Superoxide is a potential culprit of caspase-3 dependent endothelial cell death induced by lysophosphatidylcholine

• Autorzy: Park S. , Kim J.A. , Choi S. , Suh S.A.
• Języki publikacji: EN

Abstrakty

EN

Oxidative stress in the vascular wall has intimately been implicated in the apoptosis of human umbilical vein endothelial cells (HUVECs) by lysophosphatidylcholine (LPC). However, the major type of reactive oxygen species (ROS) in this apoptotic signaling pathway remains to be clarified. In this study, we report that superoxide mediate LPC-induced caspase-3 dependent apoptosis in cultured HUVECs. The stimulation of HUVECs with LPC evoked apoptosis and ROS generation, and inhibited nitric oxide (NO) production in a dose-dependent manner. The classical caspase-3 dependent apoptosis was determined after 16 hours treatment by Western blotting using an antibody against cleaved caspase-3. The caspase-3 activation induced by LPC was prominently inhibited by antioxidants or NO donors and enhanced by NO inhibitors. Especially, LPC-induced caspase-3 activation was inhibited by superoxide dismutase (SOD) and enhanced by ammonium tetrathiomolybdate, SOD inhibitor. Additionally, xanthine/xanthine oxidase mixture increased the caspase-3 activation but catalase failed to reduce this superoxide-induced caspase-3 activation. These findings indicate that the superoxide generation caused by LPC activates the caspase-3 which results in HUVECs death. This study reveals some evidences linking superoxide with caspase-3 activation and provides a new dimension to superoxide-mediated caspase-3 activation in developing the endothelial dysfunction and atherosclerosis.

Słowa kluczowe

EN

superoxide; caspase-3; endothelial cell; lysophosphatidylcholine; oxidative stress; vascular wall; apoptosis; human umbilical vein endothelial cell; reactive oxygen species; immunoblotting; endothelial dysfunction; nitric oxide; atherosclerosis

• Wydawca: -
• Czasopismo: Journal of Physiology and Pharmacology
• Rocznik: 2010
• Tom: 61
• Numer: 4
• Opis fizyczny: p.375-381,fig.,ref.

Twórcy

autor

Park S.

• Ewha Womans University, 911-1 Mok-6-dong, Yang Chun-gu, Seoul, Republic of Korea 158-710

autor

Kim J.A.

autor

Choi S.

autor

Suh S.A.

