Roles of insulin-like growth factor II in cardiomyoblast apoptosis and in hypertensive rat heart with abdominal aorta ligation

Lee, Shin-Da; Chu, Chun Hsien; Huang, Erh Jung; Lü, Min; Liu, Jer Yuh; Liu, Chung‐Jung; Hsu, Hsi Hsien; Lin, James A.; Kuo, Wei Wen; Huang, Chih Yang

doi:10.1152/ajpendo.00127.2005

Cited by 98 publications

(114 citation statements)

References 22 publications

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“…These results suggested that the apoptotic effect of ANG II might be caused by activation of the IGF-IIR signaling cascade. 10,28 In this study, we have demonstrated that JNK1/2 activation positively regulated IGF-IIR gene expression. IGF-IIR, whose expression was enhanced, translocated to the plasma membrane and sensitized IGF-II to induce apoptosis.…”

Section: Discussionmentioning

confidence: 50%

“…These results indicate that the different kinases regulated IGF-IIR via distinct mechanisms and that primarily JNK participated in the ANG II-induced upregulation of IGF-IIR gene expression, consistent with our previous studies. 10 To demonstrate that JNK activation was involved in IGF-IIR gene expression, the JNK activator anisomycin was used to challenge H9c2 cells. As shown in Figure 3a, the expression of IGF-IIR was gradually enhanced by anisomycin in a dosedependent manner.…”

Section: Resultsmentioning

confidence: 99%

“…7,8 Our previous studies found that the upregulation of the IGF-II and IGF-IIR genes is essential for ANG II-induced cell apoptosis and correlates with the promotion of cardiomyocyte apoptosis in hypertensive rat hearts. [9][10][11][12][13] However, the detailed mechanisms underlying IGF-IIR gene regulation and the upregulation of IGF-IIR expression by ANG II remain unknown.…”

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confidence: 99%

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ANG II promotes IGF-IIR expression and cardiomyocyte apoptosis by inhibiting HSF1 via JNK activation and SIRT1 degradation

Huang

et al. 2014

Cell Death Differ

115

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Hypertension-induced cardiac hypertrophy and apoptosis are major characteristics of early-stage heart failure. Our previous studies found that the activation of insulin-like growth factor receptor II (IGF-IIR) signaling was critical for hypertensive angiotensin II (ANG II)-induced cardiomyocyte apoptosis. However, the detailed mechanism by which ANG II regulates IGF-IIR in heart cells remains elusive. In this study, we found that ANG II activated its downstream kinase JNK to increase IGF-IIR expression through the ANG II receptor angiotensin type 1 receptor. JNK activation subsequently led to sirtuin 1 (SIRT1) degradation via the proteasome, thus preventing SIRT1 from deacetylating heat-shock transcription factor 1 (HSF1). The resulting increase in the acetylation of HSF1 impaired its ability to bind to the IGF-IIR promoter region (nt À 748 to À 585). HSF1 protected cardiomyocytes by acting as a repressor of IGF-IIR gene expression, and ANG II diminished this HSF1-mediated repression through enhanced acetylation, thus activating the IGF-IIR apoptosis pathway. Taken together, these results suggest that HSF1 represses IGF-IIR gene expression to protect cardiomyocytes. ANG II activates JNK to degrade SIRT1, resulting in HSF1 acetylation, which induces IGF-IIR expression and eventually results in cardiac hypertrophy and apoptosis. HSF1 could be a valuable target for developing treatments for cardiac diseases in hypertensive patients. Apoptosis has been implicated in a wide variety of cardiovascular disorders, including myocardial infarction and heart failure, suggesting that activation of apoptotic pathways contributes to cardiomyocyte loss and subsequently cardiac dysfunction. Previous studies reported that several extracellular molecules, such as insulin-like growth factors (IGFs) and angiotensin II (ANG II), are involved in the development of cardiac hypertrophy and apoptosis.

