Synergism of simvastatin with losartan prevents angiotensin II-induced cardiomyocyte apoptosis &lt;I&gt;in vitro&lt;/I&gt;

Xu, Jian; Lu, Xuanyong; Huang, Yan; Zhu, Pengli; Li, Jun

doi:10.1211/jpp/61.04.0013

Cited by 7 publications

(8 citation statements)

References 34 publications

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“…Cardiac myocytes undergo apoptosis in response to a myriad of stimuli including β ‐adrenergic agonists, Ang II, TNF‐ α and so on. Several studies have demonstrated that inhibition of myocardial apoptosis provided beneficial effects on cardiac remodelling and left ventricular function [41–43] . In our study, myocardial apoptosis was obviously induced by isoproterenol injection.…”

Section: Discussionsupporting

confidence: 48%

Icariin attenuates cardiac remodelling through down-regulating myocardial apoptosis and matrix metalloproteinase activity in rats with congestive heart failure

Song

Cai

et al. 2011

Journal of Pharmacy and Pharmacology

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Section: Discussionsupporting

confidence: 48%

Icariin attenuates cardiac remodelling through down-regulating myocardial apoptosis and matrix metalloproteinase activity in rats with congestive heart failure

Song

Cai

et al. 2011

Journal of Pharmacy and Pharmacology

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“…In contrast, the pro-apoptotic factor BAX binds to Bcl-2 and inhibits its protective effect [29]. It is pointed out that Akt is considered to play a central role in cell survival and resistance to apoptosis [30] and an increase in the activity of which has been reported in females [4,31]. We have previously shown that there occurred a downregulation in the Akt dependent survival signal involving Bcl-2 whereas the pro-apoptotic protein BAX was upregulated in the male heart and these alterations may play a role in the occurrence of cardiomyocyte apoptosis seen in heart failure due to volume overload [10].…”

Section: Discussionmentioning

confidence: 99%

“…There are many triggers to induce apoptosis such as angiotensin II (Ang II)/Ang II type 1 receptor (AT 1 R); in fact, Ang II induced a significant increase in BAX protein where Bcl-2 was decreased [34,35]. Losartan and AT 1 receptor blocker alone or in combination with simvastatin blocked the increase in BAX and caused an increase in Bcl-2 [30]. It is also well known that activation of Ang II/AT 1 R pathway can cause an increase in intracellular Ca 2?…”

Section: Discussionmentioning

confidence: 99%

Gender differences in apoptotic signaling in heart failure due to volume overload

2009

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This study examined sex differences in the regulation of pro- and anti-apoptotic proteins in cardiac hypertrophy and heart failure due to volume overload induced by arteriovenous (AV) shunt in rats. General characteristics and hemodynamic assessment revealed the presence of cardiac hypertrophy at 4 weeks of AV shunt in male (n = 12) and female (n = 12) rats, whereas heart failure was seen at 16 weeks in male rats only. Although a decrease in apoptosis was seen in hearts of both sexes at 4 weeks, an increase in apoptosis in males and a reduction in the female heart were observed at 16 weeks of AV shunt. Unlike females, increases in the pro-apoptotic proteins, BAX, caspases 3 and 9 were seen in 16 weeks post-AV shunt in male rats. While an increase in phospho-Bad was detected, phospho-Bcl-2 protein was decreased in males. Females showed an increase in only phospho-Bcl-2 protein at 16 weeks post-AV shunt. Ovariectomy (n = 12) abolished the increase in phospho-Bcl-2 protein, but this was restored by treatment with 17-beta estradiol. These data suggest that downregulation of phospho-Bcl-2 and an upregulation of BAX may play a major role in cardiomyocyte apoptosis in heart failure due to volume overload in male rats. Furthermore, upregulation of phospho-Bcl-2 in the heart due to estrogen may confer resistance against cardiomyocyte apoptosis in females.

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“…The absorbance was measured at a wavelength of 570 nm using a microplate reader (Bio-Tek Instruments Inc., Richmond, Va). Background absorbance of medium in the absence of cells was subtracted [14]. Percent viability was defined as the relative absorbance of treated versus untreated control cells.…”

Section: Methodsmentioning

confidence: 99%

Calcium-sensing receptors regulate cardiomyocyte Ca2+ signaling via the sarcoplasmic reticulum-mitochondrion interface during hypoxia/reoxygenation

Tian

Zhang

et al. 2010

J Biomed Sci

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Communication between the SR (sarcoplasmic reticulum, SR) and mitochondria is important for cell survival and apoptosis. The SR supplies Ca2+ directly to mitochondria via inositol 1,4,5-trisphosphate receptors (IP3Rs) at close contacts between the two organelles referred to as mitochondrion-associated ER membrane (MAM). Although it has been demonstrated that CaR (calcium sensing receptor) activation is involved in intracellular calcium overload during hypoxia/reoxygenation (H/Re), the role of CaR activation in the cardiomyocyte apoptotic pathway remains unclear. We postulated that CaR activation plays a role in the regulation of SR-mitochondrial inter-organelle Ca2+ signaling, causing apoptosis during H/Re. To investigate the above hypothesis, cultured cardiomyocytes were subjected to H/Re. We examined the distribution of IP3Rs in cardiomyocytes via immunofluorescence and Western blotting and found that type 3 IP3Rs were located in the SR. [Ca2+]i, [Ca2+]m and [Ca2+]SR were determined using Fluo-4, x-rhod-1 and Fluo 5N, respectively, and the mitochondrial membrane potential was detected with JC-1 during reoxygenation using laser confocal microscopy. We found that activation of CaR reduced [Ca2+]SR, increased [Ca2+]i and [Ca2+]m and decreased the mitochondrial membrane potential during reoxygenation. We found that the activation of CaR caused the cleavage of BAP31, thus generating the pro-apoptotic p20 fragment, which induced the release of cytochrome c from mitochondria and the translocation of bak/bax to mitochondria. Taken together, these results reveal that CaR activation causes Ca2+ release from the SR into the mitochondria through IP3Rs and induces cardiomyocyte apoptosis during hypoxia/reoxygenation.

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Synergism of simvastatin with losartan prevents angiotensin II-induced cardiomyocyte apoptosis <I>in vitro</I>

Abstract: Our data provide the first evidence that synergism of simvastatin with losartan prevents angiotensin II-induced cardiomyocyte apoptosis in vitro. Synergism between simvastatin and losartan may provide a new therapeutic approach to the prevention of cardiac remodelling.

Cited by 7 publications

References 34 publications

Icariin attenuates cardiac remodelling through down-regulating myocardial apoptosis and matrix metalloproteinase activity in rats with congestive heart failure

Icariin attenuates cardiac remodelling through down-regulating myocardial apoptosis and matrix metalloproteinase activity in rats with congestive heart failure

Gender differences in apoptotic signaling in heart failure due to volume overload

Calcium-sensing receptors regulate cardiomyocyte Ca2+ signaling via the sarcoplasmic reticulum-mitochondrion interface during hypoxia/reoxygenation

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