ACE2 activation by xanthenone prevents leptin-induced increases in blood pressure and proteinuria during pregnancy in Sprague-Dawley rats
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| date | 2014-10-28 16:19:09 |
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| id | 11327 |
| institution | UniSZA |
| internalnotes | [1] Thadhani R, Stampfer MJ, Hunter DJ, Manson JE, Solomon CG, Curhan GC. High body mass index and hypercholesterolemia: risk of hypertensive disorders of pregnancy. Obstetr Gynecol 1999;94(4):543. [2] Igel M, Becker W, Herberg L, Joost HG. Hyperleptinemia, leptin resistance, and polymorphic leptin receptor in the New Zealand obese mouse. Endocrinology 1997;138(10):4234. [3] Teppa RJ, Ness RB, Crombleholme WR, Roberts JM. Free leptin is increased in normal pregnancy and further increased in preeclampsia* 1. Metabolism 2000;49(8):1043–8. [4] Iftikhar U, Khoja A, Mehjabeen AI, Karira KA. Evaluation of serum leptin levels during normal pregnancy and in pre-eclampsia. J Ayub Med Coll Abbottabad 2008;20(4):137–40. [5] Miehle K, Stepan H, Fasshauer M. Leptin, adiponectin, and other adipokines in gestational diabetes mellitus and preeclampsia. Clin Endocrinol 2011. [6] Singh HJ, Abu Bakar A, Che Romli A, Nila A. Raised leptin concentrations in feto-placental tissues from women with preeclampsia. Hypertension Pregnancy 2005;24(2):191–9. [7] Chambers JC, Fusi L, Malik IS, Haskard DO, De Swiet M, Kooner JS. Association of maternal endothelial dysfunction with preeclampsia. Am Med Assoc 2001;285:1607–12. [8] Roberts JM, Lain KY. Recent insights into the pathogenesis of pre-eclampsia. Placenta 2002;23(5):359–72. [9] Mikat B, Gellhaus A, Wagner N, Birdir C, Kimmig R, Köninger A. Early detection of maternal risk for preeclampsia. ISRN Obstetr Gynecol 2012:2012. [10] Greenberg AS, Obin MS. Obesity and the role of adipose tissue in inflammation and metabolism. Am J Clin Nutr 2006;83(2):461S. [11] Mehta S, Farmer JA. Obesity and inflammation: a new look at an old problem. Curr Atherosclerosis Rep 2007;9(2):134–8. [12] Van Dielen FM, Van’t Veer C, Schols AM, Soeters PB, Buurman WA, Greve JW. Increased leptin concentrations correlate with increased concentrations of inflammatory markers in morbidly obese individuals. Int J Obesity Relat Metabolic Disord 2001;25(12):1759. [13] Madan JC, Davis JM, Craig WY, et al. Maternal obesity and markers of inflammation in pregnancy. Cytokine 2009;47(1):61–4. [14] Ibrahim HS, Omar E, Froemming GRA, Singh HJ. Leptin increases blood pressure and markers of endothelial activation during pregnancy in rats. BioMed Res Int 2013;2013:6. [15] Cha JJ, HyunYY, JeeYH, et al. Plasma concentration of soluble intercellular adhesion molecule-1 (sICAM-1) is elevated in type 2 diabetic patients, and sICAM-1 synthesis is associated with leptin-induced activation of the mitogen-activated protein kinase (MAPK) pathway. Inflammation 2013:1–10. [16] Izzo JL, Sica DA, Black HR. Hypertension primer. Lippincott Williams & Wilkins; 2008. [17] Brosnihan KB, Neves LAA, Joyner JN, et al. Enhanced renal immunocytochemical expression of ANG-(1-7) and ACE2 during pregnancy. Hypertension 2003;42(4):749–53. [18] Neves LAA, Stovall K, Joyner JN, et al. ACE2 and ANG-(1-7) in the rat uterus during early and late gestation. Am J Physiol-Regulat Integrative Comparat Physiol 2008;294(1):R151–61. [19] Valdes G, Neves LAA, Anton L, et al. Distribution of angiotensin-(1-7) and ACE2 in human placentas of normal and pathological pregnancies. Placenta 2006;27(2–3):200–7. [20] Prada JAH, Ferreira