Hypertension resulting from overexpression of translationally controlled tumor protein increases the severity of atherosclerosis in apolipoprotein E knock-out mice

详细信息    查看全文

• 作者：Yujeong Cho (1)
  Jeehye Maeng (1)
  Jungmin Ryu (1)
  Hyekyoung Shin (1)
  Miyoung Kim (1)
  Goo Taeg Oh (2)
  Moo-Yeol Lee (3)
  Kyunglim Lee (1)
  
• 关键词：Apolipoprotein E ; Atherosclerosis ; Blood pressure ; Hypertension ; Translationally controlled tumor protein (TCTP)
• 刊名：Transgenic Research
• 出版年：2012
• 出版时间：December 2012
• 年：2012
• 卷：21
• 期：6
• 页码：1245-1254
• 全文大小：623KB
• 参考文献：1. Banerjee S, Rao PN (1966) Certain aspects of protein metabolism in hypercholesteremic chickens. Proc Soc Exp Biol Med 121(1):12-5
  2. Bommer UA, Thiele BJ (2004) The translationally controlled tumour protein (TCTP). Int J Biochem Cell Biol 36(3):379-85 CrossRef
  3. Cachofeiro V, Miana M, Heras N de las, Martín-Fernandez B, Ballesteros S, Balfagon G, Lahera V (2009) Inflammation: a link between hypertension and atherosclerosis. Curr Hypertens Rev 5:40-8
  4. da Cunha V, Tham DM, Martin-McNulty B, Deng G, Ho JJ, Wilson DW, Rutledge JC, Vergona R, Sullivan ME, Wang YX (2005) Enalapril attenuates angiotensin II-induced atherosclerosis and vascular inflammation. Atherosclerosis 178(1):9-7 CrossRef
  5. Hollander W (1976) Role of hypertension in atherosclerosis and cardiovascular disease. Am J Cardiol 38(6):786-00 CrossRef
  6. Ivey ME, Osman N, Little PJ (2008) Endothelin-1 signalling in vascular smooth muscle: pathways controlling cellular functions associated with atherosclerosis. Atherosclerosis 199(2):237-47 CrossRef
  7. Jung J, Kim M, Kim MJ, Kim J, Moon J, Lim JS, Lee K (2004) Translationally controlled tumor protein interacts with the third cytoplasmic domain of Na, K-ATPase alpha subunit and inhibits the pump activity in HeLa cells. J Biol Chem 279(48):49868-9875 CrossRef
  8. Ketonen J, Merasto S, Paakkari I, Mervaala EM (2005) High sodium intake increases vascular superoxide formation and promotes atherosclerosis in apolipoprotein E-deficient mice. Blood Press 14(6):373-82 CrossRef
  9. Kim MJ, Kwon JS, Suh SH, Suh JK, Jung J, Lee SN, Kim YH, Cho MC, Oh GT, Lee K (2008) Transgenic overexpression of translationally controlled tumor protein induces systemic hypertension via repression of Na+, K+-ATPase. J Mol Cell Cardiol 44(1):151-59 CrossRef
  10. Krishnamoorthy RR, Prasanna G, Dauphin R, Hulet C, Agarwal N, Yorio T (2003) Regulation of Na, K-ATPase expression by endothelin-1 in transformed human ciliary non-pigmented epithelial (HNPE) cells. J Ocul Pharmacol Ther 19(5):465-81 CrossRef
  11. Mandal A, Shahidullah M, Beimgraben C, Delamere N (2011) The effect of endothelin-1 on Src-family tyrosine kinases and Na,K-ATPase activity in porcine lens epithelium. J Cell Physiol 226(10):2555-561. doi:10.1002/jcp.22602
  12. Nakashima Y, Plump AS, Raines EW, Breslow JL, Ross R (1994) ApoE-deficient mice develop lesions of all phases of atherosclerosis throughout the arterial tree. Arterioscler Thromb 14(1):133-40 CrossRef
  13. Okafor MC, Mukhopadhyay P, Delamere NA (2002) Studies on endothelin release and Na, K transport in porcine lens. Invest Ophthalmol Vis Sci 43(3):790-96
  14. Paigen B, Morrow A, Holmes PA, Mitchell D, Williams RA (1987) Quantitative assessment of atherosclerotic lesions in mice. Atherosclerosis 68(3):231-40 CrossRef
  15. Pendse AA, Arbones-Mainar JM, Johnson LA, Altenburg MK, Maeda N (2009) Apolipoprotein E knock-out and knock-in mice: atherosclerosis, metabolic syndrome, and beyond. J Lipid Res 50(Suppl):S178–S182. doi:10.1194/jlr.R800070-JLR200 CrossRef
  16. Prasanna G, Dibas A, Hulet C, Yorio T (2001) Inhibition of Na(+)/K(+)-atpase by endothelin-1 in human nonpigmented ciliary epithelial cells. J Pharmacol Exp Ther 296(3):966-71
  17. Roche M, Rondeau P, Singh NR, Tarnus E, Bourdon E (2008) The antioxidant properties of serum albumin. FEBS Lett 582(13):1783-787. doi:10.1016/j.febslet.2008.04.057 CrossRef
  18. Scheiner-Bobis G, Eva A, Kirch U (2006) Signalling pathways involving sodium pump stimulate endothelin-1 secretion and nitric oxide production in endothelial cells. Cell Mol Biol (Noisy-le-grand) 52(8):58-3
  19. Standridge JB (2005) Hypertension and atherosclerosis: clinical implications from the ALLHAT Trial. Curr Atheroscler Rep 7(2):132-39 CrossRef
  20. Weiss D, Taylor WR (2008) Deoxycorticosterone acetate salt hypertension in apolipoprotein E-/- mice results in accelerated atherosclerosis: the role of angiotensin II. Hypertension 51(2):218-24 CrossRef
  21. Weiss D, Kools JJ, Taylor WR (2001) Angiotensin II-induced hypertension accelerates the development of atherosclerosis in apoE-deficient mice. Circulation 103(3):448-54 CrossRef
  22. Zhang SH, Reddick RL, Piedrahita JA, Maeda N (1992) Spontaneous hypercholesterolemia and arterial lesions in mice lacking apolipoprotein E. Science 258(5081):468-71 CrossRef
  