Bibliografia

• Deanfield JE, Halcox JP, Rabelink TJ. Endothelial function and dysfunction. Testing and clinical relevance. Circulation 2007; 115: 1285-1295.
• Lerman A, Zeiher AM. Endothelial function: cardiac events. Circulation 2005; 111: 363-368.
• Matsumoto T, Kobayashi T, Kamata K. Role of lysophosphatidylcholine (LPC) in atherosclerosis. Curr Med Chem 2007; 14: 3209-3220.
• Davignon J, Ganz P. Role of endothelial dysfunction in atherosclerosis. Circulation 2004; 109: III27-III32.
• Choy JC, Granville DJ, Hunt DW, McManus BM. Endothelial cell apoptosis: biochemical characteristics and potential implications for atherosclerosis. J Mol Cell Cardiol 2001; 33: 1673-1690.
• Matsubara M, Hasegawa K. Benidipine, a dihydropyridine-calcium channel blocker, prevents lysophosphatidylcholine-induced injury and reactive oxygen species production in human aortic endothelial cells. Atherosclerosis 2005; 178: 57-66.
• Matsubara M, Yao K, Hasegawa K. Benidipine, a dihydropyridine-calcium channel blocker, inhibits lysophosphatidylcholine-induced endothelial injury via stimulation of nitric oxide release. Pharmacol Res 2006; 53: 35-43.
• Takahashi M, Okazaki H, Ogata Y, Takeuchi K, Ikeda U, Shimada K. Lysophosphatidylcholine induces apoptosis in human endothelial cells through a p38-mitogen-activated protein kinase-dependent mechanism. Atherosclerosis 2002; 161: 387-394.
• Jin Z, El-Deiry WS. Overview of cell death signaling pathways. Cancer Biol Ther 2005; 4: 139-163.
• Yu BP. Cellular defenses against damage from reactive oxygen species. Physiol Rev 1994; 74: 139-162.
• Guzik TJ, Korbut R, Adamek-Guzik T. Nitric oxide and superoxide in inflammation and immune regulation. J Physiol Pharmacol 2003; 54: 469-487.
• Kurzelewski M, Czarnowska E, Beresewicz A. Superoxide- and nitric oxide-derived species mediate endothelial dysfunction, endothelial glycocalyx disruption, and enhanced neutrophil adhesion in the post-ischemic guinea-pig heart. J Physiol Pharmacol 2005; 56: 163-178.
• Madamanchi NR, Hakim ZS, Runge MS. Oxidative stress in atherogenesis and arterial thrombosis: the disconnect between cellular studies and clinical outcomes. J Thromb Haemost 2005; 3: 254-267.
• Yokoyama M. Oxidant stress and atherosclerosis. Curr Opin Pharmacol 2004; 4: 110-115.
• Guzik TJ, Sadowski J, Guzik B, et al. Coronary artery superoxide production and nox isoform expression in human coronary artery disease. Arterioscler Thromb Vasc Biol 2006; 26: 333-339.
• Watanabe N, Zmijewski JW, Takabe W, et al. Activation of mitogen-activated protein kinases by lysophosphatidylcholine-induced mitochondrial reactive oxygen species generation in endothelial cells. Am J Pathol 2006; 168: 1737-1748.
• Kugiyama K, Sugiyama S, Ogata N, et al. Burst production of superoxide anion in human endothelial cells by lysophosphatidylcholine. Atherosclerosis 1999; 143: 201-204.
• Wink DA, Miranda KM, Espey MG, et al. Mechanisms of the antioxidant effects of nitric oxide. Antioxid Redox Signal 2001; 3: 203-213.
• Mohanakumar KP, Thomas B, Sharma SM, Muralikrishnan D, Chowdhury R, Chiueh CC. Nitric oxide: an antioxidant and neuroprotector. Ann NY Acad Sci 2002; 962: 389-401.
• Takeshita S, Inoue N, Gao D, et al. Lysophosphatidylcholine enhances superoxide anions production via endothelial nadh/nadph oxidase. J Atheroscler Thromb 2000; 7: 238-246.
• Ohara Y, Peterson TE, Zheng B, Kuo JF, Harrison DG. Lysophosphatidylcholine increases vascular superoxide anion production via protein kinase c activation. Arterioscler Thromb 1994; 14: 1007-1013.
• Nishioka H, Horiuchi H, Arai H, Kita T. Lysophosphatidylcholine generates superoxide anions through activation of phosphatidylinositol 3-kinase in human neutrophils. FEBS Lett 1998; 441: 63-66.
• Choi S, Park S, Liang GH, Kim JA, Suh SH. Superoxide generated by lysophosphatidylcholine induces endothelial nitric oxide synthase downregulation in human endothelial cells. Cell Physiol Biochem 2010; 25: 233-240.
• Jameel NM, Thirunavukkarasu C, Wu T, Watkins SC, Friedman SL, Gandhi CR. P38-mapk- and caspase-3-mediated superoxide-induced apoptosis of rat hepatic stellate cells: reversal by retinoic acid. J Cell Physiol 2009; 218: 157-166.
• Newaz MA, Yousefipour Z, Nawal N, Adeeb N. Nitric oxide synthase activity in blood vessels of spontaneously hypertensive rats: antioxidant protection by gamma-tocotrienol. J Physiol Pharmacol 2003; 54: 319-327.
• Safaya R, Chai H, Kougias P, et al. Effect of lysophosphatidylcholine on vasomotor functions of porcine coronary arteries. J Surg Res 2005; 126: 182-188.
• Liao JK, Shin WS, Lee WY, Clark SL. Oxidized low-density lipoprotein decreases the expression of endothelial nitric oxide synthase. J Biol Chem 1995; 270: 319-324.
• Yang Z, Ming XF. Recent advances in understanding endothelial dysfunction in atherosclerosis. Clin Med Res 2006; 4: 53-65.
• Channon KM, Guzik TJ. Mechanisms of superoxide production in human blood vessels: relationship to endothelial dysfunction, clinical and genetic risk factors. J Physiol Pharmacol 2002; 53: 515-524.
• Croset M, Brossard N, Polette A, Lagarde M. Characterization of plasma unsaturated lysophosphatidylcholines in human and rat. Biochem J 2000; 345(Pt 1): 61-67.
• Okajima F, Sato K, Tomura H, et al. Stimulatory and inhibitory actions of lysophosphatidylcholine, depending on its fatty acid residue, on the phospholipase c/Ca2+ system in hl-60 leukaemia cells. Biochem J 1998; 336: 491-500.
• Okita M, Gaudette DC, Mills GB, Holub BJ. Elevated levels and altered fatty acid composition of plasma lysophosphatidylcholine(lysopc) in ovarian cancer patients. Int J Cancer 1997; 71: 31-34.
• Gillett MP, Besterman EM. Plasma concentrations of lysolecithin and other phospholipids in the healthy population and in men suffering from atherosclerotic diseases. Atherosclerosis 1975; 22: 111-124.
• Chen L, Liang B, Froese DE, et al. Oxidative modification of low density lipoprotein in normal and hyperlipidemic patients: effect of lysophosphatidylcholine composition on vascular relaxation. J Lipid Res 1997; 38: 546-553.