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1 Physiology Department, Pontificia Universidad Catolica de Chile, Santiago, Chile
* To whom correspondence should be addressed. E-mail: svillanu{at}bio.puc.cl.
Recovery from acute renal failure (ARF) requires the replacement of injured cells
with new cells that restore tubule epithelial integrity. We described recently the
expression of a wide range of nephrogenic proteins in tubular cells after ARF
induced by ischemia/reperfusion (I/R) (Villanueva et al., 2006). These markers,
namely, Vimentin, Ncam, bFGF, Pax-2, BMP-7, Noggin, Lim-1, Engrailed, Smad, p-
Smad, HIF-1
, VEGF and Tie-2, are expressed in a time frame similar to that observed in normal kidney development
bFGF participates in early kidney development as a morphogen involved in
mesenchyme/epithelial transition, and it is re-expressed in the recovery phase of
ARF. With the hypothesis that bFGF could accelerate the regeneration after renal
damage, we used recombinant bFGF and studied the expression pattern of the
above described morphogens in ARF. Male Sprague Dawley rats were subjected to
30 minutes of renal ischemic injury and were injected with bFGF 30 µg/kg followed by reperfusion. Rats were sacrificed and the expression of nephrogenic proteins were analyzed by immunohistochemistry and Western blot.
In the animals subjected to I/R treated with bFGF we observed a 12 to 24 hours
earlier and more abundant re-expression of the proteins Ncam, bFGF, Pax-2, BMP-
7, Noggin, Lim-1, Engrailed, VEGF and Tie-2, than the I/R untreated rats. In
addition we observed a reduction in renal damage markers ED-1 and -SMA. These results indicate that bFGF can participate in the regeneration process and suggest that the treatment with bFGF can induce an earlier regeneration process after ischemic acute renal failure.
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