http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Yangmi Kim,Wun-Jae Kim,Eun-Jong Cha 대한생리학회-대한약리학회 2011 The Korean Journal of Physiology & Pharmacology Vol.15 No.5
Quercetin (3,3 ,4 ,5,7-pentahydroxyflavone) is an attractive therapeutic flavonoid for cancer treatment because of its beneficial properties including apoptotic, antioxidant, and antiproliferative effects on cancer cells. However, the exact mechanism of action of quercetin on ion channel modulation is poorly understood in bladder cancer 253J cells. In this study, we demonstrated that large conductance Ca<sup>2+</sup>- activated K<sup>+</sup> (BK<sub>Ca</sub>) or MaxiK channels were functionally expressed in 253J cells, and quercetin increased BK<sub>Ca</sub> current in a concentration dependent and reversible manner using a whole cell patch configuration. The half maximal activation concentration (IC<sub>50</sub>) of quercetin was 45.5±7.2ՌM. The quercetin-evoked BK<sub>Ca</sub> current was inhibited by tetraethylammonium (TEA; 5 mM) a non-specific BK<sub>Ca</sub> blocker and iberiotoxin (IBX; 100 nM) a BK<sub>Ca</sub>-specific blocker. Quercetin-induced membrane hyper</SUB>polarization was measured by fluorescence-activated cell sorting (FACS) with voltage sensitive dye, bis (1,3-dibutylbarbituric acid) trimethine oxonol (DiBAC<sub>4</sub>(3); 100 nM). Quercetin-evoked hyperpolarization was prevented by TEA. Quercetin produced an antiproliferative effect (30.3±13.5%) which was recovered to 53.3±10.5% and 72.9±3.7% by TEA and IBX, respectively. Taken together our results indicate that activation of BK<sub>Ca</sub> channels may be considered an important target related to the action of quercetin on human bladder cancer cells.
Yangmi Kim, Kyung Sun Park 충북대학교 동물의학연구소 2013 Journal of Biomedical and Translational Research Vol.14 No.2
Bladder cancer is a common cancer in smoking men and may correlate with mechanosensitive potassium channels because the urinary bladder is a stretch sensing organ. Two-pore K+ channels (K2P), such as TASK3 and TREK1, have recently been shown to play a critical role in both cell apoptosis and tumorigenesis. Of the channels, TREK1 can be activated by many physiological stimuli, including polyunsaturated fatty acids, and intracellular pH, hypoxia, and neurotransmitters. Here we attempted to determine whether TREK1 is functionally expressed in bladder cancer 253J cells. K2P channels, including TREK1, TREK2, TASK1, TASK3, and TWIK1, were quantified in cultured human bladder cancer 253J cells using real time quantitative RT-PCR (qRT-PCR) analysis. Among them, TREK1-like channel was recorded at a single channel level using the patch-clamp technique. The TREKl-like channel, with single-channel conductance of ~90 pS at −80 mV, was recorded in symmetrical 150 mM KCl using an excised inside-out patch configuration. The current-voltage relationships were linear and were insensitive to tetraethylammonium. The channel was activated by membrane stretch, free fatty acids, and intracellular acidosis. These results with electrophysiological properties resemble to those of K2P channel, for instance, TREK1. Therefore, we conclude that TREK1 channel is functionally present in bladder cancer 253J cells.
Lim, Yangmi,Jo, Dong Hyun,Kim, Jin Hyoung,Ahn, Jin-Hyung,Hwang, Yu Kyeong,Kang, Dong-Ku,Chang, Soo-Ik,Yu, Young Suk,Yoon, Yeup,Kim, Jeong Hun American Diabetes Association 2012 Diabetes Vol.61 No.6
<P><B/></P><P>Retinal neovascularization is observed in progression of diabetic retinopathy. New vessels grow into the vitreous cavity in proliferative diabetic retinopathy, resulting in traction retinal detachment and vitreous hemorrhage. To overcome the catastrophic visual loss due to these complications, efforts have been focused on the treatment of retinal neovascularization. In this study, we demonstrated the inhibitory effect of recombinant human apolipoprotein(a) kringle V (rhLK8) in an animal model of ischemia-induced retinal neovascularization. rhLK8 induced no definite toxicity on endothelial cells and retinal tissues at the therapeutic dosage. Interestingly, rhLK8 showed antiangiogenic effect, particularly on fibronectin-mediated migration of endothelial cells. Further experiments demonstrated high binding affinity of rhLK8 to α3β1 integrin, and suppression of it might be the mechanism of antiangiogenic effect of rhLK8. Furthermore, rhLK8 inhibited phosphorylation of focal adhesion kinase, resulting in suppression of activation of consequent p130CAS-Jun NH<SUB>2</SUB>-terminal kinase. Taken together, our data suggested the possible application of rhLK8 in the treatment of retinal neovascularization by suppression of fibronectin-mediated angiogenesis.</P>