Transduced PEP-1-AMPK inhibits the LPS-induced expression of COX-2 and iNOS in Raw264.7 cells

Shin, Min Jea; Lee, Yeom Pyo; Kim, Dae Won; An, Jung Nam; Jang, Sang Ho; Cho, Sung Min; Sheen, Seung-Hoon; Lee, Hae-Ran; Kweon, HaeYong; Sw, Kang; Lee, Kwang-Gill; Park, Jinseu; Eum, Won Sik; Cho, Yong‐Jun; Choi, Soo Young

doi:10.5483/bmbrep.2010.43.1.040

Cited by 13 publications

(8 citation statements)

References 41 publications

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“…In the tube formation assay of HUVEC cells, both total tube length and the number of branching points were increased in the FFA treatment group compared to the control group and cell proliferation was not significantly affected at the time when tube formation assay was performed. AMP-activated protein kinase (AMPK) is a key regulator of metabolic homeostasis (35) and has anti-inflammatory effects (37,38). In addition, it promotes angiogenesis, and protects cells from apoptosis (39)(40)(41).…”

Section: Discussionmentioning

confidence: 99%

Flufenamic acid promotes angiogenesis through AMPK activation

Tai

et al. 2013

International Journal of Oncology

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Abstract. Angiogenesis plays critical roles in development, tumor growth and metastasis. Flufenamic acid (FFA) is an anti-inflammatory agent known to alter ion fluxes across the plasma membrane. Its role in angiogenesis has not been fully addressed to date. Here, we report that FFA treatment promotes angiogenesis both in vitro and in vivo. Applying FFA for 12 h promoted tube formation of human umbilical vein endothelial cells (HUVECs) without affecting cell proliferation. Three angiogenesis-related genes, VEGF, e-NOS and AAMP, were analyzed by RT-PCR. A significant difference was found between the FFA group and the control; the FFA group had significantly higher mRNA accumulation levels of all the three genes (p<0.05). Moreover, in the chick embryo chorioallantoic membrane (CAM) assay, FFA promoted the formation of macroscopic blood vessels. Finally, western blotting showed that the FFA-treated group had significantly higher phosphorylated AMPK levels, compared with the control (p<0.05). These results suggest that FFA promotes angiogenesis both in vitro and in vivo likely via promoting tube formation through AMPK activation.

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Section: Discussionmentioning

confidence: 99%

Flufenamic acid promotes angiogenesis through AMPK activation

Tai

et al. 2013

International Journal of Oncology

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“…Activation of AMPK also underlies the anti-inflammatory actions of FFA (Pilon et al, 2004;Cheng et al, 2007;Jeong et al, 2009;Aoki et al, 2010;Cai et al, 2010;Shin et al, 2010). A series of studies demonstrated that AMPK mediates the anti-inflammatory effects of a variety of agents, including nicotine, berberine, cilostazol, and adiponectin (Pilon et al, 2004;Cheng et al, 2007;Jeong et al, 2009;Aoki et al, 2010;Cai et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

“…First, AMPK can be activated by Ca 2ϩ through the CaMKK␤ pathway (Stahmann et al, 2006). Second, similar to FFA, AMPK has both anti-inflammatory and channel-regulatory activity (Pilon et al, 2004;Carattino et al, 2005;Cheng et al, 2007;Mace et al, 2008;Jeong et al, 2009;Klein et al, 2009;Kongsuphol et al, 2009;Kréneisz et al, 2009;Aoki et al, 2010;Cai et al, 2010;Shin et al, 2010). For example, both FFA and AMPK have been reported to suppress the inflammatory mediator-induced expression of inducible nitric-oxide synthase (iNOS) (Paik et al, 2000;Aoki et al, 2010) and inhibit sodium channel (Carattino et al, 2005;Yau et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

“…pathways and switches on ATP-producing pathways. In addition to its regulatory functions on cellular metabolic pathways, AMPK has anti-inflammatory effects (Pilon et al, 2004;Cheng et al, 2007;Jeong et al, 2009;Aoki et al, 2010;Cai et al, 2010;Shin et al, 2010). In addition, it promotes angiogenesis, protects cells from apoptosis (Shaw et al, 2004), and modulates a variety of channel activities (Carattino et al, 2005;Mace et al, 2008;Klein et al, 2009;Kongsuphol et al, 2009;Kréneisz et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

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Nonsteroidal Anti-Inflammatory Drug Flufenamic Acid Is a Potent Activator of AMP-Activated Protein Kinase

Chi

Li²,

Yan³

et al. 2011

J Pharmacol Exp Ther

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Flufenamic acid (FFA) is a nonsteroidal anti-inflammatory drug (NSAID). It has anti-inflammatory and antipyretic properties. In addition, it modulates multiple channel activities. The mechanisms underlying the pharmacological actions of FFA are presently unclear. Given that AMP-activated protein kinase (AMPK) has both anti-inflammatory and channel-regulating functions, we examined whether FFA induces AMPK activation. 1) Exposure of several different types of cells to FFA resulted in an elevation of AMPK␣ phosphorylation at Thr172. This effect of FFA was reproduced by functionally and structurally similar mefenamic acid, tolfenamic acid, niflumic acid, and meclofenamic acid. 2) FFA-induced activation of AMPK was largely abolished by the treatment of cells with 1,2-bis(2-aminophenoxy)ethane-N,N,NЈ,NЈ-tetraacetic acid tetrakis(acetoxymethyl ester) (an intracellular Ca 2ϩ chelator) or depletion of extracellular Ca 2ϩ , whereas it was mimicked by stimulation of cells with the Ca

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“…Although the transduction mechanism remains unclear, PTD fusion proteins have been used to deliver therapeutic proteins in vitro and in vivo. We have shown previously that various PTD fusion proteins transduced into neuronal cells cross the blood-brain barrier and efficiently protect against cell death (14)(15)(16)(17)(18)(19)(20). In this study, we investigated the protective effects of PEP-1-p18 against MPP + -induced dopaminergic neuronal cell death and MPTP-induced PD mouse models.…”

Section: Introductionmentioning

confidence: 99%

Transduced PEP-1-AMPK inhibits the LPS-induced expression of COX-2 and iNOS in Raw264.7 cells

Abstract: AMP-activated protein kinase (AMPK) is a heterotrimeric

Cited by 13 publications

References 41 publications

Flufenamic acid promotes angiogenesis through AMPK activation

Flufenamic acid promotes angiogenesis through AMPK activation

Nonsteroidal Anti-Inflammatory Drug Flufenamic Acid Is a Potent Activator of AMP-Activated Protein Kinase

PEP-1-p18 prevents neuronal cell death by inhibiting oxidative stress and Bax expression

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