186
Views
18
CrossRef citations to date
0
Altmetric
Research Article

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

, , , , &
Pages 903-911 | Received 03 Feb 2012, Accepted 16 Apr 2012, Published online: 14 May 2012

References

  • 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.
  • Fine LG, Norman J. Cellular events in renal hypertrophy. Annu Rev Physiol 1989;51:19–32.
  • Chade AR, Rodriguez-Porcel M, Grande JP, Krier JD, Lerman A, Romero JC, . Distinct renal injury in early atherosclerosis and renovascular disease. Circulation 2002;106: 1165–1171.
  • Garovic VD, Textor SC. Renovascular hypertension and ischemic nephropathy. Circulation 2005;112:1362–1374.
  • Textor SC. Ischemic nephropathy: where are we now? J Am Soc Nephrol 2004;15:1974–1982.
  • Tokuyama H, Kelly DJ, Zhang Y, Gow RM, Gilbert RE. Macrophage infiltration and cellular proliferation in the non-ischemic kidney and heart following prolonged unilateral renal ischemia. Nephron Physiol 2007;106:p54–p62.
  • Kim J, Seok YM, Jung KJ, Park KM. Reactive oxygen species/oxidative stress contributes to progression of kidney fibrosis following transient ischemic injury in mice. Am J Physiol Renal Physiol 2009;297:F461–F470.
  • Kwak W, Jang HS, Belay T, Kim J, Ha YS, Lee SW, . Evaluation of kidney repair capacity using (99 m)Tc-DMSA in ischemia/reperfusion injury models. Biochem Biophys Res Commun 2011;406:7–12.
  • Yang L, Besschetnova TY, Brooks CR, Shah JV, Bonventre JV. Epithelial cell cycle arrest in G2/M mediates kidney fibrosis after injury. Nat Med 2010;16:535–543, 531p following 143.
  • 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.
  • 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 inflammation by remote transient ureteral obstruction. J Biol Chem 2002;277:2040–2049.
  • Kim J, Kil IS, Seok YM, Yang ES, Kim DK, Lim DG, . 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.
  • Jang HS, Kim J, Park YK, Park KM. Infiltrated macrophages contribute to recovery after ischemic injury but not to ischemic preconditioning in kidneys. Transplantation 2008;85:447–455.
  • 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.
  • 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.
  • Zielonka J, Hardy M, Kalyanaraman B. HPLC study of oxidation products of hydroethidine in chemical and biological systems: ramifications in superoxide measurements. Free Radic Biol Med 2009;46:329–338.
  • Bedard K, Krause KH. The NOX family of ROS-generating NADPH oxidases: physiology and pathophysiology. Physiol Rev 2007;87:245–313.
  • Djamali A, Vidyasagar A, Adulla M, Hullett D, Reese S. Nox-2 is a modulator of fibrogenesis in kidney allografts. Am J Transplant 2009;9:74–82.
  • 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.
  • Aldieri E, Riganti C, Polimeni M, Gazzano E, Lussiana C, Campia I, Ghigo D. Classical inhibitors of NOX NAD(P)H oxidases are not specific. Curr Drug Metab 2008;9: 686–696.
  • Ozeki M, Nagasu H, Satoh M, Namikoshi T, Haruna Y, Tomita N, . Reactive oxygen species mediate compensatory glomerular hypertrophy in rat uninephrectomized kidney. J Physiol Sci 2009;59:397–404.
  • Gorin Y, Block K, Hernandez J, Bhandari B, Wagner B, Barnes JL, Abboud HE. Nox4 NAD(P)H oxidase mediates hypertrophy and fibronectin expression in the diabetic kidney. J Biol Chem 2005;280:39616–39626.
  • Golab F, Kadkhodaee M, Zahmatkesh M, Hedayati M, Arab H, Schuster R, . Ischemic and non-ischemic acute kidney injury cause hepatic damage. Kidney Int 2009;75: 783–792.
  • 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.
  • 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.
  • 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.
  • D’Autreaux B, Toledano MB. ROS as signalling molecules: mechanisms that generate specificity in ROS homeostasis. Nat Rev Mol Cell Biol 2007;8:813–824.
  • Droge W. Free radicals in the physiological control of cell function. Physiol Rev 2002;82:47–95.
  • Maejima Y, Kuroda J, Matsushima S, Ago T, Sadoshima J. Regulation of myocardial growth and death by NADPH oxidase. J Mol Cell Cardiol 2011;50:408–416.
  • 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.
  • Haddad F, Adams GR. Inhibition of MAP/ERK kinase prevents IGF-I-induced hypertrophy in rat muscles. J Appl Physiol 2004;96:203–210.
  • Beissenhirtz MK, Scheller FW, Lisdat F. A superoxide sensor based on a multilayer cytochrome c electrode. Anal Chem 2004;76:4665–4671.
  • Griendling KK, Sorescu D, Ushio-Fukai M. NAD(P)H oxidase: role in cardiovascular biology and disease. Circ Res 2000;86:494–501.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.