Bone marrow derived cells and reactive oxygen species in hypertrophy of contralateral kidney of transient unilateral renal ischemia-induced mouse

Free Radical Research

Volumn 46, Issue 7, 2012, Pages 903-911

  Jang, Hee Seong ^a   Kim, Jee In ^a   Kim, Jinu ^a   Na, Yeon Kyung ^b   Park, Jeen Woo ^b   Park, Kwon Moo ^a  

^a Kyungpook National University School of Medicine   (South Korea)

^b Kyungpook National University   (South Korea)

Author keywords

Kidney hypertrophy; NADPH oxidase; Reactive oxygen species; Superoxide dismutase mimetic; Unilateral ischemia

Indexed keywords

APOCYNIN; PORPHYRIN; REACTIVE OXYGEN METABOLITE; REDUCED NICOTINAMIDE ADENINE DINUCLEOTIDE PHOSPHATE OXIDASE 2; SUPEROXIDE; SUPEROXIDE DISMUTASE;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; B LYMPHOCYTE; BONE MARROW CELL; CONTROLLED STUDY; DISEASE ASSOCIATION; KIDNEY HYPERTROPHY; KIDNEY ISCHEMIA; LIPID PEROXIDATION; MALE; MOUSE; NONHUMAN; PROTEIN EXPRESSION;

ACETOPHENONES; ANIMALS; BIOMIMETIC MATERIALS; BONE MARROW CELLS; CELL MOVEMENT; ENZYME INHIBITORS; GENE EXPRESSION; HYPERTROPHY; KIDNEY; MALE; METALLOPORPHYRINS; MICE; MICE, INBRED C57BL; NADPH OXIDASE; ORGAN SIZE; REACTIVE OXYGEN SPECIES; REPERFUSION INJURY; SUPEROXIDE DISMUTASE;

EID: 84862185871     PISSN: 10715762     EISSN: 10292470     Source Type: Journal    
DOI: 10.3109/10715762.2012.686664     Document Type: Article

References (33)

