Tags

Type your tag names separated by a space and hit enter

Reactive oxygen species/oxidative stress contributes to progression of kidney fibrosis following transient ischemic injury in mice.
Am J Physiol Renal Physiol. 2009 Aug; 297(2):F461-70.AJ

Abstract

Recently, kidney fibrosis following transplantation has become recognized as a main contributor of chronic allograft nephropathy. In transplantation, transient ischemia is an inescapable event. Reactive oxygen species (ROS) play a critical role in ischemia and reperfusion (I/R)-induced acute kidney injury, as well as progression of fibrosis in various diseases such as hypertension, diabetes, and ureteral obstruction. However, a role of ROS/oxidative stress in chronic kidney fibrosis following I/R injury remains to be defined. In this study, we investigated the involvement of ROS/oxidative stress in kidney fibrosis following kidney I/R in mice. Mice were subjected to 30 min of bilateral kidney ischemia followed by reperfusion on day 0 and then administered with either manganese (III) tetrakis(1-methyl-4-pyridyl) porphyrin (MnTMPyP, 5 mg/kg body wt ip), a cell permeable superoxide dismutase (SOD) mimetic, or 0.9% saline (vehicle) beginning at 48 h after I/R for 14 days. I/R significantly increased interstitial extension, collagen deposition, apoptosis of tubular epithelial cells, nitrotyrosine expression, hydrogen peroxide production, and lipid peroxidation and decreased copper-zinc SOD, manganese SOD, and glucose 6-phosphate dehydrogenase activities in the kidneys 16 days after the procedure. MnTMPyP administration minimized these postischemic changes. In addition, MnTMPyP administration significantly attenuated the increases of alpha-smooth muscle actin, PCNA, S100A4, CD68, and heat shock protein 47 expression following I/R. We concluded that kidney fibrosis develops chronically following I/R injury, and this process is associated with the increase of ROS/oxidative stress.

Authors+Show Affiliations

Department of Anatomy and BK 21 Project, Kyungpook National University School of Medicine, Daegu, Republic of Korea.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19458120

Citation

Kim, Jinu, et al. "Reactive Oxygen Species/oxidative Stress Contributes to Progression of Kidney Fibrosis Following Transient Ischemic Injury in Mice." American Journal of Physiology. Renal Physiology, vol. 297, no. 2, 2009, pp. F461-70.
Kim J, Seok YM, Jung KJ, et al. Reactive oxygen species/oxidative stress contributes to progression of kidney fibrosis following transient ischemic injury in mice. Am J Physiol Renal Physiol. 2009;297(2):F461-70.
Kim, J., Seok, Y. M., Jung, K. J., & Park, K. M. (2009). Reactive oxygen species/oxidative stress contributes to progression of kidney fibrosis following transient ischemic injury in mice. American Journal of Physiology. Renal Physiology, 297(2), F461-70. https://doi.org/10.1152/ajprenal.90735.2008
Kim J, et al. Reactive Oxygen Species/oxidative Stress Contributes to Progression of Kidney Fibrosis Following Transient Ischemic Injury in Mice. Am J Physiol Renal Physiol. 2009;297(2):F461-70. PubMed PMID: 19458120.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Reactive oxygen species/oxidative stress contributes to progression of kidney fibrosis following transient ischemic injury in mice. AU - Kim,Jinu, AU - Seok,Young Mi, AU - Jung,Kyong-Jin, AU - Park,Kwon Moo, Y1 - 2009/05/20/ PY - 2009/5/22/entrez PY - 2009/5/22/pubmed PY - 2009/8/28/medline SP - F461 EP - 70 JF - American journal of physiology. Renal physiology JO - Am J Physiol Renal Physiol VL - 297 IS - 2 N2 - Recently, kidney fibrosis following transplantation has become recognized as a main contributor of chronic allograft nephropathy. In transplantation, transient ischemia is an inescapable event. Reactive oxygen species (ROS) play a critical role in ischemia and reperfusion (I/R)-induced acute kidney injury, as well as progression of fibrosis in various diseases such as hypertension, diabetes, and ureteral obstruction. However, a role of ROS/oxidative stress in chronic kidney fibrosis following I/R injury remains to be defined. In this study, we investigated the involvement of ROS/oxidative stress in kidney fibrosis following kidney I/R in mice. Mice were subjected to 30 min of bilateral kidney ischemia followed by reperfusion on day 0 and then administered with either manganese (III) tetrakis(1-methyl-4-pyridyl) porphyrin (MnTMPyP, 5 mg/kg body wt ip), a cell permeable superoxide dismutase (SOD) mimetic, or 0.9% saline (vehicle) beginning at 48 h after I/R for 14 days. I/R significantly increased interstitial extension, collagen deposition, apoptosis of tubular epithelial cells, nitrotyrosine expression, hydrogen peroxide production, and lipid peroxidation and decreased copper-zinc SOD, manganese SOD, and glucose 6-phosphate dehydrogenase activities in the kidneys 16 days after the procedure. MnTMPyP administration minimized these postischemic changes. In addition, MnTMPyP administration significantly attenuated the increases of alpha-smooth muscle actin, PCNA, S100A4, CD68, and heat shock protein 47 expression following I/R. We concluded that kidney fibrosis develops chronically following I/R injury, and this process is associated with the increase of ROS/oxidative stress. SN - 1522-1466 UR - https://www.unboundmedicine.com/medline/citation/19458120/Reactive_oxygen_species/oxidative_stress_contributes_to_progression_of_kidney_fibrosis_following_transient_ischemic_injury_in_mice_ L2 - https://journals.physiology.org/doi/10.1152/ajprenal.90735.2008?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -