17β-Estradiol reduces cardiac hypertrophy mediated through the up-regulation of PI3K/Akt and the suppression of calcineurin/NF-AT3 signaling pathways in rats

Wu, Chieh Hsi; Liu, Jer Yuh; Wu, Jia; Hsieh, Yi‐Hsien; Liu, Chung‐Jung; Hwang, Jin Ming; Lee, Shin-Da; Chen, Li Mien; Chang, Mu Hsin; Kuo, Wei Wen; Shyu, Jyh Cherng; Tsai, Jer‐Chia; Huang, Chih Yang

doi:10.1016/j.lfs.2005.04.077

Cited by 28 publications

(27 citation statements)

References 36 publications

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“…The recovery of the heart from OVX-PO-induced cardiac injury is likely mediated by the increased eNOS expression and/or phosphorylation. Our results are consistent with inhibition of cardiac hypertrophy by 17β-estradiol in OVX-PO female rats (77), in which upregulation of PI3-K /Akt and suppression of calcineurin/NF-AT3 mediated the 17β-estradiol effects. In this context, we should examine the calcineurin/NF-AT3 signaling in the VO(OPT)-treated heart in the future.…”

Section: +supporting

confidence: 90%

Cardioprotection by Vanadium Compounds Targeting Akt-Mediated Signaling

Bhuiyan

Fukunaga

2009

J Pharmacol Sci

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Abstract. Treatment with inorganic and organic compounds of vanadium has been shown to exert a wide range of cardioprotective effects in myocardial ischemia/reperfusion-induced injury, myocardial hypertrophy, hypertension, and vascular diseases. Furthermore, administration of vanadium compounds improves cardiac performance and smooth muscle cell contractility and modulates blood pressure in various models of hypertension. Like other vanadium compounds, we documented bis(1-oxy-2-pyridinethiolato) oxovanadium (IV) [VO(OPT)] as a potent cardioprotective agent to elicit cardiac functional recovery in myocardial infarction and pressure overload-induced hypertrophy. Vanadium compounds activate Akt signaling through inhibition of protein tyrosine phosphatases, thereby eliciting cardioprotection in myocardial ischemia / reperfusion-induced injury and myocardial hypertrophy. Vanadium compounds also promote cardiac functional recovery by stimulation of glucose transport in diabetic heart. We here discuss the current understanding of mechanisms underlying vanadium compound-induced cardioprotection and propose a novel therapeutic strategy targeting for Akt signaling to rescue cardiomyocytes from heart failure.

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Section: +supporting

confidence: 90%

Cardioprotection by Vanadium Compounds Targeting Akt-Mediated Signaling

Bhuiyan

Fukunaga

2009

J Pharmacol Sci

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“…Meanwhile, it is also known that females have higher nuclear localization of phosphorylated-Akt and higher Akt activity in myocardium [21]. Interestingly, E2 has demonstrated to enhance the activation of Akt and to improve survival in murine cardiomyocytes [5,7,21]. More studies have identified that ERα specifically mediate the E2 induced activation of PI3K/Akt signaling pathway in vascular endothelial cells [22][23][24].…”

Section: Discussionmentioning

confidence: 99%

“…17β-estradiol (E2) has been shown to reduce cardiomyocyte apoptosis through activating phospho-inositide-3-kinase (PI3K)/Akt signaling in ovariectomized rats [5]. Previous studies in this lab also demonstrated that 17β-estradiol (E2) could prevent ovariectomy-induced cardiac hypertrophy, Fas-dependent and mitochondria-dependent apoptotic pathways in rat models [6,7].…”

Section: Introductionmentioning

confidence: 97%

17β-Estradiol and/or Estrogen Receptor β Attenuate the Autophagic and Apoptotic Effects Induced by Prolonged Hypoxia Through HIF-1α-Mediated BNIP3 and IGFBP-3 Signaling Blockage

Hsieh

Kuo

Lai

et al. 2015

Cell Physiol Biochem

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Background/Aims: The risk of heart disease is higher in males than in females. However, this advantage of females declines with increasing age, presumably a consequence of decreased estrogen secretion and malfunctioning of the estrogen receptor. We previously demonstrated that 17β-estradiol (E2) prevents cardiomyocyte hypertrophy, autophagy and apoptosis via estrogen receptor α (ERα), but the effects of ERβ on myocardial injury remained elusive. The present paper thus, investigated the cardioprotective effects of estrogen (E2) and ERβ against hypoxia-induced cell death. Methods: Transient transfection of Tet-On ERβ gene construct was used to overexpress ERβ in hypoxia-treated H9c2 cardiomyoblast cells. Results: Our data revealed that IGF1R, Akt phosphorylation and Bcl-2 expression are enhanced by ERβ in H9c2 cells. Moreover, ERβ overexpression reduced accumulation of hypoxia-related proteins, autophagy-related proteins and mitochondria-apoptotic proteins and enhanced the protein levels of Bcl-2, pAkt and Bad under hypoxic condition. In neonatal rat ventricular myocytes (NRVMs), we observed that hypoxia induced cell apoptosis as measured by TUNEL staining, and E2 and/or ERβ could totally abolish hypoxia-induced apoptosis. The suppressive effects of E2 and/or ERβ in hypoxia-treated NRVMs were totally reversed by ER antagonist, ICI. Taken together, E2 and/or ERβ exert the protective effect through repressed hypoxia-inducible HIF-1α, BNIP3 and IGFBP-3 levels to restrain the hypoxia-induced autophagy and apoptosis effects in H9c2 cardiomyoblast cells. Conclusion: The results suggest that females probably could tolerate better prolonged hypoxia condition than males, and E2/ERβ treatment could be a potential therapy to prevent hypoxia-induced heart damage.”

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“…Our recent studies have shown that MFG-E8 is downregulated in septic mice [15] and that a deficiency in MFG-E8 is harmful in sepsis [17]. Investigators MFG-E8 exerts its effects, looking at the MAPK and NF-jB signaling pathways [28], CD14 or TLR4 [15], fractalkine [29], Akt [29][30][31][32], and osteopontin (OPN) [33]. However, the exact mechanism is unknown.…”

Section: Discussionmentioning

confidence: 99%