Direct monitoring pressure overload predicts cardiac hypertrophy in mice

Duan, Si‐Bo; Ivashchenko, Christine Y.; Whitesall, Steven E.; DʼAlecy, Louis G.; Mortensen, Richard M.

doi:10.1088/0967-3334/28/11/001

Cited by 5 publications

(4 citation statements)

References 30 publications

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“…Male mice (8–10 weeks old, body weight larger than 23 grams) were randomly divided into the following four groups: (1) LC + sham operation (n = 4); (2) LC + abdominal aortic constriction (AAC) (n = 7); (3) MMRKO + sham operation (n = 5); (4) MMRKO + AAC (n = 6). AAC or sham operation was performed as previously described [15] . Briefly, the mice were anesthetized with 2% isoflurane inhalation.…”

Section: Methodsmentioning

confidence: 99%

Myeloid Mineralocorticoid Receptor Deficiency Inhibits Aortic Constriction-Induced Cardiac Hypertrophy in Mice

Zhang

Frieler

et al. 2014

PLoS ONE

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Mineralocorticoid receptor (MR) blockade has been shown to suppress cardiac hypertrophy and remodeling in animal models of pressure overload (POL). This study aims to determine whether MR deficiency in myeloid cells modulates aortic constriction-induced cardiovascular injuries. Myeloid MR knockout (MMRKO) mice and littermate control mice were subjected to abdominal aortic constriction (AAC) or sham operation. We found that AAC-induced cardiac hypertrophy and fibrosis were significantly attenuated in MMRKO mice. Expression of genes important in generating reactive oxygen species was decreased in MMRKO mice, while that of manganese superoxide dismutase increased. Furthermore, expression of genes important in cardiac metabolism was increased in MMRKO hearts. Macrophage infiltration in the heart was inhibited and expression of inflammatory genes was decreased in MMRKO mice. In addition, aortic fibrosis and inflammation were attenuated in MMRKO mice. Taken together, our data indicated that MR deficiency in myeloid cells effectively attenuated aortic constriction-induced cardiac hypertrophy and fibrosis, as well as aortic fibrosis and inflammation.

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Section: Methodsmentioning

confidence: 99%

Myeloid Mineralocorticoid Receptor Deficiency Inhibits Aortic Constriction-Induced Cardiac Hypertrophy in Mice

Zhang

Frieler

et al. 2014

PLoS ONE

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“…AAC mice were performed as previously described. ( Duan et al, 2007 ). Briefly, after anesthesia with 2% isoflurane, the mice were placed in the supine position on the platform and cut along the midline of the abdomen to expose the abdominal cavity.…”

Section: Methodsmentioning

confidence: 99%

Dapagliflozin Mediates Plin5/PPARα Signaling Axis to Attenuate Cardiac Hypertrophy

Zhao

et al. 2021

Front. Pharmacol.

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Objective: The purpose of this study was to investigate the effect of dapagliflozin (DAPA), a sodium-glucose cotransporter 2 inhibitor, on relieving cardiac hypertrophy and its potential molecular mechanism.Methods: Cardiac hypertrophy induced by abdominal aortic constriction (AAC) in mice, dapagliflozin were administered in the drinking water at a dose of 25 mg/kg/d for 12 weeks was observed. Echocardiography was used to detect the changes of cardiac function, including LVEF, LVFS, LVEDd, LVEDs, HR and LV mass. Histological morphological changes were evaluated by Masson trichrome staining and wheat germ agglutinin (WGA) staining. The enrichment of differential genes and signal pathways after treatment was analyzed by gene microarray cardiomyocyte hypertrophy was induced by AngII (2 μM) and the protective effect of dapagliflozin (1 μM) was observed in vitro. The morphological changes of myocardial cells were detected by cTnI immunofluorescence staining. ELISA and qRT-PCR assays were performed to detect the expressions levels of cardiac hypertrophy related molecules.Results: After 12 weeks of treatment, DAPA significantly ameliorated cardiac function and inhibited cardiac hypertrophy in AAC-induced mice. In vitro, DAPA significantly inhibited abnormal hypertrophy in AngII-induced cardiacmyocytes. Both in vivo and in vitro experiments have confirmed that DAPA could mediate the Plin5/PPARα signaling axis to play a protective role in inhibiting cardiac hypertrophy.Conclusion: Dapagliflozin activated the Plin5/PPARα signaling axis and exerts a protective effect against cardiac hypertrophy.

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“…Cardiac expression of fibrosis-related genes, such as collagen I, collagen III, connective tissue growth factor precursor (CTGF), and transforming growth factor β (TGFβ1), was also inhibited in TMRKO mice after AAC ( Figure 2E). Telemetric monitoring 23 showed no difference in either systolic or diastolic blood pressure between littermate control and TMRKO mice after AAC ( Figure S4), excluding the influence of different pressure to the heart.…”

Section: T-cell Mr Deficiency Attenuates Aac-induced Cardiac Hypertromentioning

confidence: 95%

“…Blood pressure was measured using radiotelemetry system as previously described with modifications. 23,24 Pressure transmitters (PA-C10; Data Sciences International) were placed 3 days after AAC, and data were collected after recovery for another 4 days.…”

Section: Animals and Surgeriesmentioning

confidence: 99%

Mineralocorticoid Receptor Deficiency in T Cells Attenuates Pressure Overload–Induced Cardiac Hypertrophy and Dysfunction Through Modulating T-Cell Activation

Sun

et al. 2017

Hypertension

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Although antagonists of mineralocorticoid receptor (MR) have been widely used to treat heart failure, the underlying mechanisms are incompletely understood. Recent reports show that T cells play important roles in pathologic cardiac hypertrophy and heart failure. However, it is unclear whether and how MR functions in T cells under these pathologic conditions. We found that MR antagonist suppressed abdominal aortic constriction–induced cardiac hypertrophy and decreased the accumulation and activation of CD4 + and CD8 + T cells in mouse heart. T-cell MR knockout mice manifested suppressed cardiac hypertrophy, fibrosis, and dysfunction compared with littermate control mice after abdominal aortic constriction. T-cell MR knockout mice had less cardiac inflammatory response, which was illustrated by decreased accumulation of myeloid cells and reduced expression of inflammatory cytokines. Less amounts and activation of T cells were observed in the heart of T-cell MR knockout mice after abdominal aortic constriction. In vitro studies showed that both MR antagonism and deficiency repressed activation of T cells, whereas MR overexpression elevated activation of T cells. These results demonstrated that MR blockade in T cells protected against abdominal aortic constriction–induced cardiac hypertrophy and dysfunction. Mechanistically, MR directly regulated T-cell activation and modulated cardiac inflammation. Targeting MR in T cells specifically may be a feasible strategy for more effective treatment of pathologic cardiac hypertrophy and heart failure.

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Direct monitoring pressure overload predicts cardiac hypertrophy in mice

Cited by 5 publications

References 30 publications

Myeloid Mineralocorticoid Receptor Deficiency Inhibits Aortic Constriction-Induced Cardiac Hypertrophy in Mice

Myeloid Mineralocorticoid Receptor Deficiency Inhibits Aortic Constriction-Induced Cardiac Hypertrophy in Mice

Dapagliflozin Mediates Plin5/PPARα Signaling Axis to Attenuate Cardiac Hypertrophy

Mineralocorticoid Receptor Deficiency in T Cells Attenuates Pressure Overload–Induced Cardiac Hypertrophy and Dysfunction Through Modulating T-Cell Activation

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