Luteolin Suppresses the Differentiation of THP-1 Cells through the Inhibition of NOX2 mRNA Expression and the Membrane Translocation of p47phox

Makino, Junya; Nakanishi, Ryohei; Kamiya, Tetsuro; Hara, Hirokazu; Ninomiya, Masayuki; Koketsu, Mamoru; Adachi, Tetsuo

doi:10.1021/np400224w

Cited by 19 publications

(26 citation statements)

References 34 publications

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“…These results are consistent with our previous findings, in which luteolin exhibited potent radical scavenger activity and significantly suppressed monocytic differentiation into macrophages. 25) These results indicate that luteolin maintains good redox homeostasis, particularly in extracellular spaces.…”

Section: Discussionmentioning

confidence: 88%

“…Luteolin functions as an inhibitor of TPA-induced monocytic differentiation 25) and oxidized low-density lipoprotein-elicited EC-SOD decreases in human vascular smooth cells. 51) In the present study, we tested whether some flavonoids suppress CoCl 2 -elicited decreases in EC-SOD, and found that luteolin exerted a potent inhibitory effect against this phenomenon.…”

Section: Discussionmentioning

confidence: 99%

“…[22][23][24] We previously reported that luteolin significantly suppressed phorbol ester (TPA)-induced human monocytic differentiation into macrophages, and these events were closely associated with the inhibition of intracellular ROS signaling. 25) Accordingly, some flavonoids may be seed compounds that maintain redox homeostasis.…”

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confidence: 99%

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CoCl2 Decreases EC-SOD Expression through Histone Deacetylation in COS7 Cells

Hattori

Kamiya

Hara

et al. 2016

Biological & Pharmaceutical Bulletin

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Extracellular-superoxide dismutase (EC-SOD), one of the SOD isozymes, is negatively regulated under hypoxic conditions, and decreases in its expression may exacerbate vascular diseases. Moreover, epigenetics, such as DNA methylation and histone modifications, are known to play a critical role in the progression of cancer, type 2 diabetes, and atherosclerosis. We previously investigated the involvement of reactive oxygen species (ROS) and p38 mitogen-activated protein kinase (MAPK) in decreases in EC-SOD expression in hypoxic COS7 cells; however, the role of epigenetics in this process currently remains unknown. In the present study, we demonstrated that the hypoxia mimetic cobalt chloride (CoCl 2 ) decreased histone acetylation levels, and a pretreatment with 4-phenyl butyric acid (PBA), an inhibitor of histone deacetylase, significantly suppressed CoCl 2 -elicited histone deacetylation and decreases in EC-SOD. We found that CoCl 2 -elicited decreases in EC-SOD were accompanied by reductions in histone H3 acetylation levels within its promoter region. Furthermore, luteolin, a well-known flavonoid, significantly suppressed the CoCl 2 -elicited accumulation of ROS, p38-MAPK activation, and histone deacetylation. Collectively, the results of the present study showed for the first time that CoCl 2 decreases the expression of EC-SOD through its deacetylation and luteolin may be one of the seed compounds that maintain redox homeostasis, even under hypoxic conditions.

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Section: Discussionmentioning

confidence: 88%

Section: Discussionmentioning

confidence: 99%

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CoCl2 Decreases EC-SOD Expression through Histone Deacetylation in COS7 Cells

Hattori

Kamiya

Hara

et al. 2016

Biological & Pharmaceutical Bulletin

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“…B). We previously reported that luteolin suppressed monocytic THP‐1 differentiation [Makino et al, ]. Therefore, the effects of luteolin on oxLDL‐elicited reductions in EC‐SOD expression were investigated.…”

