Glial cell line‐derived neurotrophic factor and basic fibroblast growth factor derived from skeletal muscle pericytes increase the barrier function of endothelial cells in the endomysium

2021 ◽  
Author(s):  
Eri Ishiguchi ◽  
Yasuteru Sano ◽  
Toshihiko Maeda ◽  
Fumitaka Shimizu ◽  
Miwako Fujisawa ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Endothelial Cells ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Cell Line ◽  
Glial Cell ◽  
Basic Fibroblast Growth Factor ◽  
Neurotrophic Factor ◽  
Barrier Function ◽  
Fibroblast Growth

Effects of glial cell line-derived neurotrophic factor, fibroblast growth factor 2 and epidermal growth factor on proliferation and the expression of some genes in buffalo (Bubalus bubalis) spermatogonial cells

2013 ◽  
Vol 25 (8) ◽  
pp. 1149 ◽  
Author(s):  
Prashant H. Kadam ◽  
Sushila Kala ◽  
Himanshu Agrawal ◽  
Karn P. Singh ◽  
Manoj K. Singh ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Fibroblast Growth Factor ◽  
Cell Line ◽  
Glial Cell ◽  
Sertoli Cell ◽  
Neurotrophic Factor ◽  
Feeder Layer ◽  
Fibroblast Growth ◽  
Epidermal Growth

The present study evaluated the effects of glial cell line-derived neurotrophic factor (GDNF), fibroblast growth factor (FGF) 2 and epidermal growth factor (EGF) on proliferation and the expression of some genes in spermatogonial cells. Spermatogonial cells were isolated from prepubertal buffalo testes and enriched by double enzyme treatment, filtration through 80- and 60-μm nylon mesh filters, differential plating on lectin-coated dishes and Percoll density gradient centrifugation. Cells were then cultured on a buffalo Sertoli cell feeder layer and formed colonies within 15–18 days. The colonies were found to predominantly contain undifferentiated Type A spermatogonia because they bound Dolichos biflorus agglutinin and did not express c-kit. The colonies expressed alkaline phosphatase, NANOG, octamer-binding transcription factor (OCT)-4 and tumour rejection antigen (TRA)-1–60. Cells were subcultured for 15 days, with or without growth factor supplementation. After 15 days, colony area and the relative mRNA abundance of PLZF were higher (P < 0.05) following supplementation with 40 ng mL–1 GDNF + 10 ng mL–1 EGF + 10 ng mL–1 FGF2 than with the same concentrations of GDNF alone or GDNF plus either EGF or FGF2. Expression of TAF4B was higher (P < 0.05) in the presence of FGF2, whereas the expression of THY1 was not affected by growth factor supplementation. In the Sertoli cell feeder layer, EGF and FGF2 decreased (P < 0.05), whereas GDNF increased (P < 0.05), the relative mRNA abundance of ETV5 compared with control. In conclusion, an in vitro culture system that incorporates various growth factors was developed for the short-term culture of buffalo spermatogonia.

scholarly journals The Fibrinogen Globe of Tenascin-C Promotes Basic Fibroblast Growth Factor-induced Endothelial Cell Elongation

1999 ◽  
Vol 10 (9) ◽  
pp. 2933-2943 ◽  
Author(s):  
Susanne Schenk ◽  
Ruth Chiquet-Ehrismann ◽  
Edouard J. Battegay
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Fibroblast Growth ◽  
Aortic Endothelial Cells ◽  
Tenascin C ◽  
Cytoskeleton Organization ◽  
Actin Cytoskeleton Organization

To investigate the potential role of tenascin-C (TN-C) on endothelial sprouting we used bovine aortic endothelial cells (BAECs) as an in vitro model of angiogenesis. We found that TN-C is specifically expressed by sprouting and cord-forming BAECs but not by nonsprouting BAECs. To test whether TN-C alone or in combination with basic fibroblast growth factor (bFGF) can enhance endothelial sprouting or cord formation, we used BAECs that normally do not sprout and, fittingly, do not express TN-C. In the presence of bFGF, exogenous TN-C but not fibronectin induced an elongated phenotype in nonsprouting BAECs. This phenotype was due to altered actin cytoskeleton organization. The fibrinogen globe of the TN-C molecule was the active domain promoting the elongated phenotype in response to bFGF. Furthermore, we found that the fibrinogen globe was responsible for reduced cell adhesion of BAECs on TN-C substrates. We conclude that bFGF-stimulated endothelial cells can be switched to a sprouting phenotype by the decreased adhesive strength of TN-C, mediated by the fibrinogen globe.

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