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(American Journal of Pathology. 1999;155:1977-1984.)
© 1999 American Society for Investigative Pathology

Regular Articles

Basic Fibroblast Growth Factor Synthesis by Human Peritoneal Mesothelial Cells

Induction by Interleukin-1

Marcus Victor Cronauer^*, Sylvia Stadlmann, Helmut Klocker^*, Burghard Abendstein, Iris Elisabeth Eder^*, Hermann Rogatsch, Alain Gustave Zeimet, Christian Marth and Felix Albert Offner

From the Departments of Pathology,
Urology,^*
and Obstetrics and Gynecology,
University of Innsbruck, Innsbruck, Austria

Peritoneal mesothelial cells are uniquely located to regulate cellular events in the peritoneal cavity and are an important source for various cytokines and growth factors. This study was conducted to analyze the capacity of human peritoneal mesothelial cells (HPMCs) to synthesize and release basic fibroblast growth factor (bFGF) and to characterize its regulation by inflammatory cytokines. HPMCs constitutively synthesized and released considerable amounts of bFGF as detected by a specific immunoassay. Almost 80% of bFGF (1547 ± 173 pg/10⁵ cells) was localized intracellularly. Approximately 20% of the bFGF (357 ± 27 pg/10⁵ cells) was associated with extracellular matrix components on the HPMC surface. Small amounts of bFGF (<1%) were detectable in tissue culture supernatants (8.4 ± 1.4 pg/10⁵ cells). Treatment of HPMCs with interleukin-1ß (IL-1ß; 1 ng/ml) resulted in a significant increase in bFGF production. The intracellular bFGF content showed a rapid but only transient increase, which was significant above background levels after 24 hours (41% increase; P < 0.05). This increase in intracellular bFGF concentration was associated with an induction of the release of bFGF. Within 96 hours, the release of bFGF to the cell surface and into the supernatant increased by 58% (564 ± 52.4 pg/10⁵ cells; P < 0.01) and by 214% (26.4 ± 3.2 pg/10⁵ cells; P < 0.001), respectively. Neither tumor necrosis factor- nor interferon- affected bFGF synthesis by HPMCs. Stimulation of HPMCs with IL-1ß increased steady-state levels of bFGF-specific mRNA. Immunohistochemical analyses of peritoneal tissue revealed constitutive expression of bFGF by HPMCs. This in situ expression proved to be most pronounced in areas of serosal inflammation in activated HPMCs. Our study demonstrates that HPMCs synthesize and release significant amounts of bFGF and that the expression of this growth factor is significantly up-regulated by the proinflammatory cytokine IL-1ß. The data support the view that HPMCs are key regulators of abdominal disease processes such as peritonitis, peritoneal fibrosis, or peritoneal tumor metastasis.

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