Angiotensin II Induces Apoptosis of Adult Ventricular MyocytesIn Vitro

Kajstura, Jan; Cigola, Elena; Malhotra, Ashwani; Li, Peng; Cheng, Wei; Meggs, Leonard G.; Anversa, Piero

doi:10.1006/jmcc.1996.0333

Cited by 393 publications

(269 citation statements)

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“…Angiotensin II, an IP 3 -generating agonist, is a potent stimulator of cardiomyocyte hypertrophy that can elevate cytoplasmic Ca 2+ during vasoconstriction, increased blood pressure, and hemodynamic stress. A number of studies have demonstrated that angiotensin II treatment leads to an increase in basal Ca 2+ levels in adult and neonatal cardiomyocytes (Kem et al 1991;Shao et al 1998;Hunton et al 2004), with sustained exposure affecting numerous cellular pathways (Meldrum et al 1996;Liu et al 2004b;Zhang et al 2004) and eventually resulting in cell death (Goldenberg et al 2001;Kajstura et al 1997). Elevating UDP-GlcNAc and O-GlcNAc levels through treatment with glucosamine or the O-GlcNAcase inhibitor PUGNAc attenuates angiotensin IIinduced CCE during I/R injury (Nagy et al 2006).…”

Section: Calcium Homeostasismentioning

confidence: 99%

Dynamic O-GlcNAcylation and its roles in the cellular stress response and homeostasis

Groves

Lee

Yildirir

et al. 2013

Cell Stress and Chaperones

120

112

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O-linked N-acetyl-β-D-glucosamine (O-GlcNAc) is a ubiquitous and dynamic post-translational modification known to modify over 3,000 nuclear, cytoplasmic, and mitochondrial eukaryotic proteins. Addition of O-GlcNAc to proteins is catalyzed by the O-GlcNAc transferase and is removed by a neutral-N-acetyl-β-glucosaminidase (OGlcNAcase). O-GlcNAc is thought to regulate proteins in a manner analogous to protein phosphorylation, and the cycling of this carbohydrate modification regulates many cellular functions such as the cellular stress response. Diverse forms of cellular stress and tissue injury result in enhanced O-GlcNAc modification, or O-GlcNAcylation, of numerous intracellular proteins. Stress-induced OGlcNAcylation appears to promote cell/tissue survival by regulating a multitude of biological processes including: the phosphoinositide 3-kinase/Akt pathway, heat shock protein expression, calcium homeostasis, levels of reactive oxygen species, ER stress, protein stability, mitochondrial dynamics, and inflammation. Here, we will discuss the regulation of these processes by O-GlcNAc and the impact of such regulation on survival in models of ischemia reperfusion injury and trauma hemorrhage. We will also discuss the misregulation of O-GlcNAc in diseases commonly associated with the stress response, namely Alzheimer's and Parkinson's diseases. Finally, we will highlight recent advancements in the tools and technologies used to study the O-GlcNAc modification.

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Section: Calcium Homeostasismentioning

confidence: 99%

Dynamic O-GlcNAcylation and its roles in the cellular stress response and homeostasis

Groves

Lee

Yildirir

et al. 2013

Cell Stress and Chaperones

120

112

View full text Add to dashboard Cite

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“…Increased cardiomyocyte apoptosis has been recently demonstrated in SHRs and patients with essential hypertension [12] . Although apoptosis could be induced by pressure overload, in vitro and in vivo findings indicated that angiotensin II could be critical in cardiac apoptosis [13,14] . A study of patients with essential hypertension by González and his colleagues indicated that the efficacy of antihypertensive treatment in reducing blood pressure does not predict its capacity to reduce myocardial apoptosis in hypertensive patients [15] .…”

Section: Discussionmentioning

confidence: 99%

Recombinant adeno-associated virus-mediated human kallikrein gene therapy protects against hypertensive target organ injuries through inhibiting cell apoptosis

Yan

Wang

2009

Acta Pharmacol Sin

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Aim: Overexpression of human tissue kallikrein (HK), mediated by recombinant adeno-associated virus (rAAV), decreased blood pressure in spontaneous hypertensive rats (SHRs) and reduced injury to the heart, aorta and kidney. In this study, we used both an in vivo animal model and in vitro cell culture system to investigate whether rAAV-mediated HK gene therapy protects against organ damage by inhibiting cell apoptosis. Methods: rAAV encoding HK (rAAV-HK) or LacZ (rAAV-lacZ) were delivered as a control to spontaneously hypertensive rats (SHRs) and cultured human embryonic kidney (HEK) 293 cells. Results: Treatment with rAAV-HK decreased cell apoptosis in the target organs of SHRs and also inhibited lipopolysaccharide (LPS)-induced HEK 293 apoptosis. The rAAV-HK delivery system also increased the levels of apoptosis-inhibiting proteins bcl-2 and bcl-x L , and decreased the level of Bax and the activity of caspase 3, two promoters of apoptosis. In addition to its role in the inhibition of apoptosis, rAAV-HK also activated the cell survival and proliferation signaling pathways ERK1/2 and PI3K/AKT. Conclusion: rAAV-mediated HK gene delivery has multiple therapeutic possibilities for treating hypertension, not only by decreasing blood pressure, but also by directly inhibiting end-organ damage.

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“…Myocyte apoptosis has been demonstrated to contribute in rats and mice to the transition from hypertrophy to early heart failure. 33,34 The demonstrations that angiotensin II applied directly, or released in response to mechanical stretch, induced apoptosis in adult rat cardiomyocytes in vitro 35,36 suggest a further pathophysiological role for the hormone in the progression of myocardial disease in aortic stenosis.…”

Section: Transition To Heart Failurementioning

confidence: 99%

“…AT 1 -receptor blockade (losartan) but not AT 2 blockade, was shown to prevent the five-fold increase in apoptosis caused by angiotensin II in rat cardiomyocytes. 35,36 Thus, another possible target for the use of ACE inhibitors in aortic stenosis may be prevention of a reduction…”

Section: Ace Inhibitors and Prevention Of LV Dilatation And Remodellingmentioning

confidence: 99%

ACE inhibition in aortic stenosis: dangerous medicine or golden opportunity?

Routledge

Townend

2001

J Hum Hypertens

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Conventionally angiotensin-converting enzyme (ACE) inhibitors are contraindicated in patients with aortic stenosis. Abundant evidence is now available showing that angiotensin II has a central role in the development of left ventricular hypertrophy (LVH), myocardial contractile failure and diastolic dysfunction in response to pressure overload. In animal models, ACE inhibitors have been shown to attenuate these pathological responses. In humans there is no such evidence available, however uncontrolled studies have shown that

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Angiotensin II Induces Apoptosis of Adult Ventricular MyocytesIn Vitro

Cited by 393 publications

References 0 publications

Dynamic O-GlcNAcylation and its roles in the cellular stress response and homeostasis

Dynamic O-GlcNAcylation and its roles in the cellular stress response and homeostasis

Recombinant adeno-associated virus-mediated human kallikrein gene therapy protects against hypertensive target organ injuries through inhibiting cell apoptosis

ACE inhibition in aortic stenosis: dangerous medicine or golden opportunity?

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