Section: Resultsmentioning

confidence: 99%

Suppression of EC‐SOD by oxLDL During Vascular Smooth Muscle Cell Proliferation

Makino

Asai

Hashimoto

et al. 2016

J of Cellular Biochemistry

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Reactive oxygen species (ROS) produced by endothelial cells and macrophages play important roles in atherogenesis because they promote the formation of oxidized low-density lipoproteins (oxLDL). Extracellular-superoxide dismutase (EC-SOD) is mainly produced by vascular smooth muscle cells (VSMCs), is secreted into the extracellular space, and protects cells from the damaging effects of the superoxide anion. Thus, the expression of EC-SOD in VSMCs is crucial for protecting cells against atherogenesis; however, oxLDL-induced changes in the expression of EC-SOD in VSMCs have not yet been examined. We herein showed that oxLDL decreased EC-SOD mRNA and protein levels by binding to lectin-like oxidized LDL receptor-1 (LOX-1). Moreover, we demonstrated the significant role of mitogen-activated protein kinase (MEK)/extracellular-regulated protein kinase (ERK) signaling in oxLDL-elicited reductions in the expression of EC-SOD and proliferation of VSMCs. The results obtained with the FCS treatment indicate that oxLDL-elicited reductions in the expression of EC-SOD are related to the proliferation of VSMCs. We herein showed for the first time that luteolin, a natural product, restored oxLDL-induced decreases in the expression of EC-SOD and proliferation of VSMCs. Collectively, the results of the present study suggest that oxLDL accelerates the development of atherosclerosis by suppressing the expression of EC-SOD and also that luteolin has potential as a treatment for atherosclerosis. J. Cell. Biochem. 117: 2496-2505, 2016. © 2016 Wiley Periodicals, Inc.

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“…(34,35) It has been reported that CAPE is decomposed into caffeic acid and phenethyl alcohol by intracellular esterase, and caffeic acid with catechol skeleton possess anti-oxidative properties. (8,36) We recently reported that a treatment with CAPE suppressed monocyte adhesion to endothelial cells by inhibiting the accumulation of intracellular ROS.…”

Section: Discussionmentioning

confidence: 99%

CAPE increases the expression of SOD3 through epigenetics in human retinal endothelial cells

Ohashi

Yasuda

Kamiya

et al. 2017

J. Clin. Biochem. Nutr.

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Extracellular-superoxide dismutase (EC-SOD or SOD3), which catalyzes the dismutation of superoxide anions into hydrogen peroxide, plays a key role in vascular protection against reactive oxygen species (ROS). The excess generation of ROS is closely involved in the pathogenesis of diabetic retinopathy (DR); therefore, the maintenance of SOD3 expression at high levels is important for the prevention of DR. In the present study, we showed that caffeic acid phenethyl ester (CAPE) increased the expression of SOD3 through the acetylation of histone within the SOD3 promoter region in human retinal endothelial cells (HRECs). Histone acetylation within its promoter was focused on the inhibition of histone deacetylase (HDAC), and we examined the involvement of myocyte enhancer factor 2 (MEF2) and HDAC1 in CAPE-elicited SOD3 expression. Our results demonstrate that SOD3 silencing in basal HRECs is regulated by HDAC1 composed with MEF2A/2D hetero dimers. Moreover, phosphorylation of threonine 312 in MEF2A and dissociation of HDAC1 from SOD3 promoter play pivotal roles in CAPE-elicited SOD3 expression. Overall, our findings provide that CAPE may be one of the seed compounds that maintain redox homeostasis.

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Luteolin Suppresses the Differentiation of THP-1 Cells through the Inhibition of NOX2 mRNA Expression and the Membrane Translocation of p47^phox

Cited by 19 publications

References 34 publications

CoCl<sub>2</sub> Decreases EC-SOD Expression through Histone Deacetylation in COS7 Cells

CoCl<sub>2</sub> Decreases EC-SOD Expression through Histone Deacetylation in COS7 Cells

Suppression of EC‐SOD by oxLDL During Vascular Smooth Muscle Cell Proliferation

CAPE increases the expression of SOD3 through epigenetics in human retinal endothelial cells

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