Phosphatidylinositol and inositolphosphatide metabolism in hypertrophied rat heart.

Shoki, Mikako; Kawaguchi, Hideaki; Okamoto, Hiroshi; Sano, Hitoshi; Sawa, Hirofumi; Kudo, Toshiyuki; Hirao, N.; Sakata, Yoshihito; Yasuda, Hisakazu

doi:10.1253/jcj.56.142

Cited by 24 publications

(14 citation statements)

References 32 publications

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“…Our previous studies have shown increased generation of Ins(1,4,5)P 3 in atrial tissue from patients with valve disease, in hypertrophied ventricle from mice following chronic pressure overload, in atria and ventricles of the murine DCM model and in rodent hearts subjected to acute ischemia/reperfusion 4, 8, 26–28 . Other laboratories have also reported heightened Ins(1,4,5)P 3 generation in hearts undergoing hypertrophy 29 or following ischemia or ischemia/reperfusion 30–32 . Thus, heightened generation of Ins(1,4,5)P 3 , like increased IP 3 -R expression, may be a common feature in cardiac pathologies.…”

Section: Discussionmentioning

confidence: 86%

No Contribution of IP ₃ -R(2) to Disease Phenotype in Models of Dilated Cardiomyopathy or Pressure Overload Hypertrophy

Cooley

Ouyang

McMullen

et al. 2013

Circ: Heart Failure

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Background We investigated the contribution of inositol(1,4,5)trisphosphate (Ins(1,4,5)P3, IP3) receptors (IP3-R) to disease progression in mouse models of dilated cardiomyopathy (DCM) and pressure overload hypertrophy. Mice expressing mammalian sterile 20 like kinase and dominant negative phosphatidylinositol-3-kinase in heart (Mst1 x dn-PI3K-2Tg; DCM-2Tg) develop severe DCM and conduction block, associated with increased expression of IP3-R(2) and heightened generation of Ins(1,4,5)P3. Similar increases in Ins(1,4,5)P3 and IP3-R(2) are caused by thoracic aortic constriction (TAC). Methods and Results To evaluate the contribution of IP3-R(2) to disease progression, the DCM-2Tg mice were further crossed with mice in which the type 2 IP3-R (IP3-R(2)−/−) had been deleted (DCM-2Tg x IP3-R(2) −/−) and TAC was performed on IP3-R(2) −/−mice. Hearts from DCM-2Tg mice and DCM-2Tg x IP3-R(2) −/− were similar in terms of chamber dilatation, atrial enlargement and ventricular wall thinning. Electrophysiological changes were also similar in the DCM-2Tg mice, with and without IP3-R(2). Deletion of IP3-R(2) did not alter the progression of heart failure, as DCM-2Tg mice with and without IP3-R(2) had similarly reduced contractility, increased lung congestion, atrial thrombus and both strains died between 10 and 12 weeks of age. Loss of IP3-R(2) did not alter the progression of hypertrophy following TAC. Conclusions We conclude that IP3-R(2) do not contribute to the progression of DCM or pressure overload hypertrophy despite increased expression and heightened generation of the ligand, Ins(1,4,5)P3.

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Section: Discussionmentioning

confidence: 86%

No Contribution of IP ₃ -R(2) to Disease Phenotype in Models of Dilated Cardiomyopathy or Pressure Overload Hypertrophy

Cooley

Ouyang

McMullen

et al. 2013

Circ: Heart Failure

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“…Although the mechanism causing cardiac hypertrophy in the former two animals is suspected to be in the abnormality of the cardiac cellular membrane [28,29], this is still not clear. The c-myc transgenic mice show cardiac hyperplasty, rather than cardiac hypertrophy.…”

