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Age-Dependent Expression of Fibrosis-Related Genes and Collagen Deposition in Rat Kidney Cortex

^a Department of Internal Medicine and Geriatrics, Milan and Milan-Bicocca University, Ospedale Maggiore Istituto di Ricovero e Cura a Carattere Scientifico, Milan, Italy.
^b Prassis, Istituto di Ricerche Sigma-Tau, Milan, Italy.
^c Department of Cardiovascular Research, Istituto di Ricerche Farmacologiche "Mario Negri," Milan, Italy.

Giorgio Annoni, Department of Internal Medicine and Geriatrics, Ospedale Maggiore IRCCS, Via Pace 9, 20122 Milan, Italy E-mail: geriatri{at}polic.cilea.it.

Decision Editor: Jay Roberts, PhD

Because progressive fibrosis is a histological hallmark of the aging kidney, we sought to characterize the course of some fibrosis-related genes [pro-2(I)collagen (COL-I), pro-1(III)collagen (COL-III), and transforming growth factors ß1 and ß3 (TGF-ß1 and TGF-ß3)] of interstitial collagen accumulation [COL-I and COL-III proteins, hydroxyproline (PRO-OH), histology] and its degradation (matrix metalloproteinase MMP-1 and -2) during maturation and early aging in rats. During the lifespan considered we observed no changes in the mRNA, except that COL-I mRNA tended to be up-regulated from 2 to 19 months of age. However, progressive fibrosis was histologically detectable, with COL-I accumulation ( p < .05 and p < .01 in 12-month- and 19-month-old rats vs the youngest), and confirmed by the PRO-OH tissue levels ; COL-III seemed to be less involved. The MMP-1 protein level decreased significantly in the cortex of 12-month- and 19-month-old rats (p < .05), whereas MMP-2 protein level and activity remained essentially unchanged. These results show that, during aging of the kidney, (i) renal cortex fibrosis is explained by COL-I accumulation as a consequence of an altered balance between its synthesis and degradation, and (ii) the expression of the pleiotropic factor TGF-ß in the renal cortex is not modified.