Activation of JNK/c-Jun is required for the proliferation, survival, and angiogenesis induced by EET in pulmonary artery endothelial cells

Ma, Jun; Zhang, Lei; Han, Wei-Na; Shen, Tingting; Ma, Cui; Liu, Yun; Nie, Xiaowei; Liu, Mengmeng; Ran, Yajuan; Zhu, Daling

doi:10.1194/jlr.m024398

Cited by 68 publications

(52 citation statements)

References 39 publications

(38 reference statements)

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“…c-Jun can transduce a variety of signals from the external environment, and is activated by phosphorylation, which then lead cells to adapt to external stimuli. It has been reported that c-Jun plays a positive role in angiogenesis [18]. Therefore, it is reasonable to speculate that c-Jun may act as an index of proliferation of SMCs after exposure to CSE.…”

Section: Cse Can Induce Proliferation Of Smcsmentioning

confidence: 98%

The p-ERK–p-c-Jun–cyclinD1 pathway is involved in proliferation of smooth muscle cells after exposure to cigarette smoke extract

Song

et al. 2014

Biochemical and Biophysical Research Communications

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Section: Cse Can Induce Proliferation Of Smcsmentioning

confidence: 98%

The p-ERK–p-c-Jun–cyclinD1 pathway is involved in proliferation of smooth muscle cells after exposure to cigarette smoke extract

Song

et al. 2014

Biochemical and Biophysical Research Communications

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“…2B). 33 Kandhi et al 65 demonstrated that jugular administration of EET led to an increase in RVSP in a dose-dependent manner. Thus, the effect of EET on RVSP seems synergic with hypoxia.…”

Section: Role Of Other Metabolites Of Aa In Pahmentioning

confidence: 99%

Role of Oxidized Lipids in Pulmonary Arterial Hypertension

et al. 2016

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Pulmonary arterial hypertension (PAH) is a multifactorial disease characterized by interplay of many cellular, molecular, and genetic events that lead to excessive proliferation of pulmonary cells, including smooth muscle and endothelial cells; inflammation; and extracellular matrix remodeling. Abnormal vascular changes and structural remodeling associated with PAH culminate in vasoconstriction and obstruction of pulmonary arteries, contributing to increased pulmonary vascular resistance, pulmonary hypertension, and right ventricular failure. The complex molecular mechanisms involved in the pathobiology of PAH are the limiting factors in the development of potential therapeutic interventions for PAH. Over the years, our group and others have demonstrated the critical implication of lipids in the pathogenesis of PAH. This review specifically focuses on the current understanding of the role of oxidized lipids, lipid metabolism, peroxidation, and oxidative stress in the progression of PAH. This review also discusses the relevance of apolipoprotein A-I mimetic peptides and microRNA-193, which are known to regulate the levels of oxidized lipids, as potential therapeutics in PAH.

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“…Bodiga et al, 2009;Chen et al, 2009Chen et al, , 2011Ma et al, 2010Ma et al, , 2012Batchu et al, 2011;Liu et al, 2011;Zhao et al, 2012) suggests that the renoprotective properties of sEH inhibition might also be related to their effects on cisplatin-induced apoptosis. The antiapoptotic effects of EETs have been linked to phosphoinositide 3-kinase/protein kinase B and MAPK signaling pathways (Yang et al, 2007;Dhanasekaran et al, 2008;Chen et al, 2009Chen et al, , 2011Batchu et al, 2011;Liu et al, 2011;Zhao et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Epoxyeicosatrienoic Acids Prevent Cisplatin-Induced Renal Apoptosis through a p38 Mitogen-Activated Protein Kinase–Regulated Mitochondrial Pathway

et al. 2013

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Soluble epoxide hydrolase (sEH) catalyzes the conversion of epoxyeicosatrienoic acids into less active eicosanoids, and inhibitors of sEH have anti-inflammatory and antiapoptotic properties. Based on previous observations that sEH inhibition attenuates cisplatin-induced nephrotoxicity by modulating nuclear factor-kB signaling, we hypothesized that this strategy would also attenuate cisplatin-induced renal apoptosis. Inhibition of sEH with AR9273 [1-adamantan-1-yl-3-(1-methylsulfonyl-piperidin-4-ylurea)] reduced cisplatin-induced apoptosis through mechanisms involving mitochondrial apoptotic pathways and by reducing reactive oxygen species. Renal mitochondrial Bax induction following cisplatin treatment was significantly decreased by treatment of mice with AR9273 and these antiapoptotic effects involved p38 mitogen-activated protein kinase signaling. Similar mechanisms contributed to reduced apoptosis in Ephx2 2/2 mice treated with cisplatin. Moreover, in pig kidney proximal tubule cells, cisplatin-induced mitochondrial trafficking of Bax and cytochrome c, caspase-3 activation, and oxidative stress are significantly attenuated in the presence of epoxyeicosatrienoic acids (EETs). Collectively, these in vivo and in vitro studies demonstrate a role for EETs in limiting cisplatin-induced renal apoptosis. Inhibition of sEH represents a novel therapeutic strategy for protection against cisplatin-induced renal damage.

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Activation of JNK/c-Jun is required for the proliferation, survival, and angiogenesis induced by EET in pulmonary artery endothelial cells

Cited by 68 publications

References 39 publications

The p-ERK–p-c-Jun–cyclinD1 pathway is involved in proliferation of smooth muscle cells after exposure to cigarette smoke extract

The p-ERK–p-c-Jun–cyclinD1 pathway is involved in proliferation of smooth muscle cells after exposure to cigarette smoke extract

Role of Oxidized Lipids in Pulmonary Arterial Hypertension

Epoxyeicosatrienoic Acids Prevent Cisplatin-Induced Renal Apoptosis through a p38 Mitogen-Activated Protein Kinase–Regulated Mitochondrial Pathway

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