Effects of Shear Stress on the Growth of Hybridoma Cells Cultivated in Serum-Free Medium Coupled with Ammonia Removing System

1991 ◽  
pp. 95-101
Author(s):  
F. R. Nayve ◽  
M. Matsumura ◽  
H. Kataoka
Keyword(s):  
Shear Stress ◽  
Hybridoma Cells ◽  
Serum Free Medium ◽  
Free Medium ◽  
Serum Free

Apoptosis of pulmonary microvascular endothelial cells stimulates vascular smooth muscle cell growth

2006 ◽  
Vol 291 (3) ◽  
pp. L362-L368 ◽  
Author(s):  
Seiichiro Sakao ◽  
Laimute Taraseviciene-Stewart ◽  
Kathy Wood ◽  
Carlyne D. Cool ◽  
Norbert F. Voelkel
Keyword(s):  
Shear Stress ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Transforming Growth Factor ◽  
Vegf Receptor ◽  
Serum Free Medium ◽  
Free Medium ◽  
Serum Free ◽  
Vsmc Proliferation ◽  
Tgf Β1

We have previously hypothesized that the development of severe angioproliferative pulmonary hypertension is associated with not only initial endothelial cell (EC) apoptosis followed by the emergence of apoptosis-resistant proliferating EC but also with proliferation of vascular smooth muscle cells (VSMC). We have demonstrated that EC death results in the selection of an apoptosis-resistant, proliferating, and phenotypically altered EC phenotype. We postulate here that the initial apoptosis of EC induces the release of mediators that cause VSMC proliferation. We cultured EC in an artificial capillary CellMax system designed to simulate the highly efficient functions of the human capillary system. We induced apoptosis of microvascular EC using shear stress and the combined VEGF receptor (VEGFR-1 and -2) inhibitor SU-5416. Flow cytometry for the proliferation marker bromodeoxyuridine showed that serum-free medium conditioned by apoptosed EC induced proliferation of VSMC, whereas serum-free medium conditioned by nonapoptosed EC did not. We also show that medium conditioned by apoptosed EC is characterized by increased concentrations of transforming growth factor (TGF)-β1 and VEGF compared with medium conditioned by nonapoptosed EC and that TGF-β1 blockade prevented the proliferation of cultured VSMC. In conclusion, EC death induced by high shear stress and VEGFR blockade leads to the production of factors, in particular TGF-β1, that activate VSMC proliferation.

scholarly journals Growth of hybridoma cells in serum-free medium: ethanolamine is an essential component.

1982 ◽  
Vol 79 (4) ◽  
pp. 1158-1162 ◽  
Author(s):  
H. Murakami ◽  
H. Masui ◽  
G. H. Sato ◽  
N. Sueoka ◽  
T. P. Chow ◽  
...  
Keyword(s):  
Hybridoma Cells ◽  
Serum Free Medium ◽  
Free Medium ◽  
Serum Free ◽  
Essential Component

Exogeneous factors are not necessary in attachment, spreading and polarization of hela cells

1978 ◽  
Vol 36 (2) ◽  
pp. 310-311
Author(s):  
W. Liebrich
Keyword(s):  
Hela Cells ◽  
Calf Serum ◽  
Glass Tube ◽  
Serum Free Medium ◽  
Nacl Solution ◽  
Free Medium ◽  
Minimum Essential Medium ◽  
Serum Free ◽  
All Solutions ◽  
Glass Support

HeLa cells were grown for 2-3 days in EAGLE'S minimum essential medium with 10% calf serum (S-MEM; Seromed, München) and then incubated for 24 hours in serum free medium (MEM). After detaching the cells with a solution of 0. 14 % EDTA and 0. 07 % trypsin (Difco, 1 : 250) they were suspended in various solutions (S-MEM = control, MEM, buffered salt solutions with or without Me++ions, 0. 9 % NaCl solution) and allowed to settle on glass tube slips (Leighton-tubes). After 5, 10, 15, 20, 25, 30, 1 45, 60 minutes 2, 3, 4, 5 hours cells were prepared for scanning electron microscopy as described by Paweletz and Schroeter. The preparations were examined in a Jeol SEM (JSM-U3) at 25 KV without tilting.The suspended spherical HeLa cells are able to adhere to the glass support in all solutions. The rate of attachment, however, is faster in solutions without serum than in the control. The latter is in agreement with the findings of other authors.

Hemoglobin Enhances the Binding of Bacterial Endotoxin to Human Endothelial Cells

1996 ◽  
Vol 76 (02) ◽  
pp. 258-262 ◽  
Author(s):  
Robert I Roth
Keyword(s):  
Endothelial Cells ◽  
Binding Protein ◽  
Bacterial Endotoxin ◽  
Dependent Manner ◽  
Serum Free Medium ◽  
Free Medium ◽  
Human Endothelial Cells ◽  
Serum Factors ◽  
Serum Free ◽  
Lps Binding

SummaryHuman endothelial cells, when incubated with bacterial endotoxin (lipopolysaccharide, LPS), modify their surface in association with prominent production of procoagulant tissue factor (TF) activity. This deleterious biological effect of LPS has been shown previously to be enhanced approximately 10-fold by the presence of hemoglobin (Hb), a recently recognized LPS binding protein that causes disaggregation of LPS and increases the biological activity of LPS in a number of in vitro assays. The present study was performed to test the hypothesis that Hb enhances the LPS-induced procoagulant activity of human umbilical vein endothelial cells (HUVEC) by increasing LPS binding to the cells. The binding of 3H-LPS to HUVEC was determined in the absence or presence of Hb or two other known LPS-binding proteins, human serum albumin (HSA) and IgG. LPS binding was substantially increased in the presence of Hb, in a Hb concentration-dependent manner, but was not increased by HSA or IgG. Hb enhancement of LPS binding was observed in serum-free medium, indicating that there was no additional requirement for any of the serum factors known to participate in the interaction of LPS with cells (e.g., lipopolysaccharide (LPS)-binding protein (LBP) and soluble CD14 (sCD14)). Hb enhancement of LPS binding also was observed in the more physiologic condition of 100% plasma. LPS-induced TF activity was stimulated by Hb, but not by HSA or IgG. In serum-free medium, TF activity was not stimulated under any of the conditions tested. Ultrafiltration of LPS was dramatically increased after incubation with Hb but not with HSA or IgG, suggesting that LPS disaggregation by Hb was responsible for the enhanced binding of LPS to HUVEC and the subsequent stimulation of TF activity.

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