Section: Discussionmentioning

confidence: 99%

Cardiac hypertrophy in juvenile visceral steatosis (jvs) mice with systemic carnitine deficiency

et al. 1993

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We have reported the clinical and biochemical findings in juvenile visceral steatosis (jvs) mice with systemic carnitine deficiency. This paper is the first report about cardiomyopathy injvs mice. Adult jvs mice (at the age of 2 3 months) show cardiac hypertrophy which is caused by enlargement of the cardiac muscle cell associated with increases of non-collagen protein and DNA content. Carnitine administration (2 mg/head, twice a day, from 1 month of age) significantly suppresses the cardiac hypertrophy, showing that carnitine deficiency plays an important role in the development of the cardiac hypertrophy. The discovery of cardiac hypertrophy in carnitine-deficient jvs mice will lead to clarification of the pathophysiology of cardiomyopathy in systemic carnitine deficiency in human beings.Cardiac hypertrophy; Systemic carnitine deficiency; Animal model; Juvenile visceral steatosis mice

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“…In characterized cultured myocardial cell models, several features of hypertrophy can be induced after stimulation with an a-adrenergic agent and endothelin 1 (40)(41)(42)(43) (47). The mechanism causing cardiac hypertrophy in the former two animals is suspected to be the abnormality of the cardiac cellular membrane (48,49) but still remains unclear. Cardiac hypertrophy in juvenile visceral steatosis mice is related to carnitine deficiency because it is curable by carnitine administration (46).…”

Section: Discussionmentioning

confidence: 99%

Continuous activation of gp130, a signal-transducing receptor component for interleukin 6-related cytokines, causes myocardial hypertrophy in mice.

Hirota

Yoshida

Kishimoto

et al. 1995

Proc. Natl. Acad. Sci. U.S.A.

463

258

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To investigate the physiological roles of gpl30 in detail and to determine the pathological consequence of abnormal activation of gpl30, transgenic mice having continuously activated gpl30 were created. This was carried out by mating mice from interleukin 6 (IL-6) and IL-6 receptor (IL-6R) transgenic lines. Offspring overexpressing both IL-6 and IL-6R showed constitutive tyrosine phosphorylation of gpl30 and a downstream signaling molecule, acute phase response factor/signal transducer and activator of transcription 3. Surprisingly, the distinguishing feature of such offspring was hypertrophy of ventricular myocardium and consequent thickened ventricular walls of the heart, where gpl30 is also expressed, in adulthood. Transgenic mice overexpressing either IL-6 or IL-6R alone did not show detectable myocardial abnormalities. Neonatal heart muscle cells from normal mice, when cultured in vitro, enlarged in response to a combination of IL-6 and a soluble form of IL-6R. The results suggest that activation of the gpl30 signaling pathways leads to cardiac hypertrophy and that these signals might be involved in physiological regulation of myocardium. gpl30 was initially identified as a signal-transducing receptor component that associates with the interleukin 6 receptor (IL-6R) when the receptor is occupied with interleukin 6

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Phosphatidylinositol and inositolphosphatide metabolism in hypertrophied rat heart.

Cited by 24 publications

References 32 publications

No Contribution of IP ₃ -R(2) to Disease Phenotype in Models of Dilated Cardiomyopathy or Pressure Overload Hypertrophy

No Contribution of IP ₃ -R(2) to Disease Phenotype in Models of Dilated Cardiomyopathy or Pressure Overload Hypertrophy

Cardiac hypertrophy in juvenile visceral steatosis (jvs) mice with systemic carnitine deficiency

Continuous activation of gp130, a signal-transducing receptor component for interleukin 6-related cytokines, causes myocardial hypertrophy in mice.

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Phosphatidylinositol and inositolphosphatide metabolism in hypertrophied rat heart.

Cited by 24 publications

References 32 publications

No Contribution of IP 3 -R(2) to Disease Phenotype in Models of Dilated Cardiomyopathy or Pressure Overload Hypertrophy

No Contribution of IP 3 -R(2) to Disease Phenotype in Models of Dilated Cardiomyopathy or Pressure Overload Hypertrophy

Cardiac hypertrophy in juvenile visceral steatosis (jvs) mice with systemic carnitine deficiency

Continuous activation of gp130, a signal-transducing receptor component for interleukin 6-related cytokines, causes myocardial hypertrophy in mice.

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No Contribution of IP ₃ -R(2) to Disease Phenotype in Models of Dilated Cardiomyopathy or Pressure Overload Hypertrophy

No Contribution of IP ₃ -R(2) to Disease Phenotype in Models of Dilated Cardiomyopathy or Pressure Overload Hypertrophy