Fibroblast growth factor-1 (acidic fgf) in normal and regenerating
kidney: expression in mononuclear, interstitial and regenerating
epithelial cells.
Ichimura, Takaharu, Jeanette A.-M. Maier, Thomas Maciag, Guohong
Zhang, and James L. Stevens.
The W. Alton Jones Cell Science Center, Old Barn Road, Lake Placid,
NY 12946, Phone: 518-523-1253, FAX:518-523-1849, Laboratory of
Molecular Biology, Holland Laboratory, American Red Cross, Rockville,
MD 20855
APStracts 2:0073F, 1995.
The proximal tubule epithelium regenerates following nephrotoxic
damage. To determine the role of fibroblast growth factors (FGFs) in
the regeneration of rat proximal tubule epithelial cells (RPTE), we
investigated proliferation, differentiation and FGF-1 expression in
vivo in rat kidney before and after nephrotoxic damage to the
proximal tubule epithelium caused by S-(1,1,2,2-tetrafluoroethyl)-L
-cysteine administration. In undamaged kidneys, FGF-1 was expressed in
distal tubule elements, including cortical and medullary collecting
ducts, as well as blood vessels and glomeruli, but was absent in
RPTE. One day after damage there was an increase in proliferation of
surviving proximal tubule epithelial cells and a coincident increase
in FGF-1 expression in invading mononuclear cells. After this initial
burst of proliferation, FGF-1 expression increased in poorly
differentiated vimentin-positive regenerative epithelial cells
indicating that autocrine FGF-1 expression in the regenerative
epithelium is a later event in the regeneration process. FGF-1
staining persisted in foci of macrophages, interstitial cells and
nephropathic tubules within areas of interstitial expansion two weeks
after damage. We concluded that transient paracrine and autocrine
expression of FGF-1 could play mitogenic and/or morphogenic roles
during tubular regeneration. Persistent expression in macrophages,
fibroblasts and nephropathic tubules may be associated with tubular
degeneration. FGF-1 expression may be an important contributor to
both tubular regeneration and degenerative disease following toxicant
exposure.
Received 28 November 1994; accepted in final form 26 April 1995.
APS Manuscript Number F419-4.
Article publication pending Am. J. Physiol. (Renal Fluid Electrolyte
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 2 May 1995.