1. Chen JK, Chen J, Thomas G, Kozma SC, Harris RC. S6 kinase 1 knockout inhibits uninephrectomy-or diabetes-induced renal hypertrophy. Am J Physiol Renal Physiol 2009;297:F585-F593.
2. Fine LG, Norman J. Cellular events in renal hypertrophy. Annu Rev Physiol 1989;51:19-32.
3. Chade AR, Rodriguez-Porcel M, Grande JP, Krier JD, Lerman A, Romero JC, et al. Distinct renal injury in early atherosclerosis and renovascular disease. Circulation 2002;106: 1165-1171.
4. Garovic VD, Textor SC. Renovascular hypertension and ischemic nephropathy. Circulation 2005;112:1362-1374.
5. Textor SC. Ischemic nephropathy: where are we now? J Am Soc Nephrol 2004;15:1974-1982.
6. Tokuyama H, Kelly DJ, Zhang Y, Gow RM, Gilbert RE. Mac-rophage infi ltration and cellular proliferation in the non-ischemic kidney and heart following prolonged unilateral renal ischemia. Nephron Physiol 2007;106:p54-p62.
7. Kim J, Seok YM, Jung KJ, Park KM. Reactive oxygen species/oxidative stress contributes to progression of kidney fi brosis following transient ischemic injury in mice. Am J Physiol Renal Physiol 2009;297:F461-F470.
8. Kwak W, Jang HS, Belay T, Kim J, Ha YS, Lee SW, et al. Evaluation of kidney repair capacity using (99 m)Tc-DMSA in ischemia/reperfusion injury models. Biochem Biophys Res Commun 2011;406:7-12.
9. Yang L, Besschetnova TY, Brooks CR, Shah JV, Bonventre JV. Epithelial cell cycle arrest in G2/M mediates kidney fi brosis after injury. Nat Med 2010;16:535-543, 531p following 143.
10. Park KM, Chen A, Bonventre JV. Prevention of kidney ischemia/reperfusion- induced functional injury and JNK, p38, and MAPK kinase activation by remote ischemic pretreatment. J Biol Chem 2001;276:11870-11876.
11. Park KM, Kramers C, Vayssier-Taussat M, Chen A, Bonventre JV. Prevention of kidney ischemia/reperfusion-induced functional injury, MAPK and MAPK kinase activation, and infl am-mation by remote transient ureteral obstruction. J Biol Chem 2002;277:2040-2049.
12. Kim J, Kil IS, Seok YM, Yang ES, Kim DK, Lim DG, et al. Orchiectomy attenuates post-ischemic oxidative stress and ischemia/reperfusion injury in mice. A role for manganese superoxide dismutase. J Biol Chem 2006;281:20349-20356.
13. Jang HS, Kim J, Park YK, Park KM. Infi ltrated macrophages contribute to recovery after ischemic injury but not to ischemic preconditioning in kidneys. Transplantation 2008;85:447-455.
14. Duffield JS, Park KM, Hsiao LL, Kelley VR, Scadden DT, Ichimura T, Bonventre JV. Restoration of tubular epithelial cells during repair of the postischemic kidney occurs independently of bone marrow-derived stem cells. J Clin Invest 2005;115:1743-1755.
15. Liang HL, Hilton G, Mortensen J, Regner K, Johnson CP, Nilakantan V. MnTMPyP, a cell-permeant SOD mimetic, reduces oxidative stress and apoptosis following renal ischemia-reperfusion. Am J Physiol Renal Physiol 2009;296: F266-F276.
16. Zielonka J, Hardy M, Kalyanaraman B. HPLC study of oxidation products of hydroethidine in chemical and biological systems: ramifi cations in superoxide measurements. Free Radic Biol Med 2009;46:329-338.
17. Bedard K, Krause KH. The NOX family of ROS-generating NADPH oxidases: physiology and pathophysiology. Physiol Rev 2007;87:245-313.
18. Djamali A, Vidyasagar A, Adulla M, Hullett D, Reese S. Nox-2 is a modulator of fi brogenesis in kidney allografts. Am J Transplant 2009;9:74-82.
19. Cristovao AC, Choi DH, Baltazar G, Beal MF, Kim YS. The role of NADPH oxidase 1-derived reactive oxygen species in paraquat-mediated dopaminergic cell death. Antioxid Redox Signal 2009;11:2105-2118.
20. Aldieri E, Riganti C, Polimeni M, Gazzano E, Lussiana C, Campia I, Ghigo D. Classical inhibitors of NOX NAD(P)H oxidases are not specifi c. Curr Drug Metab 2008;9: 686-696.
21. Ozeki M, Nagasu H, Satoh M, Namikoshi T, Haruna Y, Tom-ita N, et al. Reactive oxygen species mediate compensatory glomerular hypertrophy in rat uninephrectomized kidney. J Physiol Sci 2009;59:397-404.
22. Gorin Y, Block K, Hernandez J, Bhandari B, Wagner B, Barnes JL, Abboud HE. Nox4 NAD(P)H oxidase mediates hypertrophy and fi bronectin expression in the diabetic kidney. J Biol Chem 2005;280:39616-39626.
23. Golab F, Kadkhodaee M, Zahmatkesh M, Hedayati M, Arab H, Schuster R, et al. Ischemic and non-ischemic acute kidney injury cause hepatic damage. Kidney Int 2009;75: 783-792.
24. Meldrum KK, Meldrum DR, Meng X, Ao L, Harken AH. TNF-alpha-dependent bilateral renal injury is induced by unilateral renal ischemia-reperfusion. Am J Physiol Heart Circ Physiol 2002;282:H540-H546.
25. Lee HT, Park SW, Kim M, D'Agati VD. Acute kidney injury after hepatic ischemia and reperfusion injury in mice. Lab Invest 2009;89:196-208.
26. Weinbroum AA, Hochhauser E, Rudick V, Kluger Y, Karchevsky E, Graf E, Vidne BA. Multiple organ dysfunction after remote circulatory arrest: common pathway of radical oxygen species? J Trauma 1999;47:691-698.
27. D'Autreaux B, Toledano MB. ROS as signalling molecules: mechanisms that generate specifi city in ROS homeostasis. Nat Rev Mol Cell Biol 2007;8:813-824.
28. Droge W. Free radicals in the physiological control of cell function. Physiol Rev 2002;82:47-95.
29. Maejima Y, Kuroda J, Matsushima S, Ago T, Sadoshima J. Regulation of myocardial growth and death by NADPH oxi-dase. J Mol Cell Cardiol 2011;50:408-416.
30. Fujita H, Omori S, Ishikura K, Hida M, Awazu M. ERK and p38 mediate high-glucose-induced hypertrophy and TGF-beta expression in renal tubular cells. Am J Physiol Renal Physiol 2004;286:F120-F126.
31. Haddad F, Adams GR. Inhibition of MAP/ERK kinase prevents IGF-I-induced hypertrophy in rat muscles. J Appl Phys-iol 2004;96:203-210.
32. Beissenhirtz MK, Scheller FW, Lisdat F. A superoxide sensor based on a multilayer cytochrome c electrode. Anal Chem 2004;76:4665-4671.
33. Griendling KK, Sorescu D, Ushio-Fukai M. NAD(P)H oxi-dase: role in cardiovascular biology and disease. Circ Res 2000;86:494-501.