AJ, Katovich MJ, et al. Structure-based identification of small-molecule angiotensin-converting enzyme 2 activators as novel antihypertensive agents. Hypertension 2008;51(5):1312–7. [21] Ferreira AJ, Shenoy V, Yamazato Y, et al. Evidence for angiotensin-converting enzyme 2 as a therapeutic targetfor the prevention of pulmonary hypertension. Am J Respir Crit Care Med 2009;179(11):1048. [22] Fraga-Silva RA, Sorg BS, Wankhede M. ACE2 activation promotes antithrombotic activity. Mol Med 2010;16(5–6):210. [23] Ferreira AJ, Shenoy V, Qi Y, et al. Angiotensin-converting enzyme 2 activation protects against hypertension-induced cardiac fibrosis involving extracellular signal-regulated kinases. Exp Physiol 2011;96(3):287–94. [24] Bella J, Kolatkar PR, Marlor CW, Greve JM, Rossmann MG. The structure of the two amino-terminal domains of human ICAM-1 suggests how it functions as a rhinovirus receptor and as an LFA-1 integrin ligand. Proc Natl Acad Sci 1998;95(8):4140–5. [25] Vadasz Z, Haj T, Halasz K, et al. Semaphorin 3A is a marker for disease activity and a potential immunoregulator in systemic lupus erythematosus. Arthritis Res Therapy 2012;14(3):R146. [26] Bustin SA, Benes V, Garson JA, et al. The MIQE guidelines: minimum information for publication of quantitative real-time PCR experiments. Clin Chem 2009;55(4):611–22. [27] Vandesompele J, De Preter K, Pattyn F, et al. Accurate normalization of real-time quantitative RT-PCR data by geometric averaging of multiple internal control genes. Genome Biol 2002;3(7), research0034. [28] Livak KJ, Schmittgen TD. Analysis of relative gene expression data using real-time quantitative PCR and the 2−CT method. Methods 2001;25(4):402–8. [29] Haynes WG, Morgan DA, Walsh SA, Mark AL, Sivitz WI. Receptor-mediated regional sympathetic nerve activation by leptin. J Clin Invest 1997;100(2):270. [30] Dunbar JC, Hu Y, Lu H. Intracerebroventricular leptin increases lumbar and renal sympathetic nerve activity and blood pressure in normal rats. Diabetes 1997;46(12):2040–3. [31] Correia MLG, Rahmouni K. Role of leptin in the cardiovascular and endocrine complications of metabolic syndrome. Diabet Obesity Metabol 2006;8(6):603–10. [32] Madajka M, Korda M, White J, Malinski T. Effect of aspirin on constitutive nitric oxide synthase and the biovailability of NO. Thrombosis Res 2003;110(5):317–21. [33] Ecelbarger CA. Proteomics and sodium transport. Proteomics Nephrol 2003;141:124–41. [34] Bridges JP, Gilbert JS, Colson D, et al. Oxidative stress contributes to soluble fms-like tyrosine kinase-1 induced vascular dysfunction in pregnant rats. Am J Hypertension 2009;22(5):564–8. [35] Murphy SR, LaMarca BBD, Cockrell K, Granger JP. Role of endothelin in mediating soluble fms-like tyrosine kinase 1-induced hypertension in pregnant rats. Hypertension 2010;55(2):394–8. [36] Wu FT, Stefanini MO, Gabhann FM, Kontos CD, Annex BH, Popel AS. A systems biology perspective on sVEGFR1: its biological function, pathogenic role and therapeutic use. J Cell Mol Med 2010;14(3):528–52. [37] Quehenberger P, Exner M, Sunder-Plassmann R, et al. Leptin induces endothelin-1 in endothelial cells in vitro. Circulat Res 2002;90(6): 711–8. [38] Schinzari F, Tesauro M, Rovella V, et al. Leptin stimulates both endothelin-1 and nitric oxide activity in lean subjects but not in patients with obesity-related metabolic syndrome. J Clin Endocrinol Metabol 2013;98(3):1235–41. [39] George EM, Palei AC, Granger JP. Endothelin as a final common pathway in the pathophysiology of preeclampsia: therapeutic