scholarly journals Preconditioning by aerobic exercise reduces acute ischemic renal injury in rats

2019 ◽  
Vol 7 (14) ◽  
Author(s):  
Weslei V. Lima ◽  
Iria Visona ◽  
Nestor Schor ◽  
Waldemar S. Almeida
Keyword(s):  
Aerobic Exercise ◽  
Renal Injury ◽  
Ischemic Renal Injury

Poly(ADP-ribose) polymerase-1 gene ablation protects mice from ischemic renal injury

2005 ◽  
Vol 288 (2) ◽  
pp. F387-F398 ◽  
Author(s):  
Jianfeng Zheng ◽  
Kishor Devalaraja-Narashimha ◽  
Kurinji Singaravelu ◽  
Babu J. Padanilam
Keyword(s):  
Dna Damage ◽  
Cell Death ◽  
Mouse Model ◽  
Renal Injury ◽  
Atp Depletion ◽  
Inflammatory Cascade ◽  
Renal Functions ◽  
Atp Levels ◽  
Ischemic Renal Injury ◽  
Parp 1

Increased generation of reactive oxygen species (ROS) and the subsequent DNA damage and excessive activation of poly(ADP-ribose) polymerase-1 (PARP-1) have been implicated in the pathogenesis of ischemic injury. We previously demonstrated that pharmacological inhibition of PARP protects against ischemic renal injury (IRI) in rats (Martin DR, Lewington AJ, Hammerman MR, and Padanilam BJ. Am J Physiol Regul Integr Comp Physiol 279: R1834–R1840, 2000). To further define the role of PARP-1 in IRI, we tested whether genetic ablation of PARP-1 attenuates tissue injury after renal ischemia. Twenty-four hours after reperfusion following 37 min of bilateral renal pedicle occlusion, the effects of the injury on renal functions in PARP−/− and PARP+/+ mice were assessed by determining glomerular filtration rate (GFR) and the plasma levels of creatinine. The levels of plasma creatinine were decreased and GFR was augmented in PARP−/− mice. Morphological evaluation of the kidney tissues showed that the extent of damage due to the injury in PARP−/− mice was less compared with their wild-type counterparts. The levels of ROS and DNA damage were comparable in the injured kidneys of PARP+/+ and PARP−/− mice. PARP activity was induced in ischemic kidneys of PARP+/+ mice at 6–24 h postinjury. At 6, 12, and 24 h after injury, ATP levels in the PARP+/+ mice kidney declined to 28, 26, and 43%, respectively, whereas it was preserved close to normal levels in PARP−/− mice. The inflammatory cascade was attenuated in PARP−/− mice as evidenced by decreased neutrophil infiltration and attenuated expression of inflammatory molecules such as TNF-α, IL-1β, and intercellular adhesion molecule-1. At 12 h postinjury, no apoptotic cell death was observed in PARP−/− mice kidneys. However, by 24 h postinjury, a comparable number of cells underwent apoptosis in both PARP−/− and PARP+/+ mice kidneys. Thus activation of PARP post-IRI contributes to cell death most likely by ATP depletion and augmentation of the inflammatory cascade in the mouse model. PARP ablation preserved ATP levels, renal functions, and attenuated inflammatory response in the setting of IRI in the mouse model. PARP inhibition may have clinical efficacy in preventing the progression of acute renal failure complications.

scholarly journals P-glycoprotein-deficient mice have proximal tubule dysfunction but are protected against ischemic renal injury

2007 ◽  
Vol 72 (10) ◽  
pp. 1233-1241 ◽  
Author(s):  
M. Huls ◽  
C. Kramers ◽  
E.N. Levtchenko ◽  
M.J.G. Wilmer ◽  
H.B.P.M. Dijkman ◽  
...  
Keyword(s):  
Proximal Tubule ◽  
Renal Injury ◽  
P Glycoprotein ◽  
Ischemic Renal Injury ◽  
Deficient Mice

scholarly journals Osteogenic protein-1 mRNA expression is selectively modulated after acute ischemic renal injury.

