 bait and a cardiac cDNA library to identify novel proteins involved in regulating ERK signali

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9

Leigh, Robert S., and Bogac L. Kaynak. "Vitamin A as a Transcriptional Regulator of Cardiovascular Disease." Hearts 1, no. 2 (2020): 126–45. http://dx.doi.org/10.3390/hearts1020013.

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Vitamin A is a micronutrient and signaling molecule that regulates transcription, cellular differentiation, and organ homeostasis. Additionally, metabolites of Vitamin A are utilized as differentiation agents in the treatment of hematological cancers and skin disorders, necessitating further study into the effects of both nutrient deficiency and the exogenous delivery of Vitamin A and its metabolites on cardiovascular phenotypes. Though vitamin A/retinoids are well-known regulators of cardiac formation, recent evidence has emerged that supports their role as regulators of cardiac regeneration,

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10

Prakash, Ajay, Aaron M. Udager, David A. Saenz, and Deborah L. Gumucio. "Roles for Nkx2–5 and Gata3 in the ontogeny of the murine smooth muscle gastric ligaments." American Journal of Physiology-Gastrointestinal and Liver Physiology 307, no. 4 (2014): G430—G436. http://dx.doi.org/10.1152/ajpgi.00360.2013.

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The gastric ligaments are superficial cord-like structures, located on the lesser curvature of the stomach, that extend from the pylorus to the esophagus. These ligaments have been documented in a wide variety of mammalian species, including humans, but their composition and ontogeny is unexplored. Here, we demonstrate that, during ontogeny, the gastric ligaments are first visible as extensions from a C-shaped domain of Gata3-expressing cells that surround the future pylorus; this domain will later give rise to the pyloric outer longitudinal muscle (OLM). The open ends of the C are located ven

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11

Wang, Kimberley C. W., Darran N. Tosh, Song Zhang та ін. "IGF-2R-Gαq signaling and cardiac hypertrophy in the low-birth-weight lamb". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 308, № 7 (2015): R627—R635. http://dx.doi.org/10.1152/ajpregu.00346.2014.

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The cardiac insulin-like growth factor 2 receptor (IGF-2R) can induce cardiomyocyte hypertrophy in a heterotrimeric G protein receptor-coupled manner involving αq (Gαq) or αs (Gαs). We have previously shown increased left ventricular weight and cardiac IGF-2 and IGF-2R gene expression in low-birth-weight (LBW) compared with average-birth-weight (ABW) lambs. Here, we have investigated the cardiac expression of IGF-2 gene variants, the degree of histone acetylation, and the abundance of proteins in the IGF-2R downstream signaling pathway in ABW and LBW lambs. Samples from the left ventricle of A

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12

Ishida, Hidekazu, Shigetoyo Kogaki, Jun Narita та ін. "LEOPARD-type SHP2 mutant Gln510Glu attenuates cardiomyocyte differentiation and promotes cardiac hypertrophy via dysregulation of Akt/GSK-3β/β-catenin signaling". American Journal of Physiology-Heart and Circulatory Physiology 301, № 4 (2011): H1531—H1539. http://dx.doi.org/10.1152/ajpheart.00216.2011.

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LEOPARD syndrome (LS) is an autosomal dominant inherited multisystemic disorder. Most cases involve mutations in the PTPN11 gene, which encodes the protein tyrosine phosphatase Src homology 2-containing protein phosphatase 2 (SHP2). LS frequently causes severe hypertrophic cardiomyopathy (HCM), even from the fetal period. However, the molecular pathogenesis has not been clearly elucidated. Here, we analyzed the roles of the LS-type SHP2 mutant Gln510Glu (Q510E), which showed the most severe type of HCM in LS, in cardiomyocyte differentiation, and in morphological changes. We generated mutant P

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13

Debrus, Sophie, Loulwa Rahbani, Minna Marttila, Bruno Delorme, Pierre Paradis та Mona Nemer. "The Zinc Finger-Only Protein Zfp260 Is a Novel Cardiac Regulator and a Nuclear Effector of α1-Adrenergic Signaling". Molecular and Cellular Biology 25, № 19 (2005): 8669–82. http://dx.doi.org/10.1128/mcb.25.19.8669-8682.2005.