implications. Curr Opin Nephrol Hypertension 2012;21(2):157. [40] Aggarwal P, Chandel N, Jain V, Jha V. The relationship between circulating endothelin-1, soluble fms-like tyrosine kinase-1 and soluble endoglin in preeclampsia. J Hum Hypertension 2011;26(4):236–41. [41] Sharma D, Singh A, Trivedi SS, Bhattacharjee J. Role of endothelin and inflammatory cytokines in pre-eclampsia – A Pilot North Indian Study. Am J Reprod Immunol 2011;65(4):428–32. [42] Singh HJ, Rahman A, Larmie ET, Nila A. Endothelin-1 in feto-placental tissues from normotensive pregnant women and women with pre-eclampsia. Acta Obstet Gynecol Scand 2001;80(2):99–103. [43] Bharadwaj MS, Strawn WB, Groban L, et al. Angiotensin-converting enzyme 2 deficiency is associated with impaired gestational weight gain and fetal growth restriction. Hypertension 2011;58(5):852–8. [44] Mizuiri S, Hemmi H, Arita M, et al. Expression of ACE and ACE2 in individuals with diabetic kidney disease and healthy controls. Am J Kidney Dis 2008;51(4):613–23. [45] LiuR, Qi H,Wang J, et al.Angiotensin-converting enzyme (ACE andACE2)imbalance correlates with the severity of cerulein-induced acute pancreatitis in mice. Exp Physiol 2014. [46] BrosnihanK, Neves L,AntonL, Joyner J, Valdes G, Merrill D. Enhanced expression of Ang-(1-7) during pregnancy. Brazilian J Med Biol Res 2004;37(8):1255–62. [47] Zhang H, Li Y, Zeng Y, Wu R, Ou J. Endothelin-1 downregulates angiotensin-converting enzyme-2 expression in human bronchial epithelial cells. Pharmacology 2013;91(5–6):297–304. [48] Lambert DW, Yarski M, Warner FJ, et al. Tumor necrosis factor-� convertase (ADAM17) mediates regulated ectodomain shedding of the severe-acute respiratory syndrome-coronavirus (SARS-CoV) receptor, angiotensin-converting enzyme-2 (ACE2). J Biol Chem 2005;280(34):30113–9. [49] Fiorentino L, Vivanti A, Cavalera M, et al. Increased tumor necrosis factor �- converting enzyme activity induces insulin resistance and hepatosteatosis in mice. Hepatology 2010;51(1):103–10. [50] De Caterina R, Ghiadoni L, Taddei S, et al. Soluble e-selectin in essential hypertension: a correlate of vascular structural changes&ast. Am J Hypertension 2001;14(3):259–66. [51] Zhang M, Wang G, Wang A, Tong W, Zhang Y. Association of hypertension with coexistence of abnormal metabolism and inflammation and endothelial dysfunction. Blood Pressure 2013;22(3):151–7. [52] Yudkin JS, Stehouwer C, Emeis J, Coppack S. C-reactive protein in healthy subjects: associations with obesity, insulin resistance, and endothelial dysfunction a potential role for cytokines originating from adipose tissue? Arteriosclerosis Thrombosis Vascular Biol 1999;19(4):972–8. [53] Steinberg HO, Chaker H, Leaming R, Johnson A, Brechtel G, Baron AD. Obesity/insulin resistance is associated with endothelial dysfunction. Implications for the syndrome of insulin resistance. J Clin Invest 1996;97(11):2601. [54] Hashimoto M, Akishita M, Eto M, et al. The impairment of flow-mediated vasodilatation in obese men with visceral fat accumulation. Int J Obesity Relat Metabol Disord 1998;22(5):477. [55] Hou N, Luo JD. Leptin and cardiovascular diseases. Clin Exp Pharmacol Physiol 2011;38(12):905–13. [56] Beltowski J. Leptin and atherosclerosis. Atherosclerosis 2006;189(1):47–60. [57] Thomas MC, Pickering RJ, Tsorotes D, et al. Genetic Ace2 deficiency accentuates vascular inflammation and atherosclerosis in the ApoE Knockout MouseNovelty and Significance. Circulat Res 2010;107(7):888–97. [58] Wang MY, Yan TZ, Newgard CB, Unger RH. A novel leptin receptor isoform