Hypoxic activation of the atrial natriuretic peptide gene promoter through direct and indirect actions of hypoxia-inducible factor-1

Chun, Yang Sook; Hyun, Ju Yeon; Kwak, Yong-Geun; Kim, In San; Kim, Chan Hyung; Choi, Eunhee; Kim, Myung Suk; Park, Jong-Wan

doi:10.1042/bj20021087

Cited by 87 publications

(50 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Increased VLDLR expression appears to be a general response to lack of oxygen, as we demonstrated hypoxia-induced increases in VLDLR expression in a number of different cell types (Supplemental Table 2). We therefore investigated whether the hypoxia-induced expression of VLDLR was dependent on the transcription factor HIF-1α, which has been described as being involved in regulation of cardiac peptides under conditions of low oxygen (17). As expected, HIF-1α expression was increased in hypoxic cells ( Figure 3A).…”

Section: Figurementioning

confidence: 82%

The VLDL receptor promotes lipotoxicity and increases mortality in mice following an acute myocardial infarction

Perman¹,

Boström²,

Lindbom³

et al. 2011

J. Clin. Invest.

139

View full text Add to dashboard Cite

Impaired cardiac function is associated with myocardial triglyceride accumulation, but it is not clear how the lipids accumulate or whether this accumulation is detrimental. Here we show that hypoxia/ischemia-induced accumulation of lipids in HL-1 cardiomyocytes and mouse hearts is dependent on expression of the VLDL receptor (VLDLR). Hypoxia-induced VLDLR expression in HL-1 cells was dependent on HIF-1α through its interaction with a hypoxia-responsive element in the Vldlr promoter, and VLDLR promoted the endocytosis of lipoproteins. Furthermore, VLDLR expression was higher in ischemic compared with nonischemic left ventricles from human hearts and was correlated with the total lipid droplet area in the cardiomyocytes. Importantly, Vldlr -/-mice showed improved survival and decreased infarct area following an induced myocardial infarction. ER stress, which leads to apoptosis, is known to be involved in ischemic heart disease. We found that ischemia-induced ER stress and apoptosis in mouse hearts were reduced in Vldlr -/-mice and in mice treated with antibodies specific for VLDLR. These findings suggest that VLDLR-induced lipid accumulation in the ischemic heart worsens survival by increasing ER stress and apoptosis.

show abstract

Section: Figurementioning

confidence: 82%

The VLDL receptor promotes lipotoxicity and increases mortality in mice following an acute myocardial infarction

Perman¹,

Boström²,

Lindbom³

et al. 2011

J. Clin. Invest.

139

View full text Add to dashboard Cite

show abstract

“…Furthermore, HIF-1␣ stabilization not only fails to promote, but actually decreases tumor growth (108). HIF-1␣, similar to Myc, has also been implicated in playing a role in cardiac hypertrophy (36,112). A comprehensive analysis of the role of HIF-1␣ in cardiac proliferation and hypertrophy still needs to be performed, but given Myc's critical role in mediating cardiac myocyte growth, HIF-1␣ may represent a novel endogenous antagonist.…”

Section: Hypoxia Inducible Factor-1␣mentioning

confidence: 99%

Cardiac Myocyte Cell Cycle Control in Development, Disease, and Regeneration

Ahuja

Sdek²,

MacLellan

2007

Physiological Reviews

499

475

View full text Add to dashboard Cite

Cardiac myocytes rapidly proliferate during fetal life but exit the cell cycle soon after birth in mammals. Although the extent to which adult cardiac myocytes are capable of cell cycle reentry is controversial and species-specific differences may exist, it appears that for the vast majority of adult cardiac myocytes the predominant form of growth postnatally is an increase in cell size (hypertrophy) not number. Unfortunately, this limits the ability of the heart to restore function after any significant injury. Interest in novel regenerative therapies has led to the accumulation of much information on the mechanisms that regulate the rapid proliferation of cardiac myocytes in utero, their cell cycle exit in the perinatal period, and the permanent arrest (terminal differentiation) in adult myocytes. The recent identification of cardiac progenitor cells capable of giving rise to cardiac myocyte-like cells has challenged the dogma that the heart is a terminally differentiated organ and opened new prospects for cardiac regeneration. In this review, we summarize the current understanding of cardiomyocyte cell cycle control in normal development and disease. In addition, we also discuss the potential usefulness of cardiomyocyte self-renewal as well as feasibility of therapeutic manipulation of the cardiac myocyte cell cycle for cardiac regeneration.

show abstract

“…Also, both the A‐ and B‐type peptides have a hypoxia‐responsive element in the promoter sequence of their respective genes (Chun et al . 2003, Luo et al . 2006) and hypoxia has been shown to be a direct and sufficient stimulus for the transcription of the gene encoding B‐type peptide (Weidemann et al .…”

mentioning

confidence: 99%

Hypoxia exposure and B‐type natriuretic peptide release from Langendorff heart of rats

et al. 2016

View full text Add to dashboard Cite

AimWe studied whether available oxygen without induced mechanical stretch regulates the release of the biologically active B‐type natriuretic peptide (BNP) from Langendorff heart.MethodsRat hearts were isolated and perfused with a physiological Krebs–Henseleit solution at a constant hydrostatic pressure in Langendorff set‐up. The basal O2 level of perfusate (24.4 ± 0.04 mg L−1) was gradually lowered to 3.0 ± 0.01 mg L−1 over 20 min using N2 gas (n = 7). BNP and O2 level were measured from coronary flow. During control perfusions (n = 5), the O2 concentration was kept at 26.6 ± 0.3 mg L−1.ResultsA low oxygen concentration in the perfusate was associated with a significant increase in BNP release (F = 40.4, P < 0.001). Heart rate decreased when the oxygen concentration in the perfusate reached 9.1 ± 0.02 mg L−1 and continued to fall in lower oxygen concentrations (F = 14.8, P < 0.001). There was also a significant but inverse correlation between BNP and oxygen in the coronary flow (R 2 = 0.27, P < 0.001).ConclusionIn the spontaneously beating Langendorff rat heart, a decreasing concentration of oxygen in the ingoing perfusion increased the secretion of BNP. The effect of oxygen was independent of mechanical stretch of the heart as it occurred even when the heart rate decreased but the pressure conditions remained constant. The difference in the oxygen capacitance of blood and Krebs–Henseleit solution appears to be a major factor affecting secretion of BNP, which is correlated with the oxygen tension of myocardial cells and affected both by the oxygen concentration and capacitance of solution perfusing the heart and by the coronary flow.

show abstract

Hypoxic activation of the atrial natriuretic peptide gene promoter through direct and indirect actions of hypoxia-inducible factor-1

Cited by 87 publications

References 27 publications

The VLDL receptor promotes lipotoxicity and increases mortality in mice following an acute myocardial infarction

The VLDL receptor promotes lipotoxicity and increases mortality in mice following an acute myocardial infarction

Cardiac Myocyte Cell Cycle Control in Development, Disease, and Regeneration

Hypoxia exposure and B‐type natriuretic peptide release from Langendorff heart of rats

Contact Info

Product

Resources

About