Microarray analysis of gene expression after transverse aortic constriction in mice

Zhao, Mingming; Chow, Amy; Powers, Jennifer; Fajardo, Giovanni; Bernstein, Daniel

doi:10.1152/physiolgenomics.00040.2004

Cited by 71 publications

(76 citation statements)

References 51 publications

(34 reference statements)

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“…We assessed the effects of TAC on heart weight/body weight ratios and gene expression after only 7 days, and as such we addressed mechanisms related to the compensatory (growth) phase of hypertrophy unrelated to a transition to heart failure. Using a similar murine pressure overload model, Zhao and coworkers [29] reported most genes were differentially regulated by 10 days, similar to the time period used in this study. Wagner and coworkers have shown that TAC resulted in stabilization of hypertrophy in as few as 20 days in mice [30].…”

Section: Discussionsupporting

confidence: 64%

Interleukin-18 knockout mice display maladaptive cardiac hypertrophy in response to pressure overload

Colston

Boylston

Feldman

et al. 2007

Biochemical and Biophysical Research Communications

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Interleukin (IL)-18 is a cardiotropic proinflammatory cytokine chronically elevated in the serum of patients with cardiac hypertrophy (LVH). The purpose of this study was to examine the role of IL-18 in pressure-overload hypertrophy using wild type (WT) and IL-18 −/− (null) mice. Adult male C57Bl/ 6 mice underwent transaortic constriction (TAC) for 7 days or sham surgery. Heart weight/body weight ratios showed blunted hypertrophy in IL-18 null TAC mice compared to WT TAC animals. Microarray analyses indicated differential expression of hypertrophy-related genes in WT versus IL-18 nulls. Northern, Western, and EMSA analyses showed Akt and GATA4 were increased in WT but unchanged in IL-18 null mice. Our results demonstrate blunted hypertrophy with reduced expression of contractile-, hypertrophy-, and remodeling-associated genes following pressure overload in IL-18 null mice, and suggest that IL-18 plays a critical role in the hypertrophic response.

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Section: Discussionsupporting

confidence: 64%

Interleukin-18 knockout mice display maladaptive cardiac hypertrophy in response to pressure overload

Colston

Boylston

Feldman

et al. 2007

Biochemical and Biophysical Research Communications

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“…During the early "asymptomatic" stage of diastolic dysfunction (1 month), there were surprisingly minimal gene expression changes, a marked contrast to previous studies of isolated PS, isolated PI, or models of LV afterload, such as transverse aortic constriction (TAC) (17)(18)(19). Only 23 genes were upregulated, including those encoding proteins involved in metabolic (insulin-like receptors, adenylate cyclase), transport (organic anion transporters), and fibrotic (fibroblast growth factors) pathways, while 33 were downregulated, including those encoding proteins involved with pathways related to oxidative stress (NADPH oxidase 4, glutathione transferase) and chemokine response (chemokine ligands, adhesion molecules).…”

Section: Model Of Pi+ps Recapitulates the Clinical Setting -Early Diacontrasting

confidence: 72%

miR-21 is associated with fibrosis and right ventricular failure

Reddy

Zhao

et al. 2017

JCI Insight

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“…TAC was performed as previously described (53). Briefly, anesthesia was induced with 3% isoflurane and maintained with 1.5% isoflurane.…”

Section: Methodsmentioning

confidence: 99%

“…We subjected ␤ 1 , ␤ 2 , and ␤ 1 ␤ 2 -AR knockout mice to transverse aortic constriction (TAC) at a level that induces stable, compensated LV hypertrophy and not cardiac failure (53). These conditions were chosen to specifically study the separate mechanisms of hypertrophy as distinct from hypertrophy-induced heart failure.…”

mentioning

confidence: 99%

Cardiac pressure overload hypertrophy is differentially regulated by β-adrenergic receptor subtypes

Zhao¹,

Fajardo²,

Urashima³

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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In isolated myocytes, hypertrophy induced by norepinephrine is mediated via ␣1-adrenergic receptors (ARs) and not ␤-ARs. However, mice with deletions of both major cardiac ␣1-ARs still develop hypertrophy in response to pressure overload. Our purpose was to better define the role of ␤-AR subtypes in regulating cardiac hypertrophy in vivo, important given the widespread clinical use of ␤-AR antagonists and the likelihood that patients treated with these agents could develop conditions of further afterload stress. Mice with deletions of ␤1, ␤2, or both ␤1-and ␤2-ARs were subjected to transverse aortic constriction (TAC). After 3 wk, ␤1Ϫ/Ϫ showed a 21% increase in heart to body weight vs. sham controls, similar to wild type, whereas ␤2 Ϫ/Ϫ developed exaggerated (49% increase) hypertrophy. Only when both ␤-ARs were ablated (␤1␤2 Ϫ/Ϫ ) was hypertrophy totally abolished. Cardiac function was preserved in all genotypes. Several known inhibitors of cardiac hypertrophy (FK506 binding protein 5, thioredoxin interacting protein, and S100A9) were upregulated in ␤1␤2 Ϫ/Ϫ compared with the other genotypes, whereas transforming growth factor-␤2, a positive mediator of hypertrophy was upregulated in all genotypes except the ␤1␤2 Ϫ/Ϫ . In contrast to recent reports suggesting that angiogenesis plays a critical role in regulating cardiac hypertrophy-induced heart failure, we found no evidence that angiogenesis or its regulators (VEGF, Hif1␣, and p53) play a role in compensated cardiac hypertrophy. Pressure overload hypertrophy in vivo is dependent on a coordination of signaling through both ␤1-and ␤2-ARs, mediated through several key cardiac remodeling pathways. Angiogenesis is not a prerequisite for compensated cardiac hypertrophy.angiogenesis; genes; G protein-coupled receptors CHRONIC LEFT VENTRICULAR (LV) PRESSURE overload is present in patients with aortic stenosis, coarctation of the aorta, and systemic hypertension, and although it is one of the leading causes of heart failure (18), moderate levels of pressure overload can be tolerated for decades. The mechanisms by which the heart adapts to pressure overload, producing either an adaptive (compensated hypertrophy) or a maladaptive (heart failure) phenotype, have been the subject of considerable investigation. One of the signaling pathways implicated in the hypertrophic response is that mediated by catecholamines acting via ␣-and ␤-adrenergic receptors (ARs; Refs. 5,15,18,33). In isolated myocytes, hypertrophy induced by norepinephrine is mediated via ␣ 1 -ARs; however, in vivo, mice with deletions of both of the major cardiac ␣ 1 -ARs still develop hypertrophy when exposed to pressure overload (29,30). This suggests that the other target for catecholamine stimulation, the ␤-ARs, must contribute to the development of cardiac hypertrophy in vivo.There is considerable heterogeneity between ␤ 1 -and ␤ 2 -ARs in their regulation of adaptive and maladaptive cardiac remodeling. In vitro, ␤ 1 -AR activation is predominantly cardiotoxic (55), whereas ␤ 2 activation can switch betwe...

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Microarray analysis of gene expression after transverse aortic constriction in mice

Abstract: Zhao, Mingming, Amy Chow, Jennifer Powers, Giovanni Fajardo, and Daniel Bernstein. Microarray analysis of gene expression after transverse aortic constriction in mice.

Cited by 71 publications

References 51 publications

Interleukin-18 knockout mice display maladaptive cardiac hypertrophy in response to pressure overload

Interleukin-18 knockout mice display maladaptive cardiac hypertrophy in response to pressure overload

miR-21 is associated with fibrosis and right ventricular failure

Cardiac pressure overload hypertrophy is differentially regulated by β-adrenergic receptor subtypes

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