in rat. FEBS Lett 1996;392(2):87–90. [59] Serradeil-Le Gal C, Raufaste D, Brossard G, et al. Characterization and localization of leptin receptors in the rat kidney. FEBS Lett 1997;404(2):185–91. [60] Han DC, Isono M, Chen S, et al. Leptin stimulates type I collagen production in db/db mesangial cells: glucose uptake and TGF-&bgr; type II receptor expression. Kidney Int 2001;59(4):1315–23. [61] Wolf G, Hamann A, Han DC, et al. Leptin stimulates proliferation and TGF-&bgr; expression in renal glomerular endothelial cells: potential role in glomerulosclerosis1. Kidney Int 1999;56(3):860–72. [62] Kasiske BL, Crosson JT. Renal disease in patients with massive obesity. Archiv Internal Med 1986;146(6):1105. [63] Sharma K, Ziyadeh FN. The emerging role of transforming growth factor-beta in kidney diseases. Am J Physiol-Renal Physiol 1994;266(6):F829–42. [64] Dhaun N, Webb DJ, Kluth DC. Endothelin-1 and the kidney-beyond BP. Br J Pharmacol 2012;167(4):720–31. [65] Giani JF, Burghi V, Veiras LC, et al. Angiotensin-(1-7) attenuates diabetic nephropathy in Zucker diabetic fatty rats. Am J Physiol-Renal Physiol 2012;302(12):F1606–15. [66] Oudit GY, Liu GC, Zhong J, et al. Human recombinant ACE2 reduces the progression of diabetic nephropathy. Diabetes 2010;59(2):529–38. [67] Dilauro M, Zimpelmann J, Robertson SJ, Genest D, Burns KD. Effect of ACE2 and angiotensin-(1-7) in a mouse model of early chronic kidney disease. Am J Physiol-Renal Physiol 2010;298(6):F1523–32. [68] Park SE,KimWJ, Park SW, et al. HighurinaryACE2 concentrations are associated with severity of glucose intolerance and microalbuminuria. Eur J Endocrinol 2013;168(2):203–10. |
| originalfilename | 5543-01-FH02-FPSK-14-01594.jpg |
| person | UniSZA Unisza unisza |
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| resourceurl | https://intelek.unisza.edu.my/intelek/pages/view.php?ref=11327 |
| spelling | 11327 https://intelek.unisza.edu.my/intelek/pages/view.php?ref=11327 https://intelek.unisza.edu.my/intelek/pages/search.php?search=!collection407072 Restricted Document Article Journal UniSZA Unisza unisza image/jpeg inches 96 96 04 04 747 1413 1413x747 2014-10-28 16:19:09 5543-01-FH02-FPSK-14-01594.jpg UniSZA Private Access ACE2 activation by xanthenone prevents leptin-induced increases in blood pressure and proteinuria during pregnancy in Sprague-Dawley rats Elsevier Inc. Reproductive Toxicology This study investigates the effect of ACE2 activation on leptin-induced changes in systolic blood pressure (SBP), proteinuria, endothelial activation and ACE2 expression during pregnancy in Sprague-Dawley rats. Pregnant rats were given subcutaneous injection of either saline, or leptin, or leptin plus xanthenone (ACE2 activator), or xanthenone (XTN) alone. SBP, serum ACE, ACE2, endothelin-1, E-selectin and ICAM-1 levels were estimated; also their gene expressions were determined in the kidney and aorta respectively. Compared to control, SBP was higher in the leptin-only treated group (P<0.001) and lower in rats treated with xanthenone alone (P<0.01). Proteinuria, markers of endothelial activation were significantly higher than controls in leptin-only treated rats (P<0.05). ACE2 activity and expression were lower in leptin-only treated rats when compared to controls (P<0.05). It seems, leptin administration during pregnancy significantly increases SBP, proteinuria, endothelial activation, but decreases ACE2 level and expression. These effects are prevented by concurrent administration of xanthenone. 