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Growth factor-dependent proliferation and invasion of muscle satellite cells require the cell-associated fibrinolytic system.
Biol Chem. 2002 Jan; 383(1):127-36.BC

Abstract

The process of muscle regeneration in normal and dystrophic muscle depends on locally produced cytokines and growth factors and requires the activity of the urokinase plasminogen activator/urokinase plasminogen activator receptor/plasminogen activator inhibitor-1 system. In this study we tested the effect of basic fibroblast growth factor (bFGF), hepatocyte growth factor (HGF) and transforming growth factor-beta (TGFbeta) on the fibrinolytic pattern of normal and dystrophic satellite cells, their mitogenic and motogenic activities and the dependence of such activities on the cell-associated fibrinolytic system. We have observed that the urokinase plasminogen activator (u-PA) receptor is weakly upregulated by bFGF in normal satellite cells, while it is strongly up-regulated by TGFbeta, mainly in dystrophic myoblasts. bFGF up-regulated u-PA in both normal and dystrophic myoblasts grown in primary culture, while a striking down-regulation was observed with TGFbeta. TGFbeta was the only growth factor able to exceptionally up-regulate plasminogen activator inhibitor-1 (PAI-1), mainly in dystrophic satellite cells. HGF did not show any activity on the fibrinolytic system. Proliferation and invasion into Matrigel matrices of normal and dystrophic cells occurred regardless of the growth factor-dependent regulation of the fibrinolytic system. Nevertheless, each growth factor required the efficiency of the constitutive cell-associated fibrinolytic system to operate, as shown by impairment of growth factor activity with antagonists of u-PA and of its receptor. Noteworthy, TGFbeta induced a dose-dependent increase of Matrigel invasion only in dystrophic myoblasts. Since TGFbeta-challenged dystrophic myoblasts undergo an exceptional up-regulation of the receptor and of PAI-1, we propose the possibility that the TGFbeta-induced fibrinolytic pattern (low urokinase plasminogen activator, high receptor and high PAI-1) may be exploited to promote survival and spreading of transplanted engineered myoblasts in Duchenne muscular dystrophy.

Authors+Show Affiliations

Department of Experimental Pathology and Oncology, University of Florence, Italy.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

11928807

Citation

Fibbi, Gabriella, et al. "Growth Factor-dependent Proliferation and Invasion of Muscle Satellite Cells Require the Cell-associated Fibrinolytic System." Biological Chemistry, vol. 383, no. 1, 2002, pp. 127-36.
Fibbi G, D'Alessio S, Pucci M, et al. Growth factor-dependent proliferation and invasion of muscle satellite cells require the cell-associated fibrinolytic system. Biol Chem. 2002;383(1):127-36.
Fibbi, G., D'Alessio, S., Pucci, M., Cerletti, M., & Del Rosso, M. (2002). Growth factor-dependent proliferation and invasion of muscle satellite cells require the cell-associated fibrinolytic system. Biological Chemistry, 383(1), 127-36.
Fibbi G, et al. Growth Factor-dependent Proliferation and Invasion of Muscle Satellite Cells Require the Cell-associated Fibrinolytic System. Biol Chem. 2002;383(1):127-36. PubMed PMID: 11928807.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Growth factor-dependent proliferation and invasion of muscle satellite cells require the cell-associated fibrinolytic system. AU - Fibbi,Gabriella, AU - D'Alessio,Silvia, AU - Pucci,Marco, AU - Cerletti,Massimiliano, AU - Del Rosso,Mario, PY - 2002/4/4/pubmed PY - 2003/2/14/medline PY - 2002/4/4/entrez SP - 127 EP - 36 JF - Biological chemistry JO - Biol Chem VL - 383 IS - 1 N2 - The process of muscle regeneration in normal and dystrophic muscle depends on locally produced cytokines and growth factors and requires the activity of the urokinase plasminogen activator/urokinase plasminogen activator receptor/plasminogen activator inhibitor-1 system. In this study we tested the effect of basic fibroblast growth factor (bFGF), hepatocyte growth factor (HGF) and transforming growth factor-beta (TGFbeta) on the fibrinolytic pattern of normal and dystrophic satellite cells, their mitogenic and motogenic activities and the dependence of such activities on the cell-associated fibrinolytic system. We have observed that the urokinase plasminogen activator (u-PA) receptor is weakly upregulated by bFGF in normal satellite cells, while it is strongly up-regulated by TGFbeta, mainly in dystrophic myoblasts. bFGF up-regulated u-PA in both normal and dystrophic myoblasts grown in primary culture, while a striking down-regulation was observed with TGFbeta. TGFbeta was the only growth factor able to exceptionally up-regulate plasminogen activator inhibitor-1 (PAI-1), mainly in dystrophic satellite cells. HGF did not show any activity on the fibrinolytic system. Proliferation and invasion into Matrigel matrices of normal and dystrophic cells occurred regardless of the growth factor-dependent regulation of the fibrinolytic system. Nevertheless, each growth factor required the efficiency of the constitutive cell-associated fibrinolytic system to operate, as shown by impairment of growth factor activity with antagonists of u-PA and of its receptor. Noteworthy, TGFbeta induced a dose-dependent increase of Matrigel invasion only in dystrophic myoblasts. Since TGFbeta-challenged dystrophic myoblasts undergo an exceptional up-regulation of the receptor and of PAI-1, we propose the possibility that the TGFbeta-induced fibrinolytic pattern (low urokinase plasminogen activator, high receptor and high PAI-1) may be exploited to promote survival and spreading of transplanted engineered myoblasts in Duchenne muscular dystrophy. SN - 1431-6730 UR - https://www.unboundmedicine.com/medline/citation/11928807/Growth_factor_dependent_proliferation_and_invasion_of_muscle_satellite_cells_require_the_cell_associated_fibrinolytic_system_ L2 - https://www.degruyter.com/document/doi/10.1515/BC.2002.013 DB - PRIME DP - Unbound Medicine ER -