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ABSTRACT α1-Adrenergic receptors mediate several biological effects of catecholamines, including the regulation of myocyte growth and contractility and transcriptional regulation of the atrial natriuretic factor (ANF) gene whose promoter contains an α1-adrenergic response element. The nuclear pathways and effectors that link receptor activation to genetic changes remain poorly understood. Here, we describe the isolation by the yeast one-hybrid system of a cardiac cDNA encoding a novel nuclear zinc finger protein, Zfp260, belonging to the Krüppel family of transcriptional regulators. Zfp260 is

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14

Reddy, Venkatapuram Seenu, Sumanth D. Prabhu, Srinivas Mummidi та ін. "Interleukin-18 induces EMMPRIN expression in primary cardiomyocytes via JNK/Sp1 signaling and MMP-9 in part via EMMPRIN and through AP-1 and NF-κB activation". American Journal of Physiology-Heart and Circulatory Physiology 299, № 4 (2010): H1242—H1254. http://dx.doi.org/10.1152/ajpheart.00451.2010.

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IL-18 and the extracellular matrix metalloproteinase (MMP) inducer (EMMPRIN) stimulate the expression of proinflammatory cytokines and MMPs and are elevated in myocardial hypertrophy, remodeling, and failure. Here, we report several novel findings in primary cardiomyocytes treated with IL-18. First, IL-18 activated multiple transcription factors, including NF-κB (p50 and p65), activator protein (AP)-1 (cFos, cJun, and JunD), GATA, CCAAT/enhancer-binding protein, myocyte-specific enhancer-binding factor, interferon regulatory factor-1, p53, and specific protein (Sp)-1. Second, IL-18 induced EMM

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15

Georges, Romain, Georges Nemer, Martin Morin, Chantal Lefebvre, and Mona Nemer. "Distinct Expression and Function of Alternatively Spliced Tbx5 Isoforms in Cell Growth and Differentiation." Molecular and Cellular Biology 28, no. 12 (2008): 4052–67. http://dx.doi.org/10.1128/mcb.02100-07.

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ABSTRACT Mutations in the T-box transcription factor Tbx5 cause Holt-Oram syndrome, an autosomal dominant disease characterized by a wide spectrum of cardiac and upper limb defects with variable expressivity. Tbx5 haploinsufficiency has been suggested to be the underlying mechanism, and experimental models are consistent with a dosage-sensitive requirement for Tbx5 in heart development. Here, we report that Tbx5 levels are regulated through alternative splicing that generates, in addition to the known 518-amino-acid protein, a C-terminal truncated isoform. This shorter isoform retains the capa

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16

van Berlo, Jop H., and Jeffery D. Molkentin. "Abstract 47: GATA Factors Caught at a Crossroad of Gene Duplication with Functional Divergence." Circulation Research 111, suppl_1 (2012). http://dx.doi.org/10.1161/res.111.suppl_1.a47.

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Background Six individual members comprise the GATA family of Zn finger-containing transcription factors that play major roles in the hematopoietic system and many mesoderm and endoderm derived tissues. The adult heart expresses both GATA4 and GATA6. Here, we examined the overlapping and diverging functional roles of GATA4 and GATA6 in the adult heart, both at baseline and under stress. Results Pressure overload by transverse aortic constriction (TAC) caused a blunted hypertrophic response when GATA4 was deleted from the adult heart, with severe heart failure ensuing after 4 weeks. Similarly,

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17

Dittrich, Gesine M., Natali Froese, Xue Wang, et al. "Fibroblast GATA-4 and GATA-6 promote myocardial adaptation to pressure overload by enhancing cardiac angiogenesis." Basic Research in Cardiology 116, no. 1 (2021). http://dx.doi.org/10.1007/s00395-021-00862-y.

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AbstractHeart failure due to high blood pressure or ischemic injury remains a major problem for millions of patients worldwide. Despite enormous advances in deciphering the molecular mechanisms underlying heart failure progression, the cell-type specific adaptations and especially intercellular signaling remain poorly understood. Cardiac fibroblasts express high levels of cardiogenic transcription factors such as GATA-4 and GATA-6, but their role in fibroblasts during stress is not known. Here, we show that fibroblast GATA-4 and GATA-6 promote adaptive remodeling in pressure overload induced c

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18

Sunagawa, Y., M. Funamoto, K. Shimizu, et al. "P4998Novel GATA4 binding proteins, RbAp48/46, regulate cardiomyocyte hypertrophy with depending on the phosphorylate State of GATA4." European Heart Journal 40, Supplement_1 (2019). http://dx.doi.org/10.1093/eurheartj/ehz746.0176.