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Section: Discussionmentioning

confidence: 50%

Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

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ANG II promotes IGF-IIR expression and cardiomyocyte apoptosis by inhibiting HSF1 via JNK activation and SIRT1 degradation

Huang

et al. 2014

Cell Death Differ

115

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“…When cytochrome c is released from mitochondria into cytosol, it is responsible for activating caspase-9, which further activates caspase-3 and executes the apoptotic program (9). One of our previous studies showed that longer duration of nocturnal sustained hypoxia at 0-, 4-, and 8-wk periods appeared to exert more deleterious effects on Fas and mitochondrial-dependent apoptotic pathways in Sprague-Dawley rats (20,21). The increased cardiac apoptosis was found in leptin-deficient and leptin-resistant mice (6), implying that leptin-signaling impairments may lead to cardiac apoptosis.…”

mentioning

confidence: 98%

“…Apoptosis, a physiological program of cellular death, may contribute to many cardiac disorders (16,20). The occurrence of apoptosis has been reported to contribute to the loss of cardiomyocytes in cardiomyopathies and is recognized as a predictor of adverse outcomes in subjects with cardiac diseases or heart failure (27).…”

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confidence: 99%

The coexistence of nocturnal sustained hypoxia and obesity additively increases cardiac apoptosis

Lee

Kuo

Bau

et al. 2008

Journal of Applied Physiology

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. The coexistence of nocturnal sustained hypoxia and obesity additively increases cardiac apoptosis. J Appl Physiol 104: 1144-1153, 2008. First published January 17, 2008 doi:10.1152 doi:10. /japplphysiol.00152.2007 nocturnal sustained hypoxia during sleeping time has been reported in severe obesity, but no information regarding the cardiac molecular mechanism in the coexistence of nocturnal sustained hypoxia and obesity is available. This study evaluates whether the coexistence of nocturnal sustained hypoxia and obesity will increase cardiac Fas death receptor and mitochondrial-dependent apoptotic pathway. Methods: 32 lean and 32 obese 5-to 6-mo-old rats with or without nocturnal sustained hypoxia were studied and assigned to one of four subgroups: normoxia lean (NL), normoxia obese (NO), hypoxia lean (HL, 12% O2 for 8 h and 21% O2 16 h/day, 1 wk), and hypoxia obese (HO). The heart weight index, tail cuff plethysmography, echocardiography, hematoxylin-eosin staining, TUNEL assays, Western blotting, and RT-PCR were performed. Results: systolic and diastolic blood pressures in HO were higher than those in NL, and fractional shortening in HO was reduced compared with others. The whole heart weight, the left ventricular weight, the abnormal myocardial architecture, and TUNEL-positive apoptotic cells, as well as the activity of cardiac Fas-dependent and mitochondrial-dependent apoptotic pathway, were significantly increased in obese group or nocturnal sustained hypoxia group and were further increased when obesity and nocturnal sustained hypoxia coexisted, the evidence for which is based on decreases in an anti-apoptotic protein Bcl2 level and Bid and increases in Fas, FADD, pro-apoptotic Bad, BNIP3, cytosolic cytochrome c, activated caspase-8, activated caspase-9, and activated caspase-3. Conclusions: The cardiac Fas receptor-and mitochondrial-dependent apoptotic pathways were more activated in obesity with coexistent nocturnal sustained hypoxia, which may represent one possible apoptotic mechanism for the development of heart failure in obesity with nocturnal sustained hypoxia.

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Reversible Mechanical Induction of Optical Activity in Solutions of Soft‐Matter Nanophases

Arteaga

Escudero

Oncins

et al. 2009

Chemistry An Asian Journal

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Nanophases of J-aggregates of several achiral amphiphilic porphyrins, which have thin long acicular shapes (nanoribbons), show the immediate and reversible formation of a stationary mechano-chiral state in the solution by vortex stirring, as detected by their circular dichroic signals measured by 2-modulator generalized ellipsometry. The results suggest that when a macroscopic chiral force creates supramolecular chirality, it also creates an enantiomeric excess of screw distortions, which may be detected by their excitonic absorption. An explanation on the effect of the shear flow gradients is proposed on the basis of the orientation of the rotating particles in the vortex and the size, shape, and mechanical properties of the nanoparticles.

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Roles of insulin-like growth factor II in cardiomyoblast apoptosis and in hypertensive rat heart with abdominal aorta ligation

Cited by 98 publications

References 22 publications

ANG II promotes IGF-IIR expression and cardiomyocyte apoptosis by inhibiting HSF1 via JNK activation and SIRT1 degradation

ANG II promotes IGF-IIR expression and cardiomyocyte apoptosis by inhibiting HSF1 via JNK activation and SIRT1 degradation

The coexistence of nocturnal sustained hypoxia and obesity additively increases cardiac apoptosis

Reversible Mechanical Induction of Optical Activity in Solutions of Soft‐Matter Nanophases

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