AMPK activation inhibits apoptosis and tau hyperphosphorylation mediated by palmitate in SH-SY5Y cells

Kim, Juhae; Park, Youn‐Jin; Jang, Yumi; Kwon, Young Hye

doi:10.1016/j.brainres.2011.08.059

Cited by 43 publications

(41 citation statements)

References 54 publications

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“…1). Our investigation group as well as others have reported that palmitic acid increases ER stress response in cortical neurons (Camacho et al, 2012), in SH-SY5Y cells (Kim et al, 2011) and in hypothalamic cell line (Mayer and Belsham, 2010). Conversely, the monounsaturated C:16:9 lipid, palmitoleic acid seems to be well tolerated on neuronal death susceptibility versus its saturated form palmitic acid (Delint-Ramirez et al, 2015).…”

Section: Discussionmentioning

confidence: 63%

Saturated lipids decrease mitofusin 2 leading to endoplasmic reticulum stress activation and insulin resistance in hypothalamic cells

Díaz¹,

Fuentes-Mera²,

Tovar³

et al. 2015

Brain Research

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Section: Discussionmentioning

confidence: 63%

Saturated lipids decrease mitofusin 2 leading to endoplasmic reticulum stress activation and insulin resistance in hypothalamic cells

Díaz¹,

Fuentes-Mera²,

Tovar³

et al. 2015

Brain Research

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“…In fact, a recent study showed that AMPK activity significantly increased in Quercetin-treated AD model mice, resulting in less learning and memory deficits, reduced senile plaques, and mitochondrial dysfunction (Wang et al, 2014). Also, activation of AMPK significantly inhibited ER stress, resulting in reduced tau hyperphosphorylation in human neuroblastoma cells SH-SY5Y treated with palmitate (Kim et al, 2011).…”

Section: Discussionmentioning

confidence: 94%

Nutraceutical activators of AMPK/Sirt1 axis inhibit viral production and protect neurons from neurodegenerative events triggered during HSV-1 infection

et al. 2015

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“…Rossi and Lord describe that AICAR treatment decreases the neutrophil apoptosis through the AMPK activation, suggesting an important role of AMPK in normal function of neutrophils (45). Similarly, Kim et al demonstrate that AICAR reduces the palmitate-induced apoptosis in neuron cells by activation of AMPK (46).…”

Section: R E S E a R C H A R T I C L Ementioning

confidence: 96%

“…Oberholzer and colleagues suggested that targeting signaling pathways that lead to apoptosis would represent a new therapeutic target for the patient with sepsis or other related clinical conditions (34). By systemic administration, AICAR has been shown to decrease the apoptosis in different cells associated with various disease conditions (44)(45)(46). Rossi and Lord describe that AICAR treatment decreases the neutrophil apoptosis through the AMPK activation, suggesting an important role of AMPK in normal function of neutrophils (45).…”

Section: R E S E a R C H A R T I C L Ementioning

confidence: 99%

Stimulation of Brain AMP-Activated Protein Kinase Attenuates Inflammation and Acute Lung Injury in Sepsis

Mulchandani

Yang

Khan

et al. 2015

Mol Med

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Sepsis and septic shock are enormous public health problems with astronomical financial repercussions on health systems worldwide. The central nervous system (CNS) is closely intertwined in the septic process but the underlying mechanism is still obscure. AMP-activated protein kinase (AMPK) is a ubiquitous energy sensor enzyme and plays a key role in regulation of energy homeostasis and cell survival. In this study, we hypothesized that activation of AMPK in the brain would attenuate inflammatory responses in sepsis, particularly in the lungs. Adult C57BL/6 male mice were treated with 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR, 20 ng), an AMPK activator, or vehicle (normal saline) by intracerebroventricular (ICV) injection, followed by cecal ligation and puncture (CLP) at 30 min post-ICV. The septic mice treated with AICAR exhibited elevated phosphorylation of AMPKα in the brain along with reduced serum levels of aspartate aminotransferase, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6), compared with the vehicle. Similarly, the expressions of TNF-α, IL-1β, keratinocyte-derived chemokine and macrophage inflammatory protein-2 as well as myeloperoxidase activity in the lungs of AICAR-treated mice were significantly reduced. Moreover, histological findings in the lungs showed improvement of morphologic features and reduction of apoptosis with AICAR treatment. We further found that the beneficial effects of AICAR on septic mice were diminished in AMPKα2 deficient mice, showing that AMPK mediates these effects. In conclusion, our findings reveal a new functional role of activating AMPK in the CNS to attenuate inflammatory responses and acute lung injury in sepsis.

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AMPK activation inhibits apoptosis and tau hyperphosphorylation mediated by palmitate in SH-SY5Y cells

Cited by 43 publications

References 54 publications

Saturated lipids decrease mitofusin 2 leading to endoplasmic reticulum stress activation and insulin resistance in hypothalamic cells

Saturated lipids decrease mitofusin 2 leading to endoplasmic reticulum stress activation and insulin resistance in hypothalamic cells

Nutraceutical activators of AMPK/Sirt1 axis inhibit viral production and protect neurons from neurodegenerative events triggered during HSV-1 infection

Stimulation of Brain AMP-Activated Protein Kinase Attenuates Inflammation and Acute Lung Injury in Sepsis

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