Zeaxanthin inhibits PDGF‐BB‐induced migration in human dermal fibroblasts

Wu, Nan-Lin; Chiang, Yuh-Chiau; Huang, Chieh-Chen; Fang, Jia‐You; Chen, Der-Fang; Hung, Chi‐Feng

doi:10.1111/j.1600-0625.2009.01036.x

Cited by 36 publications

(28 citation statements)

References 37 publications

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“…There is a report that zeaxanthin can inhibit PDGF-BB-induced migration in human dermal fibroblasts. The authors concluded that zeaxanthin affects cellular components but does not directly interact with PDGF-BB [34]. In our system, zeaxanthin was found to inhibit PDGF-BB-induced PDGFR and PLCγ activation; however surprisingly it only marginally affected Akt, ERK1/2, and p38 MAPK activation (Figure 8).…”

Section: Discussionmentioning

confidence: 52%

A naturally occurring carotenoid, lutein, reduces PDGF and H2O2 signaling and compromises migration in cultured vascular smooth muscle cells

Tsou

et al. 2012

J Biomed Sci

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BackgroundPlatelet-derived growth factor (PDGF) is a potent stimulator of growth and motility of vascular smooth muscle cells (VSMCs). Abnormalities of PDGF/PDGF receptor (PDGFR) are thought to contribute to vascular diseases and malignancy. We previously showed that a carotenoid, lycopene, can directly bind to PDGF and affect its related functions in VSMCs. In this study we examined the effect of the other naturally occurring carotenoid, lutein, on PDGF signaling and migration in VSMCs.MethodsWestern blotting was performed to examine PDGF and H2O2 signaling. Flowcytometry was used to determine PDGF binding to VSMCs. Fluorescence microscopy was performed to examine intracellular ROS production. Modified Boyden chamber system (Transwell apparatus) was used for migration assay.ResultsLutein reduced PDGF signaling, including phosphorylation of PDGFR-β and its downstream protein kinases/enzymes such as phospholipase C-γ, Akt, and mitogen-activated protein kinases (MAPKs). Although lutein possesses a similar structure to lycopene, it was striking that lutein inhibited PDGF signaling through a different way from lycopene in VSMCs. Unlike lycopene, lutein not only interacted with (bound to) PDGF but also interfered with cellular components. This was evidenced that preincubation of PDGF with lutein and treatment of VSMCs with lutein followed by removing of lutein compromised PDGF-induced signaling. Lutein reduced PDGF-induced intracellular reactive oxygen species (ROS) production and attenuated ROS- (H2O2-) induced ERK1/2 and p38 MAPK activation. A further analysis indicated lutein could inhibit a higher concentration of H2O2-induced PDGFR signaling, which is known to act through an oxidative inhibition of protein tyrosine phosphatase. Finally, we showed that lutein functionally inhibited PDGF-induced VSMC migration, whereas its stereo-isomer zeaxanthin did not, revealing a special action of lutein on VSMCs.ConclusionsOur study reveals a differential action mechanism of lutein from other reported caroteinoids and suggests a possible beneficial effect of lutein but not zeaxanthin on prevention of vascular diseases.

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Section: Discussionmentioning

confidence: 52%

A naturally occurring carotenoid, lutein, reduces PDGF and H2O2 signaling and compromises migration in cultured vascular smooth muscle cells

Tsou

et al. 2012

J Biomed Sci

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“…In order to know if the antiproliferative activity of F4 was due to the presence of zeaxanthin, the antiproliferative activity of standard zeaxanthin (Sigma-Aldrich, Saint-Quentin Fallavier, France) was studied in A-2058 melanoma cells. This study revealed that 100 µg·mL −1 zeaxanthin induced 38.4% ± 4.2% growth inhibition at 72 h ( n = 4, p = 0.0245, statistically significant in the t test ), demonstrating for the first time the antimelanoma activity of zeaxanthin, complementary to its already known ability to inhibit PDGF-induced migration of dermal fibroblasts in the skin [15]. This value was coherent with the antiproliferative activity of the F4 fraction (34.4% ± 0.2% growth inhibition at 72 h at 100 µg·mL −1 ).…”

Section: Resultsmentioning

confidence: 96%

Antiproliferative Activity of Cyanophora paradoxa Pigments in Melanoma, Breast and Lung Cancer Cells

et al. 2013

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The glaucophyte Cyanophora paradoxa (Cp) was chemically investigated to identify pigments efficiently inhibiting malignant melanoma, mammary carcinoma and lung adenocarcinoma cells growth. Cp water and ethanol extracts significantly inhibited the growth of the three cancer cell lines in vitro, at 100 µg·mL−1. Flash chromatography of the Cp ethanol extract, devoid of c-phycocyanin and allophycocyanin, enabled the collection of eight fractions, four of which strongly inhibited cancer cells growth at 100 µg·mL−1. Particularly, two fractions inhibited more than 90% of the melanoma cells growth, one inducing apoptosis in the three cancer cells lines. The detailed analysis of Cp pigment composition resulted in the discrimination of 17 molecules, ten of which were unequivocally identified by high resolution mass spectrometry. Pheophorbide a, β-cryptoxanthin and zeaxanthin were the three main pigments or derivatives responsible for the strong cytotoxicity of Cp fractions in cancer cells. These data point to Cyanophora paradoxa as a new microalgal source to purify potent anticancer pigments, and demonstrate for the first time the strong antiproliferative activity of zeaxanthin and β-cryptoxanthin in melanoma cells.

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“…By far the main reported role for zeaxanthin in human health is in ocular health, where, together with lutein, zeaxanthin provides protection against age-related macular degeneration [ 67 , 68 ]. In addition, potential antitumor properties have been described for zeaxanthin [ 69 ]. Furthermore, it was recently found that meso-zeaxanthin has an inhibitory effect on the mutagenicity of fi ve mutagenic agents, including nitro-ophenylenediamine and N -methyl-N ′-nitro-N -nitrosoguanidine [ 70 ].…”

Section: Lutein [ β ( Beta ) ε ( Epsilon )-Carotene -3 3′ -Diol ]mentioning

confidence: 99%