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Abstract Introduction Cardiac hypertrophy is being recognized as a critical event during the development of heart failure. A zinc finger protein GATA4 associates with an intrinsic histone acetyltransferase p300 and regulates myocardial transcriptional activities in response to hypertrophic stimuli. Here, we show that Retinoblastoma protein (Rb)-associated protein 48 and 46 (RbAp48, RbAp46) are novel components of p300/GATA4 complex. Both RbAp48 and 46 form a repressor complex with HDACs and has been implicated in chromatin remodeling and transcriptional repression. However, the precise functio

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19

Kwon, Duk-hwa, Gwang Hyeon Eom, Hae Jin Kee, et al. "Abstract 071: Estrogen-related Receptor Gamma Induces Cardiac Hypertrophy By Activating Gata4." Circulation Research 113, suppl_1 (2013). http://dx.doi.org/10.1161/res.113.suppl_1.a071.

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Introduction— Estrogen-related receptor gamma (ERRγ) is an orphan nuclear receptor that has biological roles mainly in metabolism and it controls metabolic switching in perinatal heart. In adult heart diseases, however, the functional roles of ERRγ have not yet been elucidated. Hypothesis— In the present study, we aimed to characterize the role of ERRγ in cardiac hypertrophy. Here we show that ERRγ provokes cardiac hypertrophy by inducing GATA4 and that its inverse agonist, GSK-5182, prevents cardiac hypertrophy. Methods and Results— The functional roles of ERRγ in association with development

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20

Sunagawa, Yoichi, Yasufumi Katanasaka, Taishi Terada, et al. "Abstract P221: Retinoblastoma Protein--Associated Proteins 48 and 46 Are Novel p300/GATA4-Binding Partners Involved in Hypertrophic Responses in Cardiomyocytes." Circulation Research 109, suppl_1 (2011). http://dx.doi.org/10.1161/res.109.suppl_1.ap221.

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Background: A zinc finger protein GATA4 is one of hypertrophy-responsive transcription factors, and increases its DNA-binding and transcriptional activities in response to hypertrophic stimuli in cardiomyocytes. Activation of GATA4 during this process is mediated, in part, through acetylation by intrinsic histone acetyltransferases such as a transcriptional coactivator p300. Here, we show that retinoblastoma protein (Rb)-associated protein 48 and 46 (RbAp48, RbAp46), components of NuRD (nucleosome remodeling and deacetylase) complex that has been implicated in chromatin remodeling and transcri

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21

Zhao, Tingwei, Hae Jin Kee, Liyan Bai, Moon-Ki Kim, Seung-Jung Kee, and Myung Ho Jeong. "Selective HDAC8 Inhibition Attenuates Isoproterenol-Induced Cardiac Hypertrophy and Fibrosis via p38 MAPK Pathway." Frontiers in Pharmacology 12 (April 20, 2021). http://dx.doi.org/10.3389/fphar.2021.677757.

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Histone deacetylase (HDAC) expression and enzymatic activity are dysregulated in cardiovascular diseases. Among Class I HDACs, HDAC2 has been reported to play a key role in cardiac hypertrophy; however, the exact function of HDAC8 remains unknown. Here we investigated the role of HDAC8 in cardiac hypertrophy and fibrosis using the isoproterenol-induced cardiac hypertrophy model system.Isoproterenol-infused mice were injected with the HDAC8 selective inhibitor PCI34051 (30 mg kg−1 body weight). Enlarged hearts were assessed by HW/BW ratio, cross-sectional area, and echocardiography. RT-PCR, wes

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22

Tenhunen, Olli, Hanna Leskinen, Raisa Serpi, et al. "Abstract 865: Gata-4 Is An Angiogenic Survival Factor Of The Infarcted Heart." Circulation 116, suppl_16 (2007). http://dx.doi.org/10.1161/circ.116.suppl_16.ii_169.

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Recent data suggest that the cardiac-restricted transcription factor GATA-4 is an anti-apoptotic factor required for adaptive responses as well as a key regulator of hypertrophy and hypertrophy-associated genes in the heart. As a leading cause of chronic heart failure, reversal of post-infarction left ventricular remodeling represents an important target for therapeutic interventions. Here we studied the role of GATA-4 as a mediator of post-infarction remodeling. Rats were subjected to experimental myocardial infarction (MI) by ligating the left anterior descending coronary artery (LAD). Ligat

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