TITLE

Basic fibroblast growth factor expression is increased in human renal fibrogenesis and may mediate autocrine fibroblast proliferation

AUTHOR(S)
Strutz, Frank; Zeisberg, Michael; Hemmerlein, Bernhard; Sattler, Burkhard; Hummel, Klaus; Becker, Volker; Müller, Gerhard A.
PUB. DATE
April 2000
SOURCE
Kidney International;Apr2000, Vol. 57 Issue 4, p1521
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
Basic fibroblast growth factor expression is increased in human renal fibrogenesis and may mediate autocrine fibroblast proliferation. Background. Interstitial fibroblasts play a critical role in renal fibrogenesis, and autocrine proliferation of these cells may account for continuous matrix synthesis. Basic fibroblast growth factor (FGF-2) is mitogenic for most cells and exerts intracrine, autocrine, and paracrine effects on epithelial and mesenchymal cells. The aims of the present studies were to localize and quantitate the expression of FGF-2 in normal and pathologic human kidneys and to study the in vitro effects of FGF-2 on proliferation, differentiation, and matrix production of isolated cortical kidney fibroblasts. Methods. FGF-2 protein expression was localized by immunofluoresence double labelings in normal and fibrotic human kidneys. Subsequently, interstitial FGF-2 labeling was determined semiquantitatively in 8 normal kidneys and 39 kidneys with variable degrees of interstitial fibrosis and was correlated with the morphometrically determined interstitial cortical volume. In addition, FGF-2 expression was quantitated by immunoblot analysis in three normal and six fibrotic kidneys. FGF-2 mRNA was localized by in situ hybridizations. Seven primary cortical fibroblast lines were established, and expression of FGF-2 and FGF receptor-1 (FGFR-1) were examined. The effects of FGF-2 on cell proliferation were determined by bromodeoxyuridine incorporation and cell counts, those on differentiation into myofibroblasts by staining for α-smooth muscle actin, and those on matrix synthesis by enzyme-linked immunosorbent assay for collagen type I and fibronectin. Finally, proliferative activity in vivo was evaluated by expression of MIB-1 (Ki-67 antigen). Results. In normal kidneys, FGF-2 expression was confined to glomerular, vascular, and a few tubular as well as interstitial fibroblast-like cells. The expression of FGF-2 protein was increased in human...
ACCESSION #
5888838

 

Related Articles

  • Fibroblast growth factor receptors and their ligands in the adult rat kidney. Cancilla, Belinda; Davies, Ann; Cauchi, Jennifer A.; Risbridger, Gail P.; Bertram, John F. // Kidney International;Jul2001, Vol. 60 Issue 1, p147 

    Fibroblast growth factor receptors and their ligands in the adult rat kidney. Background. Fibroblast growth factors (FGFs) are a family of at least 21 heparin-binding proteins involved in many biological processes, both during development and in the adult, including cell proliferation,...

  • Regulatory molecules in kidney development. Burrow, C.R. // Pediatric Nephrology;Feb2000, Vol. 14 Issue 3, p240 

    The molecular regulation of the complex inductive events associated with formation of the vertebrate excretory system has been progressively elucidated as a result of both genetic and tissue culture approaches. Kidney organogenesis is initiated and maintained by a series of reciprocal inductive...

  • Basic fibroblast growth factor is a morphogenic modulator in kidney vessel development. Kloth, Sabine; Gerdes, Johannes; Wanke, Christiane; Minuth, Will W. // Kidney International;Apr1998, Vol. 53 Issue 4, p970 

    Investigates the fibroblast growth factor in kidney vessel development. Identification of the growth factor as a morphogenic modulator; Maturation of nephrons and collecting duct system; Role of retinoic acid and aldosterone.

  • Circulating concentration of FGF-23 increases as renal function declines in patients with chronic kidney disease, but does not change in response to variation in phosphate intake in healthy volunteers. Larsson, Tobias; Nisbeth, Ulf; Ljunggren, Östen; Jüppner, Harald; Jonsson, Kenneth B. // Kidney International;Dec2003, Vol. 64 Issue 6, p2272 

    Circulating concentration of FGF-23 increases as renal function declines in patients with chronic kidney disease, but does not change in response to variation in phosphate intake in healthy volunteers. Background. Hyperphosphatemia is a risk factor for the development of several different...

  • The Authors Reply:. Ärnlöv, Johan; Larsson, Tobias E // Kidney International;Sep2013, Vol. 84 Issue 3, p621 

    A response from the author of the article regarding the stimulation of fibroblast growth factor-23 (FGF23) expression in early chronic kidney disease (CKD) and whether it can be therapeutically targeted to ease cardiovascular risk.

  • The relationship between circulating fibroblast growth factor 23 and bone metabolism factors in Korean hemodialysis patients. So-Youn Park; Kyung-Hwan Jeong; Ju-Young Moon; Sang-Ho Lee; Chun-Gyoo Ihm; Sang Rhee; Jeong-Taek Woo; In-Hwan Oh; Lee, Tae-Won // Clinical & Experimental Nephrology;Jun2010, Vol. 14 Issue 3, p239 

    Fibroblast growth factor 23 (FGF-23) is a circulating factor that acts as a phosphaturic factor in the kidneys. It is also involved in several disorders of phosphate regulation and bone metabolism. We hypothesized that increased FGF-23 levels in patients with endstage renal disease (ESRD) on...

  • In this Issue.  // Kidney International;Oct2013, Vol. 84 Issue 4, p633 

    An introduction is presented in which the editor discusses various reports within the issue on topics including peptide hormone Hepcidin (Hepc), IgG4-related kidney disease (IgG4-RD) and Fibroblast growth factor 23 (FGF23).

  • Does bone structure accurately reflect serum FGF23 levels in patients with chronic kidney disease? Yokoyama, Keitaro; Nakashima, Akio; Maruyama, Yukio; Ohkido, Ichiro; Yokoo, Takashi // Kidney International;Sep2015, Vol. 88 Issue 3, p640 

    A letter to the editor is presented in response to the article on the regulation of serum fibroblast growth factor 23 (FGF23) levels in chronic kidney patients.

  • High FGF-23 in AKI Raises Death Rises. Charnow, Jody A. // Renal & Urology News;Dec2011, Vol. 10 Issue 12, p1 

    The article reports on the result of a study which shows that the increased levels of fibroblast growth factor 23 (FGF-23) in acute kidney injury (AKI) are linked with an increased risk of death or need for renal replacement therapy (RRT).

Share

Read the Article

Courtesy of THE LIBRARY OF VIRGINIA

Sorry, but this item is not currently available from your library.

Try another library?
Sign out of this library

Other Topics