49 Elsevier Inc. Elsevier Inc. 155-161 [1] Thadhani R, Stampfer MJ, Hunter DJ, Manson JE, Solomon CG, Curhan GC. High body mass index and hypercholesterolemia: risk of hypertensive disorders of pregnancy. Obstetr Gynecol 1999;94(4):543. [2] Igel M, Becker W, Herberg L, Joost HG. Hyperleptinemia, leptin resistance, and polymorphic leptin receptor in the New Zealand obese mouse. Endocrinology 1997;138(10):4234. [3] Teppa RJ, Ness RB, Crombleholme WR, Roberts JM. Free leptin is increased in normal pregnancy and further increased in preeclampsia* 1. Metabolism 2000;49(8):1043–8. [4] Iftikhar U, Khoja A, Mehjabeen AI, Karira KA. Evaluation of serum leptin levels during normal pregnancy and in pre-eclampsia. J Ayub Med Coll Abbottabad 2008;20(4):137–40. [5] Miehle K, Stepan H, Fasshauer M. Leptin, adiponectin, and other adipokines in gestational diabetes mellitus and preeclampsia. Clin Endocrinol 2011. [6] Singh HJ, Abu Bakar A, Che Romli A, Nila A. Raised leptin concentrations in feto-placental tissues from women with preeclampsia. Hypertension Pregnancy 2005;24(2):191–9. [7] Chambers JC, Fusi L, Malik IS, Haskard DO, De Swiet M, Kooner JS. Association of maternal endothelial dysfunction with preeclampsia. Am Med Assoc 2001;285:1607–12. [8] Roberts JM, Lain KY. Recent insights into the pathogenesis of pre-eclampsia. Placenta 2002;23(5):359–72. [9] Mikat B, Gellhaus A, Wagner N, Birdir C, Kimmig R, Köninger A. Early detection of maternal risk for preeclampsia. ISRN Obstetr Gynecol 2012:2012. [10] Greenberg AS, Obin MS. Obesity and the role of adipose tissue in inflammation and metabolism. Am J Clin Nutr 2006;83(2):461S. [11] Mehta S, Farmer JA. Obesity and inflammation: a new look at an old problem. Curr Atherosclerosis Rep 2007;9(2):134–8. [12] Van Dielen FM, Van’t Veer C, Schols AM, Soeters PB, Buurman WA, Greve JW. Increased leptin concentrations correlate with increased concentrations of inflammatory markers in morbidly obese individuals. Int J Obesity Relat Metabolic Disord 2001;25(12):1759. [13] Madan JC, Davis JM, Craig WY, et al. Maternal obesity and markers of inflammation in pregnancy. Cytokine 2009;47(1):61–4. [14] Ibrahim HS, Omar E, Froemming GRA, Singh HJ. Leptin increases blood pressure and markers of endothelial activation during pregnancy in rats. BioMed Res Int 2013;2013:6. [15] Cha JJ, HyunYY, JeeYH, et al. Plasma concentration of soluble intercellular adhesion molecule-1 (sICAM-1) is elevated in type 2 diabetic patients, and sICAM-1 synthesis is associated with leptin-induced activation of the mitogen-activated protein kinase (MAPK) pathway. Inflammation 2013:1–10. [16] Izzo JL, Sica DA, Black HR. Hypertension primer. Lippincott Williams & Wilkins; 2008. [17] Brosnihan KB, Neves LAA, Joyner JN, et al. Enhanced renal immunocytochemical expression of ANG-(1-7) and ACE2 during pregnancy. Hypertension 2003;42(4):749–53. [18] Neves LAA, Stovall K, Joyner JN, et al. ACE2 and ANG-(1-7) in the rat uterus during early and late gestation. Am J Physiol-Regulat Integrative Comparat Physiol 2008;294(1):R151–61. [19] Valdes G, Neves LAA, Anton L, et al. Distribution of angiotensin-(1-7) and ACE2 in human placentas of normal and pathological pregnancies. Placenta 2006;27(2–3):200–7. [20] Prada JAH, Ferreira AJ, Katovich MJ, et al. Structure-based identification of small-molecule angiotensin-converting enzyme 2 activators as novel antihypertensive agents. Hypertension 2008;51(5):1312–7. [21] Ferreira AJ, Shenoy V, Yamazato Y, et al. Evidence for angiotensin-converting enzyme 2 as a therapeutic targetfor the prevention of pulmonary