Abstract
Fucoidan, a sulfated polysaccharide extracted from brown seaweed, has been used in traditional Chinese herbal medicine to treat thyroid tumors for many years. Although a number of its cellular effects have been investigated, the role of fucoidan in molecular signaling, particularly in Ca2+ signaling, remains largely unknown. In the present study, the effects of fucoidan on Ca2+ responses in HeLa cells, human umbilical vein endothelial cells and astrocytes were investigated using a wide range of receptor agonists. Fucoidan inhibited the increase in intracellular free calcium concentration that was induced by histamine, ATP, compound 48/80 and acetylcholine. The responses induced by the same agonists in the absence of extracellular Ca2+ were also markedly suppressed by fucoidan. Reverse transcription-polymerase chain reaction demonstrated that 0.5 and 1.0 mg/ml fucoidan treatment for 3 h decreased histamine receptor 1 expression in HeLa cells. Similarly, the expressions of purinergic receptor P2Y, G-protein coupled (P2YR)1, P2YR2 and P2YR11 were significantly downregulated within cells pretreated with 1.0 mg/ml fucoidan for 3 h, and 0.5 mg/ml fucoidan significantly inhibited P2YR1 and P2YR11 expression. The results demonstrated that fucoidan may exert a wide spectrum of inhibitory effects on Ca2+ responses and that fucoidan may inhibit a number of different G-protein coupled receptors associated with Ca2+ dynamics.
Highlights
IntroductionIt has a chain structure similar to that of heparin [1,2]
Fucoidan is a sulfated polysaccharide extracted from brown seaweed
Our results demonstrate that fucoidan exerts a wide spectrum of inhibitory effects on Ca2+ responses and inhibits various G‐protein coupled receptors related to Ca2+ dynamics, suggesting that fucoidan inhibits Ca2+ signaling by directly inhibiting G‐protein coupled receptors
Summary
It has a chain structure similar to that of heparin [1,2] It exerts various biological activities including anticoagulation and inhibition of cell proliferation [3,4,5,6,7]. Several newly identified T‐type calcium channel blockers have been shown to be able to inhibit the growth of human cancer cells by blocking Ca2+ influx into the cells [15], a process that affects cell cycle progression and cell proliferation. These blockers are potential therapeutic agents for the tumors that depend on T‐type calcium channel to grow [16]. These studies suggest that calcium signaling may participate in tumorigenesis and targeting their signaling could have therapeutic values
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