• 作者单位：Yujeong Cho (1)
  Jeehye Maeng (1)
  Jungmin Ryu (1)
  Hyekyoung Shin (1)
  Miyoung Kim (1)
  Goo Taeg Oh (2)
  Moo-Yeol Lee (3)
  Kyunglim Lee (1)
  
  1. Center for Cell Signaling and Drug Discovery Research, College of Pharmacy, Ewha Womans University, Seoul, Korea
  2. Division of Molecular Life Sciences, Ewha Womans University, Seoul, Korea
  3. College of Pharmacy, Dongguk University, Goyang, Gyeonggi-do, 410-820, Korea
  
• ISSN：1573-9368

文摘

Hypertension is a well-established etiological factor for atherogenesis. We previously showed that transgenic mice overexpressing translationally controlled tumor protein (TCTP) develop systemic arterial hypertension. In this study we explored the cardiovascular effects of TCTP overexpression and possibly of the resultant hypertension on the severity of atherosclerosis in apolipoprotein E-deficient mice. Through multiple mating of TCTP-overexpressing transgenic mice (TCTP-TG) with apolipoprotein E knock-out mice (ApoE KO), we generated non-transgenic (nTG), TCTP-TG, nTG/ApoE KO and TCTP-TG/ApoE KO mice with similar genetic background. Male mice, 7-week old, were fed a lipid-enriched Western diet for 16?weeks, and blood pressure and body weight change were monitored every 2?weeks. Plasma lipid profiles and atherosclerotic lesions in aorta were quantified at the end of study. We found that blood pressure levels of TCTP-TG and TCTP-TG/ApoE KO, were similarly elevated while nTG and nTG/ApoE KO mice were normotensive. TCTP overexpression in ApoE KO mice led to significant exacerbation of atherosclerotic lesions. Feeding Western diet resulted in increases in total cholesterol, triglyceride (TG) and low density lipoprotein, and decreased high density lipoprotein (HDL) in ApoE KO mice. No significant differences were found in plasma lipid profiles of nTG/ApoE KO and TCTP-TG/ApoE KO. This study suggests that overexpression of TCTP, which induces hypertension, also accelerates the development of atherosclerotic lesion caused by high-fat and high-cholesterol diet without significantly altering plasma lipid profiles. We conclude that TCTP-induced hypertension could increase the severity of atherosclerotic lesion and suggest that inhibition of TCTP or its signaling pathways may be a potential approach to the therapy of both diseases, hypertension and atherosclerosis.