hypertension. Am J Respir Crit Care Med 2009;179(11):1048. [22] Fraga-Silva RA, Sorg BS, Wankhede M. ACE2 activation promotes antithrombotic activity. Mol Med 2010;16(5–6):210. [23] Ferreira AJ, Shenoy V, Qi Y, et al. Angiotensin-converting enzyme 2 activation protects against hypertension-induced cardiac fibrosis involving extracellular signal-regulated kinases. Exp Physiol 2011;96(3):287–94. [24] Bella J, Kolatkar PR, Marlor CW, Greve JM, Rossmann MG. The structure of the two amino-terminal domains of human ICAM-1 suggests how it functions as a rhinovirus receptor and as an LFA-1 integrin ligand. Proc Natl Acad Sci 1998;95(8):4140–5. [25] Vadasz Z, Haj T, Halasz K, et al. Semaphorin 3A is a marker for disease activity and a potential immunoregulator in systemic lupus erythematosus. Arthritis Res Therapy 2012;14(3):R146. [26] Bustin SA, Benes V, Garson JA, et al. The MIQE guidelines: minimum information for publication of quantitative real-time PCR experiments. Clin Chem 2009;55(4):611–22. [27] Vandesompele J, De Preter K, Pattyn F, et al. Accurate normalization of real-time quantitative RT-PCR data by geometric averaging of multiple internal control genes. Genome Biol 2002;3(7), research0034. [28] Livak KJ, Schmittgen TD. Analysis of relative gene expression data using real-time quantitative PCR and the 2−CT method. Methods 2001;25(4):402–8. [29] Haynes WG, Morgan DA, Walsh SA, Mark AL, Sivitz WI. Receptor-mediated regional sympathetic nerve activation by leptin. J Clin Invest 1997;100(2):270. [30] Dunbar JC, Hu Y, Lu H. Intracerebroventricular leptin increases lumbar and renal sympathetic nerve activity and blood pressure in normal rats. Diabetes 1997;46(12):2040–3. [31] Correia MLG, Rahmouni K. Role of leptin in the cardiovascular and endocrine complications of metabolic syndrome. Diabet Obesity Metabol 2006;8(6):603–10. [32] Madajka M, Korda M, White J, Malinski T. Effect of aspirin on constitutive nitric oxide synthase and the biovailability of NO. Thrombosis Res 2003;110(5):317–21. [33] Ecelbarger CA. Proteomics and sodium transport. Proteomics Nephrol 2003;141:124–41. [34] Bridges JP, Gilbert JS, Colson D, et al. Oxidative stress contributes to soluble fms-like tyrosine kinase-1 induced vascular dysfunction in pregnant rats. Am J Hypertension 2009;22(5):564–8. [35] Murphy SR, LaMarca BBD, Cockrell K, Granger JP. Role of endothelin in mediating soluble fms-like tyrosine kinase 1-induced hypertension in pregnant rats. Hypertension 2010;55(2):394–8. [36] Wu FT, Stefanini MO, Gabhann FM, Kontos CD, Annex BH, Popel AS. A systems biology perspective on sVEGFR1: its biological function, pathogenic role and therapeutic use. J Cell Mol Med 2010;14(3):528–52. [37] Quehenberger P, Exner M, Sunder-Plassmann R, et al. Leptin induces endothelin-1 in endothelial cells in vitro. Circulat Res 2002;90(6): 711–8. [38] Schinzari F, Tesauro M, Rovella V, et al. Leptin stimulates both endothelin-1 and nitric oxide activity in lean subjects but not in patients with obesity-related metabolic syndrome. J Clin Endocrinol Metabol 2013;98(3):1235–41. [39] George EM, Palei AC, Granger JP. Endothelin as a final common pathway in the pathophysiology of preeclampsia: therapeutic implications. Curr Opin Nephrol Hypertension 2012;21(2):157. [40] Aggarwal P, Chandel N, Jain V, Jha V. The relationship between circulating endothelin-1, soluble fms-like tyrosine kinase-1 and soluble endoglin in preeclampsia. J Hum Hypertension 2011;26(4):236–41. [41] Sharma D, Singh A, Trivedi SS, Bhattacharjee J. Role of endothelin