Survivin mediates the anti-apoptotic effect of δ-opioid receptor stimulation in cardiomyocytes

Yao, Lingling; Wang, Yonggang; Cai, Wenjie; Tai, Yang; Zhu, Yi‐Chun

doi:10.1242/jcs.03393

Cited by 36 publications

(29 citation statements)

References 27 publications

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“…Our data are consistent with results in cells exposed to ciglitazone in A172 human glioma cells [49]. It has been reported that ERK or Akt can be an upstream regulator of XIAP and survivin [50][51][52]. However, whether ERK and Akt are involved in regulating XIAP and survivin in glioma cells remains to be further elucidated.…”

Section: Discussionsupporting

confidence: 91%

Kaempferol Induces Cell Death Through ERK and Akt-Dependent Down-Regulation of XIAP and Survivin in Human Glioma Cells

Jeong

Kim

et al. 2008

Neurochem Res

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The present study was undertaken to determine the molecular mechanism by which kaempferol induces cell death in human glioma cells. Kaempferol resulted in loss of cell viability and inhibition of proliferation in a dose- and time-dependent manner, which were largely attributed to cell death. Kaempferol caused an increase in reactive oxygen species (ROS) generation and the kaempferol-induced cell death was prevented by antioxidants, suggesting that ROS generation is involved in kaempferol-induced cell death. Kaempferol caused depolarization of mitochondrial membrane potential. Western blot analysis showed that kaempferol treatment caused a rapid reduction in phosphorylation of extracellular signal-regulated kinase (ERK) and Akt. The ERK inhibitor U0126 and the Akt inhibitor LY984002 increased the kaempferol-induced cell death and overexpression of MEK, the upstream kinase of ERK, and Akt prevented the cell death. The expression of anti-apoptotic proteins XIAP and survivin was down-regulated by kaempferol and its effect was prevented by overexpression of MEK and Akt. Kaempferol induced activation of caspase-3 and kaempferol-induced cell death was prevented by caspase inhibitors. Taken together, these findings suggest that kaempferol results in human glioma cell death through caspase-dependent mechanisms involving down-regulation of XIAP and survivin regulating by ERK and Akt.

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Section: Discussionsupporting

confidence: 91%

Kaempferol Induces Cell Death Through ERK and Akt-Dependent Down-Regulation of XIAP and Survivin in Human Glioma Cells

Jeong

Kim

et al. 2008

Neurochem Res

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“…Yao et al (33) reported that activation of the δ-opioid receptor reduces the apoptosis of myocardial cells through inhibition of the ERK and IP3 pathways. Furthermore, Huang et al (34) reported that activation of the δ-opioid receptor inhibits apoptosis by promoting CGRP expression in myocardial cells.…”

Section: Discussionmentioning

confidence: 99%

Activation of the δ-opioid receptor inhibits serum deprivation-induced apoptosis of human liver cells via the activation of PKC and the mitochondrial pathway

Wang¹

2011

Int J Mol Med

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Abstract. Apoptosis of human liver cells is commonly found in liver diseases and liver surgery and directly affects their prognosis. Recent studies have found that δ-opioid receptors, abundant in the membranes of hepatic cells, participate in the oncogenesis and progression of liver tumors, viral hepatitis, liver cirrhosis and other diseases. The purpose of this study was to analyze the effect of the activation of the δ-opioid receptor on liver cell apoptosis and explore its relationship with PKC and the mitochondrial pathway. Hepatic cells were serum-deprived to induce apoptosis in vitro. During the period of apoptosis, mitochondrial membrane potential decreased, protein levels of cytosolic cytochrome c increased and the expression of Bcl-2 decreased, indicating that apoptosis was specifically induced by the mitochondrial pathway. Importantly, activation of δ-opioid receptors reversed the apoptotic state of hepatic cells. Following δ-opioid receptor activation, the mitochondrial membrane potential remained stable, and the expression of cytosolic cytochrome c and Bax decreased. These data suggest that δ-opioid receptor activation specifically inhibits the mitochondrial apoptotic pathway. In addition, activation of the δ-opioid receptor apparently increased the levels of PKC; blocking the PKC pathway led to increased apoptosis of liver cells, which was not affected by the activation of δ-opioid receptor. Blocking the PKC pathway led to increased apoptosis of liver cells, which was associated with δ-opioid receptor activation. Therefore, the PKC pathway is involved in the anti-apoptotic effects of the δ-opioid receptor on liver cells.

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“…The pellet was resuspended into 30 µL of cold lysis buffer (at pH 7.5, in mmol/ L, 20 Tris, 100 NaCl, 1% Triton X-100) supplemented with 1% protease inhibitor cocktail. The supernatant was further centrifuged at 100,000 g for 60 min at 4°C, and the resultant supernatant was collected as the cytosolic fraction [16,17].…”

Section: Western Blottingmentioning

confidence: 99%

DIDS Attenuates Staurosporine-induced Cardiomyocyte Apoptosis by PI3K/Akt Signaling Pathway: Activation of eNOS/NO and Inhibition of Bax Translocation

Liu

Cao

Liu

et al. 2008

Cell Physiol Biochem

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Aims: 4,4''-diisothiocyanostilbene-2,2''-disulfonic acid (DIDS), a non-selective chloride channel blocker, has been shown to prevent cell apoptosis, however, the underlying mechanisms remain undefined, thus the present study was to explore whether phosphatidylinositol 3''-kinase (PI3K)/Akt and its downstream molecules are involved in the cytoprotective effect of DIDS. Methods: Neonatal rat cardiomyocytes were exposed to staurosporine (STS) in the presence or absence of DIDS. Cell viability, apoptosis and expressions of Akt, phospho-Akt (p-Akt), eNOS, phospho-eNOS (p-eNOS), Bcl-2/Bax and nitric oxide (NO) production were determined, and Bax translocation was assessed by double immunofluorescence labeling and Western blotting. Results: DIDS markedly improved cell viability and exerted an anti-apoptotic effect on STS-exposed cardiomyocytes. DIDS resulted in a 2.1-fold increase of p-Akt over control levels, prevented the reduction in eNOS expression and phospho-eNOS levels induced by STS and significantly increased NO production (all P<0.01 vs. STS alone). Treatment with LY294002, a selective PI3K inhibitor, abolished DIDS-induced increases in p-Akt, eNOS, p-eNOS and NO production, and completely abrogated the DIDS-induced anti-apoptotic effect (P<0.01). Treatment with L-NAME, a non-selective NOS inhibitor similarly inhibited the increased NO but only partly abolished protective effects of DIDS (P<0.05). In addition, DIDS effectively inhibited STS-induced Bax translocation to mitochondria, which was also reversed by LY294002. Conclusion: DIDS protects cardiomyocytes against STS-induced apoptosis via activating PI3K/Akt signaling pathway, including increasing eNOS phosphorylation and the subsequent NO production and inhibiting Bax translocation.

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Survivin mediates the anti-apoptotic effect of δ-opioid receptor stimulation in cardiomyocytes

Cited by 36 publications

References 27 publications

Kaempferol Induces Cell Death Through ERK and Akt-Dependent Down-Regulation of XIAP and Survivin in Human Glioma Cells

Kaempferol Induces Cell Death Through ERK and Akt-Dependent Down-Regulation of XIAP and Survivin in Human Glioma Cells

Activation of the δ-opioid receptor inhibits serum deprivation-induced apoptosis of human liver cells via the activation of PKC and the mitochondrial pathway

DIDS Attenuates Staurosporine-induced Cardiomyocyte Apoptosis by PI3K/Akt Signaling Pathway: Activation of eNOS/NO and Inhibition of Bax Translocation

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