Δ‐opioid Receptor Stimulation Enhances the Growth of Neonatal Rat Ventricular Myocytes via the Extracellular Signal‐regulated Kinase Pathway

Zhao, Min; Wang, Hongxin; Yang, Jing; Su, Yuhong; Su, Rongjian; Wong, Tak Ming

doi:10.1111/j.1440-1681.2007.04831.x

Cited by 12 publications

(13 citation statements)

References 48 publications

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“…In the opioid receptor superfamily, the δ receptor is closely associated with the viability and proliferation of cells (32,33). As demonstrated in previous studies, the activation of the δ receptor promotes the proliferation of rat ventricular muscle cells (34,35). In the current study, alpinetin was administered to rat myocardial cells, leading to an increase in the expression level of the δ receptor, a significant reduction in the myocardial apoptosis rate and an increase in cell proliferation.…”

Section: Discussionsupporting

confidence: 73%

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Alpinetin activates the δ receptor instead of the κ and μ receptor pathways to protect against rat myocardial cell apoptosis

Suo¹,

Sun

Yang³

2013

Experimental and Therapeutic Medicine

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Alpinetin is a natural flavonoid that protects cells against fatal injury in ischemia-reperfusion. δ receptor activation protects myocardial cells from trauma; however, the mechanism is unknown. The aim of this study was to explore the function of alpinetin in δ receptor-mediated myocardial apoptosis. The myocardial cells of newly born rats were cultivated and myocardial apoptosis was induced by serum deprivation. The MTT method was used to evaluate cell viability and Annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) staining was used to analyze apoptosis. The expression levels of opioid receptor mRNA and protein were tested using reverse transcription-polymerase reaction (RT-PCR) and western blot assays. In addition, an opioid receptor antagonist, as well as protein kinase C (PKC) and extracellular signal-regulated kinase (ERK) inhibitors, were used to determine the inferred signaling pathway. The results showed that that alpinetin reduced the myocardial apoptosis induced by serum deprivation in a concentration-dependent manner. However, the protection conferred to the myocardial cells by alpinetin was blocked by the δ opioid receptor antagonist naltrindole, as well as by PKC and ERK inhibitors (GF109203X and U0126, respectively). In addition, it was shown that alpinetin was able to maintain the stability of the mitochondrial membrane potential, lower the level of intracytoplasmic cytochrome c and reduce Bax displacement from the cytoplasm to the mitochondria. It was concluded that alpinetin was able to activate δ receptors to induce the endogenous protection of myocardial cells via the PKC/ERK signaling pathway.

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Section: Discussionsupporting

confidence: 73%

“…It was demonstrated in a previous study that the δ receptor acted via the ERK signaling pathway to promote the survival and proliferation of cells (35). In this study, we proposed that alpinetin exerted its protective effects on the rat myocardial cells by exciting the δ receptor to activate PKC, leading to the further activation of ERK.…”

Section: Discussionmentioning

confidence: 99%

Alpinetin activates the δ receptor instead of the κ and μ receptor pathways to protect against rat myocardial cell apoptosis

Suo¹,

Sun

Yang³

2013

Experimental and Therapeutic Medicine

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“…In addition, Zhao et al (37) found that opioid receptors promote cell survival and proliferation via the ERK1/2 pathway. We determined that the activation of the δ-opioid receptor enhances PKC expression.…”

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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“…Activation of cardiac G-protein coupled delta opioid receptors (DOR) induces an intracellular kinase pathway in which activation of mitochondrial ATP-sensitive K + -channels seem to play an important role [8][9][10]. In addition, DOR activation triggers different mechanisms at multiple levels to stabilize homeostasis, to increase pro-survival signaling and antioxidative capacity, and to stimulate the growth of neonatal rat ventricular myocytes [11][12][13].…”

Section: Introductionmentioning

confidence: 99%

Cellular localization and adaptive changes of the cardiac delta opioid receptor system in an experimental model of heart failure in rats

et al. 2015

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The role of the cardiac opioid system in congestive heart failure (CHF) is not fully understood. Therefore, this project investigated the cellular localization of delta opioid receptors (DOR) in left ventricle (LV) myocardium and adaptive changes in DOR and its endogenous ligand, the precursor peptide proenkephalin (PENK), during CHF. Following IRB approval, DOR localization was determined by radioligand binding using [H(3)]Naltrindole and by double immunofluorescence confocal analysis in the LV of male Wistar rats. Additionally, 28 days following an infrarenal aortocaval fistula (ACF) the extent of CHF and adaptions in left ventricular DOR and PENK expression were examined by hemodynamic measurements, RT-PCR, and Western blot. DOR specific membrane binding sites were identified in LV myocardium. DOR were colocalized with L-type Ca(2+)-channels (Cav1.2) as well as with intracellular ryanodine receptors (RyR) of the sarcoplasmatic reticulum. Following ACF severe congestive heart failure developed in all rats and was accompanied by up-regulation of DOR and PENK on mRNA as well as receptor proteins representing consecutive adaptations. These findings might suggest that the cardiac delta opioid system possesses the ability to play a regulatory role in the cardiomyocyte calcium homeostasis, especially in response to heart failure.

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Δ‐opioid Receptor Stimulation Enhances the Growth of Neonatal Rat Ventricular Myocytes via the Extracellular Signal‐regulated Kinase Pathway

Cited by 12 publications

References 48 publications

Alpinetin activates the δ receptor instead of the κ and μ receptor pathways to protect against rat myocardial cell apoptosis

Alpinetin activates the δ receptor instead of the κ and μ receptor pathways to protect against rat myocardial cell apoptosis

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

Cellular localization and adaptive changes of the cardiac delta opioid receptor system in an experimental model of heart failure in rats

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