and inflammatory cytokines in pre-eclampsia – A Pilot North Indian Study. Am J Reprod Immunol 2011;65(4):428–32. [42] Singh HJ, Rahman A, Larmie ET, Nila A. Endothelin-1 in feto-placental tissues from normotensive pregnant women and women with pre-eclampsia. Acta Obstet Gynecol Scand 2001;80(2):99–103. [43] Bharadwaj MS, Strawn WB, Groban L, et al. Angiotensin-converting enzyme 2 deficiency is associated with impaired gestational weight gain and fetal growth restriction. Hypertension 2011;58(5):852–8. [44] Mizuiri S, Hemmi H, Arita M, et al. Expression of ACE and ACE2 in individuals with diabetic kidney disease and healthy controls. Am J Kidney Dis 2008;51(4):613–23. [45] LiuR, Qi H,Wang J, et al.Angiotensin-converting enzyme (ACE andACE2)imbalance correlates with the severity of cerulein-induced acute pancreatitis in mice. Exp Physiol 2014. [46] BrosnihanK, Neves L,AntonL, Joyner J, Valdes G, Merrill D. Enhanced expression of Ang-(1-7) during pregnancy. Brazilian J Med Biol Res 2004;37(8):1255–62. [47] Zhang H, Li Y, Zeng Y, Wu R, Ou J. Endothelin-1 downregulates angiotensin-converting enzyme-2 expression in human bronchial epithelial cells. Pharmacology 2013;91(5–6):297–304. [48] Lambert DW, Yarski M, Warner FJ, et al. Tumor necrosis factor-� convertase (ADAM17) mediates regulated ectodomain shedding of the severe-acute respiratory syndrome-coronavirus (SARS-CoV) receptor, angiotensin-converting enzyme-2 (ACE2). J Biol Chem 2005;280(34):30113–9. [49] Fiorentino L, Vivanti A, Cavalera M, et al. Increased tumor necrosis factor �- converting enzyme activity induces insulin resistance and hepatosteatosis in mice. Hepatology 2010;51(1):103–10. [50] De Caterina R, Ghiadoni L, Taddei S, et al. Soluble e-selectin in essential hypertension: a correlate of vascular structural changes&ast. Am J Hypertension 2001;14(3):259–66. [51] Zhang M, Wang G, Wang A, Tong W, Zhang Y. Association of hypertension with coexistence of abnormal metabolism and inflammation and endothelial dysfunction. Blood Pressure 2013;22(3):151–7. [52] Yudkin JS, Stehouwer C, Emeis J, Coppack S. C-reactive protein in healthy subjects: associations with obesity, insulin resistance, and endothelial dysfunction a potential role for cytokines originating from adipose tissue? Arteriosclerosis Thrombosis Vascular Biol 1999;19(4):972–8. [53] Steinberg HO, Chaker H, Leaming R, Johnson A, Brechtel G, Baron AD. Obesity/insulin resistance is associated with endothelial dysfunction. Implications for the syndrome of insulin resistance. J Clin Invest 1996;97(11):2601. [54] Hashimoto M, Akishita M, Eto M, et al. The impairment of flow-mediated vasodilatation in obese men with visceral fat accumulation. Int J Obesity Relat Metabol Disord 1998;22(5):477. [55] Hou N, Luo JD. Leptin and cardiovascular diseases. Clin Exp Pharmacol Physiol 2011;38(12):905–13. [56] Beltowski J. Leptin and atherosclerosis. Atherosclerosis 2006;189(1):47–60. [57] Thomas MC, Pickering RJ, Tsorotes D, et al. Genetic Ace2 deficiency accentuates vascular inflammation and atherosclerosis in the ApoE Knockout MouseNovelty and Significance. Circulat Res 2010;107(7):888–97. [58] Wang MY, Yan TZ, Newgard CB, Unger RH. A novel leptin receptor isoform in rat. FEBS Lett 1996;392(2):87–90. [59] Serradeil-Le Gal C, Raufaste D, Brossard G, et al. Characterization and localization of leptin receptors in the rat kidney. FEBS Lett 1997;404(2):185–91. [60] Han DC, Isono M, Chen S, et al. Leptin stimulates type I collagen production in db/db mesangial cells: glucose uptake and TGF-&bgr; type