Faculty Opinions recommendation of Mitochondrial damage-induced impairment of angiogenesis in the aging rat kidney.

Author(s):  
Rick Schnellmann
2010 ◽  
Vol 91 (2) ◽  
pp. 190-202 ◽  
Author(s):  
Minoru Satoh ◽  
Sohachi Fujimoto ◽  
Hideyuki Horike ◽  
Masahito Ozeki ◽  
Hajime Nagasu ◽  
...  

1990 ◽  
Vol 15 (3) ◽  
pp. 244-251 ◽  
Author(s):  
Christine Baylis ◽  
Michael Fredericks ◽  
Curtis Wilson ◽  
Karen Munger ◽  
Rose Collins

2009 ◽  
Vol 1 (1) ◽  
pp. 75-83 ◽  
Author(s):  
J. A. Joles ◽  
D. V. Sculley ◽  
S. C. Langley-Evans

Nephrogenesis in the rat starts mid-gestation and continues into lactation. Maternal low protein (LP) intake leads to renal injury in rats and associates with mild renal injury in humans. We hypothesized that LP during early nephrogenesis or throughout gestation would induce more renal injury in rat offspring than when LP was only present before nephrogenesis. Pregnant rats were fed LP diet (9% casein) at early gestation (LPE, day 0–7), mid (LPM, day 8–14), late (LPL, day 15–22) or throughout gestation (LPA, day 0–22) and compared to controls on 18% casein diet. Offspring were studied at 18 months. Renal injury was assessed by 24 h proteinuria, plasma urea, antioxidant enzyme activities, and apoptosis (Bax/Bcl2). Proteinuria was higher in LPM males and LPE and LPM females. In LPM males glutathione peroxidase activity was lower, while in LPE males catalase activity was higher. Antioxidants were not much affected in females. Bax expression was higher in LPM males and females, while Bcl2 expression was higher in LPA females. Thus even before nephrogenesis (day 0–7), LP impacted on renal integrity in adult life, while LP during a later phase (day 15–22) or throughout gestation had less effect. In summary, for aging rat kidney LP poses the greatest threat when restricted to early nephrogenesis.


2007 ◽  
Vol 292 (6) ◽  
pp. F1751-F1760 ◽  
Author(s):  
Susan H. McKiernan ◽  
Victoria C. Tuen ◽  
Katherine Baldwin ◽  
Jonathan Wanagat ◽  
Arjang Djamali ◽  
...  

Adult-onset calorie restriction (A-CR) is an experimental model of life extension and healthy aging less explored, compared with calorie restriction begun at early ages, but one more realistic for human application. We examined the effect of A-CR on the aging rat kidney with respect to common structural age-dependent changes and the accumulation of mitochondrial enzyme abnormalities in tubular epithelial cells. A 40% calorie restriction was initiated in middle-aged rats, before the onset of significant age-related changes in the Fischer × Brown Norway rat kidney. This dietary intervention effectively reduced glomerulosclerosis and tubular atrophy within 6 mo and changed the rate of interstitial fibrosis formation within 1 yr and vascular wall thickening and the expression cytochrome c oxidase (COX)-deficient tubular epithelial cells in 18 mo compared with age-matched ad libitum-fed rats. Our histological approach (histochemical staining for mitochondrial enzyme activity and laser capture microdissection) coupled with mitochondrial DNA (mtDNA) PCR analyses demonstrated that COX-deficient renal tubular epithelial cells accumulated mtDNA deletion mutations and that these cells contained unique, clonally expanded mtDNA deletion mutations. Renal tubular epithelial cells with mitochondrial abnormalities presented cellular characteristics indicative of physiological dysfunction.


1991 ◽  
Vol 61 (2) ◽  
pp. 187-195 ◽  
Author(s):  
Paolo Napoleone ◽  
Elena Bronzetti ◽  
Francesco Amenta

1994 ◽  
Vol 24 (3) ◽  
pp. 499-504 ◽  
Author(s):  
Liliana Schaefer ◽  
Markus Teschner ◽  
Hong Ling ◽  
Ursula Oldakowska ◽  
August Heidland ◽  
...  
Keyword(s):  

2013 ◽  
Vol 93 (3) ◽  
pp. 334-343 ◽  
Author(s):  
Minoru Satoh ◽  
Kengo Kidokoro ◽  
Masahito Ozeki ◽  
Hajime Nagasu ◽  
Yuko Nishi ◽  
...  
Keyword(s):  

1976 ◽  
Vol 31 (1) ◽  
pp. 13-22 ◽  
Author(s):  
W. G. Couser ◽  
M. M. Stilmant
Keyword(s):  

1985 ◽  
Vol 248 (3) ◽  
pp. R282-R287 ◽  
Author(s):  
B. Corman ◽  
J. Pratz ◽  
P. Poujeol

Changes in kidney function were studied in anesthetized female WAG/Rij rats 6, 18, and 30 mo old. The growth in kidney size measured between 6 and 18 mo and 18 and 30 mo was due to enlargement of the glomeruli and lengthening of the proximal tubules, without significant changes in the number of nephrons. Glomerular filtration per gram kidney was unaffected between 6 and 18 mo but diminished 27% between 18 and 30 mo. This reduction was accompanied by an intrarenal redistribution of individual filtration rates for the superficial and deep nephrons. Fractional excretion of sodium, potassium, calcium, and magnesium declined sharply between 6 and 18 mo but did not change further between 18 and 30 mo, whereas the fractional excretion of amino acids and glucose remained constant between 6 and 18 mo but rose in the 30-mo group. Taken together, these observations indicate that, in the rat, kidney aging cannot be reduced to a loss in the number of functional nephrons but is the result of several differential and specific processes.


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