1998 ◽  
Vol 9 (8) ◽  
pp. 1456-1463
Author(s):  
M M Almanzar ◽  
K S Frazier ◽  
P H Dube ◽  
A I Piqueras ◽  
W K Jones ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Renal Injury ◽  
Tissue Repair ◽  
Western Blots ◽  
Time Points ◽  
Mrna Content ◽  
Repair Mechanisms ◽  
Osteogenic Protein ◽  
Ischemic Renal Injury ◽  
Deficient Mice

Osteogenic protein-1 (OP-1) is a morphogenetic factor highly expressed in the kidney and involved in tissue repair and development. Homozygous OP-1-deficient mice die shortly after birth due mainly to arrest of renal growth and differentiation. Because postischemic injury involves several repair mechanisms, this study examined whether kidney OP-1 mRNA expression is modulated after ischemia. Acute ischemic renal injury was achieved in rats by unilateral clamping of the renal pedicle followed by reperfusion. Rats were killed at 3, 6, 12, 24, and 48 h and 7 d after reperfusion, and kidneys were microdissected and analyzed by histology and Northern and Western blots. Changes in OP-1 mRNA were determined by measuring the ratio of OP-1/glyceraldehyde 3-phosphate dehydrogenase signals for each OP-1 transcript (4.0 and 2.4 kb) from ischemic, opposite, and sham-operated rats. The OP-1 mRNA content for transcript 4.0 kb was fivefold lower in the whole ischemic kidney compared with that in sham animals 24 h after reperfusion. In the ischemic medulla, OP-1 mRNA was strikingly downregulated 20-fold when compared with the ischemic cortex. Results for transcript 2.4 kb and for the other time points were comparable. OP-1 mRNA expression was also affected in the opposite medulla compared with the sham medulla. However, only in the ischemic medulla was the relative OP-1 content significantly lower at all time points. Similar results were obtained when analyzing OP-1 protein by Western blot at 24 h after reperfusion. Seven days after reperfusion, the levels of OP-1 mRNA returned to baseline. In conclusion, kidney OP-1 mRNA and protein are selectively downregulated in the medulla after acute ischemic renal injury. OP-1 modulation may be a key element for kidney repair.

scholarly journals Cholesterol ester accumulation: An immediate consequence of acute in vivo ischemic renal injury

2001 ◽  
Vol 59 (5) ◽  
pp. 1750-1761 ◽  
Author(s):  
Richard A. Zager ◽  
Ali Johnson ◽  
Katie Anderson ◽  
Sherry Wright
Keyword(s):  
Renal Injury ◽  
Cholesterol Ester ◽  
Ischemic Renal Injury

scholarly journals Activation of Src Kinase in Platelet-Derived Growth Factor-B-Dependent Tubular Regeneration after Acute Ischemic Renal Injury

2003 ◽  
Vol 163 (1) ◽  
pp. 277-286 ◽  
Author(s):  
Mikiko Takikita-Suzuki ◽  
Masakazu Haneda ◽  
Masakiyo Sasahara ◽  
M. Koji Owada ◽  
Takahiko Nakagawa ◽  
...  
Keyword(s):  
Growth Factor ◽  
Renal Injury ◽  
Src Kinase ◽  
Platelet Derived Growth Factor ◽  
Factor B ◽  
Ischemic Renal Injury

Fenoldopam Improves Corticomedullary Oxygen Delivery and Attenuates Angiogenesis Gene Expression in Acute Ischemic Renal Injury

2006 ◽  
Vol 29 (3) ◽  
pp. 165-174 ◽  
Author(s):  
Natarajan Aravindan ◽  
Joshua Samuels ◽  
Bernhard Riedel ◽  
Andrew Shaw
Keyword(s):  
Gene Expression ◽  
Renal Injury ◽  
Oxygen Delivery ◽  
Ischemic Renal Injury
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