II receptor expression. Kidney Int 2001;59(4):1315–23. [61] Wolf G, Hamann A, Han DC, et al. Leptin stimulates proliferation and TGF-&bgr; expression in renal glomerular endothelial cells: potential role in glomerulosclerosis1. Kidney Int 1999;56(3):860–72. [62] Kasiske BL, Crosson JT. Renal disease in patients with massive obesity. Archiv Internal Med 1986;146(6):1105. [63] Sharma K, Ziyadeh FN. The emerging role of transforming growth factor-beta in kidney diseases. Am J Physiol-Renal Physiol 1994;266(6):F829–42. [64] Dhaun N, Webb DJ, Kluth DC. Endothelin-1 and the kidney-beyond BP. Br J Pharmacol 2012;167(4):720–31. [65] Giani JF, Burghi V, Veiras LC, et al. Angiotensin-(1-7) attenuates diabetic nephropathy in Zucker diabetic fatty rats. Am J Physiol-Renal Physiol 2012;302(12):F1606–15. [66] Oudit GY, Liu GC, Zhong J, et al. Human recombinant ACE2 reduces the progression of diabetic nephropathy. Diabetes 2010;59(2):529–38. [67] Dilauro M, Zimpelmann J, Robertson SJ, Genest D, Burns KD. Effect of ACE2 and angiotensin-(1-7) in a mouse model of early chronic kidney disease. Am J Physiol-Renal Physiol 2010;298(6):F1523–32. [68] Park SE,KimWJ, Park SW, et al. HighurinaryACE2 concentrations are associated with severity of glucose intolerance and microalbuminuria. Eur J Endocrinol 2013;168(2):203–10. |
| spellingShingle | ACE2 activation by xanthenone prevents leptin-induced increases in blood pressure and proteinuria during pregnancy in Sprague-Dawley rats |
| summary | This study investigates the effect of ACE2 activation on leptin-induced changes in systolic blood pressure (SBP), proteinuria, endothelial activation and ACE2 expression during pregnancy in Sprague-Dawley rats. Pregnant rats were given subcutaneous injection of either saline, or leptin, or leptin plus xanthenone (ACE2 activator), or xanthenone (XTN) alone. SBP, serum ACE, ACE2, endothelin-1, E-selectin and ICAM-1 levels were estimated; also their gene expressions were determined in the kidney and aorta respectively. Compared to control, SBP was higher in the leptin-only treated group (P<0.001) and lower in rats treated with xanthenone alone (P<0.01). Proteinuria, markers of endothelial activation were significantly higher than controls in leptin-only treated rats (P<0.05). ACE2 activity and expression were lower in leptin-only treated rats when compared to controls (P<0.05). It seems, leptin administration during pregnancy significantly increases SBP, proteinuria, endothelial activation, but decreases ACE2 level and expression. These effects are prevented by concurrent administration of xanthenone. |
| title | ACE2 activation by xanthenone prevents leptin-induced increases in blood pressure and proteinuria during pregnancy in Sprague-Dawley rats |
| title_full | ACE2 activation by xanthenone prevents leptin-induced increases in blood pressure and proteinuria during pregnancy in Sprague-Dawley rats |
| title_fullStr | ACE2 activation by xanthenone prevents leptin-induced increases in blood pressure and proteinuria during pregnancy in Sprague-Dawley rats |
| title_full_unstemmed | ACE2 activation by xanthenone prevents leptin-induced increases in blood pressure and proteinuria during pregnancy in Sprague-Dawley rats |
| title_short | ACE2 activation by xanthenone prevents leptin-induced increases in blood pressure and proteinuria during pregnancy in Sprague-Dawley rats |
| title_sort | ace2 activation by xanthenone prevents leptin-induced increases in blood pressure and proteinuria during pregnancy in sprague-dawley rats |