Docosahexaenoic acid induces ERK1/2 activation and neuritogenesis via intracellular reactive oxygen species production in human neuroblastoma SH-SY5Y cells

Wu, Hai‐Tao; Ichikawa, Sanae; Tani, Chiharu; Zhu, Beiwei; Tada, Mikiro; Shimoishi, Yasuaki; Murata, Yoshiyuki; Nakamura, Yoshimasa

doi:10.1016/j.bbalip.2008.10.004

Cited by 48 publications

(44 citation statements)

References 72 publications

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“…Wu et al demonstrated that ROS can enhance protein tyrosine kinase activity to regulate ERK1/2 phosphorylation in neuroblastoma in vitro. 41 Chen et al also reported that activation of protein phosphatases (eg, PP2A or PP5) can inhibit hydrogen peroxide-induced ERK1/2 phosphorylation in neuronal cells. 42 However, in our study, we showed that ROS accumulation inhibited ERK1/2 activation in the NTS and induced hypertension.…”

Section: Discussionmentioning

confidence: 99%

Angiotensin II Inhibits Neuronal Nitric Oxide Synthase Activation Through the ERK1/2-RSK Signaling Pathway to Modulate Central Control of Blood Pressure

Cheng

et al. 2010

Circulation Research

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Rationale: Angiotensin (Ang) II exerts diverse physiological actions in both the peripheral and central neural systems. It was reported that the activity of Ang II is higher in the nucleus tractus solitarii (NTS) of spontaneously hypertensive rats (SHRs) and that angiotensin type-1 receptors are colocalized with NAD(P)H oxidase in the neurons of the NTS, resulting in the induction of local reactive oxygen species production by Ang II. However, the signaling mechanisms of Ang II that induce hypertension remain unclear. Objective: The aim of this study was to investigate the possible signaling pathways involved in Ang II-mediated blood pressure regulation in the NTS. Methods and Results: Male SHRs were treated with losartan or tempol for 2 weeks, after which systolic blood pressure was observed to decrease significantly. Dihydroethidium staining showed many cells with high reactive oxygen species in the NTS of SHRs. The addition of losartan or tempol decreased the numbers of reactive oxygen species-positive cells in the NTS. The systemic administration of losartan or tempol reduced the systolic blood pressure and increased NO production. Immunoblotting and immunohistochemical analysis further showed that inhibition of Ang II activity by losartan or tempol significantly increased the expression extracellular signal-regulated kinase (ERK)1/2, ribosomal protein S6 kinase (RSK), and also increased neuronal NO synthase (nNOS) phosphorylation. RSK was also found to bind directly to nNOS and induce phosphorylation at the Ser1416 position. Conclusions: Taken together, these results suggest that the ERK1/2-RSK-nNOS signaling pathway may play a significant role in Ang II-mediated central blood pressure regulation. (Circ Res. 2010;106:788-795.)Key Words: angiotensin II Ⅲ nucleus tractus solitarii Ⅲ neuronal nitric oxide synthase Ⅲ ribosomal protein S6 kinase Ⅲ reactive oxygen species T he nucleus tractus solitarii (NTS), which is located in the dorsal medulla of the brain stem, is the primary site of termination of the vagus and glossopharyngeal nerves. The NTS participates in cardiovascular, gastric, and gustatory control. Our previous studies demonstrated that several neuromodulators are involved in cardiovascular control of the NTS, including ATP, 1 adenosine, 2 neuropeptide Y, 3 angiotensin (Ang) II, 4 NO, 5 carbon monoxide, 6 and insulin. 7 Ang II is a powerful vasoconstrictor in the peripheral blood system that exerts effects on the central nervous system, regulating fluid balance and the secretion of aldosterone. Hyperactivity of Ang II has been shown to play a major role in hypertension. 8,9 Ang II is produced from enzymatic cleavage of angiotensinogen by renin and then by angiotensin converting enzyme. These pathological and physiological actions of Ang II are mediated through its type 1 receptor (AT 1 R). 10 Recent evidence suggests that hyperactivity of the brain renin-angiotensin system may play a critical role in mediating hypertension in spontaneously hypertensive rats (SHRs). 11 Significant differences in AT 1...

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Section: Discussionmentioning

confidence: 99%

Angiotensin II Inhibits Neuronal Nitric Oxide Synthase Activation Through the ERK1/2-RSK Signaling Pathway to Modulate Central Control of Blood Pressure

Cheng

et al. 2010

Circulation Research

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“…GAP-43 is mainly localized in neurites and induces neurite outgrowth ( 32,33 ), and EPA and DHA in free fatty acid form stimulate GAP-43 mRNA expression in neuroblastoma cells ( 34 ). LpE (AA), LpE (EPA), and LpE (DHA) increased GAP-43 mRNA expression in neurons ( Fig.…”

Section: Discussionmentioning

confidence: 99%

“…EPA and DHA in free fatty acid form increase GAP-43 mRNA expression in the SH-SY5Y human neuroblastoma cells ( 34 ), and neurons take up lipids contained in LpE via internalization of LpE secreted from glial cells ( 10 ). We used quantitative RT-PCR to examine GAP-43 mRNA expression in whether inhibition of LpE uptake abrogates the effects of LpE on neurite outgrowth, we incubated neurons with LpE for 24 h in the presence or absence of cytochalasin D ( Fig.…”

Section: Fatty Acid Composition Of Phospholipids In Lpe Affects Gene mentioning

confidence: 99%

Neurite outgrowth stimulation by n-3 and n-6 PUFAs of phospholipids in apoE-containing lipoproteins secreted from glial cells

Nakato

Matsuo

Kono

et al. 2015

Journal of Lipid Research

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“…Wu et al [37] demonstrated that ROS can enhance protein tyrosine kinase activity to regulate extracellular signal-regulated kinase (ERK1/2 phosphorylation in neuroblastoma in vitro). Chen et al [38] also reported that activation of protein phosphatases (e.g. PP2A or PP5) can inhibit hydrogen peroxide-induced ERK1/2 phosphorylation in neuronal cells.…”

Section: The Erk1/2-rsk-nnos Signaling Pathwaymentioning

confidence: 99%

Angiotensin-II Induced Reactive Oxygen Species: Implications in Neurogenic Hypertension

Lu¹

2012

J Hypertens

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Docosahexaenoic acid induces ERK1/2 activation and neuritogenesis via intracellular reactive oxygen species production in human neuroblastoma SH-SY5Y cells

Cited by 48 publications

References 72 publications

Angiotensin II Inhibits Neuronal Nitric Oxide Synthase Activation Through the ERK1/2-RSK Signaling Pathway to Modulate Central Control of Blood Pressure

Angiotensin II Inhibits Neuronal Nitric Oxide Synthase Activation Through the ERK1/2-RSK Signaling Pathway to Modulate Central Control of Blood Pressure

Neurite outgrowth stimulation by n-3 and n-6 PUFAs of phospholipids in apoE-containing lipoproteins secreted from glial cells

Angiotensin-II Induced Reactive Oxygen Species: Implications in Neurogenic Hypertension

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