Upregulation of cytochrome P450 2J3/11,12-epoxyeicosatrienoic acid inhibits apoptosis in neonatal rat cardiomyocytes by a caspase-dependent pathway

Wang, Hongxia; Zhang, Dongmei; Zhang, Xiangjun; Mu, Jing; Yang, Hui; Lü, Ling; Zhang, Like

doi:10.1016/j.cyto.2012.04.029

Cited by 17 publications

(8 citation statements)

References 39 publications

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“…CYP2J3 overexpression prevented the formation of arrhythmogenic substrates by maintaining gap junction integrity and reducing the development of atrial fibrosis in cardiac hypertrophy [16] . The upregulation of CYP2J3/11,12-EETs during ischemic post-conditioning (HPost) induced cardioprotection by inhibiting apoptosis via the mitochondrial pathway [18] . In the CYP2J3-expressing SHR rats, systolic blood pressure was significantly decreased, cardiac output was improved, cardiac collagen content was reduced, and ANP was increased in the myocardium and plasma [36] .…”

Section: Resultsmentioning

confidence: 99%

“…Accumulating evidence suggests that EETs have crucial and diverse protective roles within the cardiovascular system. Specifically, EETs have been reported to possess antiarrhythmic [16] , anti-inflammatory [17] , anti-apoptotic [18] , and antioxidant [19] functions. Additionally, CYP2J3 overexpression and increased levels of EETs have been reported to decrease ER stress signaling and ER stress-mediated apoptosis in rats with heart failure by maintaining SERCA2a activity and intracellular Ca 2+ homeostasis [20] .…”

Section: +mentioning

confidence: 99%

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Ophiopogonin D maintains Ca2+ homeostasis in rat cardiomyocytes in vitro by upregulating CYP2J3/EETs and suppressing ER stress

You

Zhou

et al. 2016

Acta Pharmacol Sin

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Section: Resultsmentioning

confidence: 99%

Section: +mentioning

confidence: 99%

Ophiopogonin D maintains Ca2+ homeostasis in rat cardiomyocytes in vitro by upregulating CYP2J3/EETs and suppressing ER stress

You

Zhou

et al. 2016

Acta Pharmacol Sin

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“…Protein samples were prepared from C2C12 cells and soleus muscle tissue, and western blot analysis was performed as described [24]. In total, 50µg protein was loaded on SDS-PAGE gels, transferred to PVDF membrane and incubated with primary antibodies Anti-AKT (1:1000), anti-phospho-AKT (1:800), anti-PKC (1:1000), anti-phospho-PKC (1:800), anti-ERK1/2(1:1000), anti-phospho-ERK1/2 (1:800), anti-gp91-phox (1:500), anti-p67-phox (1:500), anti-p47-phox (1:500), anti-p40-phox (1:500), anti-p22-phox (1:500) or GLUT4 (1:200).…”

Section: Methodsmentioning

confidence: 99%

Urotensin II Inhibits Skeletal Muscle Glucose Transport Signaling Pathways via the NADPH Oxidase Pathway

Wang

Yang

et al. 2013

PLoS ONE

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Our previous studies have demonstrated that the urotensin (UII) and its receptor are up-regulated in the skeletal muscle of mice with type II diabetes mellitus (T2DM), but the significance of UII in skeletal muscle insulin resistance remains unknown. The purpose of this study was to investigate the effect of UII on NADPH oxidase and glucose transport signaling pathways in the skeletal muscle of mice with T2DM and in C2C12 mouse myotube cells. KK/upj-AY/J mice (KK) mice were divided into the following groups: KK group, with saline treatment for 2 weeks; KK+ urantide group, with daily 30 µg/kg body weight injections over the same time period of urantide, a potent urotensin II antagonist peptide; Non-diabetic C57BL/6J mice were used as normal controls. After urantide treatment, mice were subjected to an intraperitoneal glucose tolerance test, in addition to measurements of the levels of ROS, NADPH oxidase and the phosphorylated AKT, PKC and ERK. C2C12 cells were incubated with serum-free DMEM for 24 hours before conducting the experiments, and then administrated with 100 nM UII for 2 hours or 24 hours. Urantide treatment improved glucose tolerance, decreased the translocation of the NADPH subunits p40-phox and p47-phox, and increased levels of the phosphorylated PKC, AKT and ERK. In contrast, UII treatment increased ROS production and p47-phox and p67-phox translocation, and decreased the phosphorylated AKT, ERK1/2 and p38MAPK; Apocynin abrogated this effect. In conclusion, UII increased ROS production by NADPH oxidase, leading to the inhibition of signaling pathways involving glucose transport, such as AKT/PKC/ERK. Our data imply a role for UII at the molecular level in glucose homeostasis, and possibly in skeletal muscle insulin resistance in T2DM.

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“…The main rat homologs, CYP2J3 and CYP2J4, have 72% and 76% sequence similar to human CYP2J2, and have a similar tissue distribution to human. Furthermore, CYP2J3 is reported to be found primarily within atrial and ventricular myocytes (Wu et al, 1997;Zhang et al, 1997), whereas increased expression of CYP2J3 in the heart after ischemic postconditioning significantly increased EET generation (Wang et al, 2012), suggesting that CYP2J3 may have epoxygenase activity analogous to CYP2J2. Therefore, rat CYP2J3 may be the closest homologous enzyme to CYP2J2 in terms of distribution and epoxygenase activity and may be applicable to investigations of cardiotoxicity.…”

Section: Animal Homologs Of Cyp2j2 To Investigate Preclinical Drug-inmentioning

confidence: 99%

Cytochrome P450 2J2: Potential Role in Drug Metabolism and Cardiotoxicity

et al. 2018

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Drug-induced cardiotoxicity may be modulated by endogenous arachidonic acid (AA)-derived metabolites known as epoxyeicosatrienoic acids (EETs) synthesized by cytochrome P450 2J2 (CYP2J2). The biologic effects of EETs, including their protective effects on inflammation and vasodilation, are diverse because, in part, of their ability to act on a variety of cell types. In addition, CYP2J2 metabolizes both exogenous and endogenous substrates and is involved in phase 1 metabolism of a variety of structurally diverse compounds, including some antihistamines, anticancer agents, and immunosuppressants. This review addresses current understanding of the role of CYP2J2 in the metabolism of xenobiotics and endogenous AA, focusing on the effects on the cardiovascular system. In particular, we have promoted here the hypothesis that CYP2J2 influences drug-induced cardiotoxicity through potentially conflicting effects on the production of protective EETs and the metabolism of drugs.

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Upregulation of cytochrome P450 2J3/11,12-epoxyeicosatrienoic acid inhibits apoptosis in neonatal rat cardiomyocytes by a caspase-dependent pathway

Cited by 17 publications

References 39 publications

Ophiopogonin D maintains Ca2+ homeostasis in rat cardiomyocytes in vitro by upregulating CYP2J3/EETs and suppressing ER stress

Ophiopogonin D maintains Ca2+ homeostasis in rat cardiomyocytes in vitro by upregulating CYP2J3/EETs and suppressing ER stress

Urotensin II Inhibits Skeletal Muscle Glucose Transport Signaling Pathways via the NADPH Oxidase Pathway

Cytochrome P450 2J2: Potential Role in Drug Metabolism and Cardiotoxicity

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