scholarly journals Bioreactor design for the mechanical stimulation by compression of 3D cell cultures

2021 ◽  
Vol 7 (2) ◽  
pp. 899-902
Author(s):  
Carina M. Micheler ◽  
Paulina A. Geck ◽  
Fiona Charitou ◽  
René Leix ◽  
Peter Foehr ◽  
...  
Keyword(s):  
Cell Cultures ◽  
Force Sensor ◽  
Bone Cell ◽  
Loading Frequency ◽  
Compression Force ◽  
3D Cell Cultures ◽  
Cell Processes ◽  
Bioreactor System ◽  
Stimulation System ◽  
Bone Cell Cultures

Abstract Bioreactors with a controlled physiological environment are being developed to study various cell processes. The influences of mechanostimulation on bone cell cultures can be investigated using a compression bioreactor. The developed bioreactor system applies a cyclic compression force to the specimen via an eccentrically mounted push rod. The compression force is monitored by a force sensor to detect changes in the material properties of the specimen. Depending on the piston setting, a stroke of 0.28 - 2.50 mm can be applied to the specimen. The bioreactor system was tested with a trial run of 18 days. A sample was continuously stimulated with a loading frequency of 2 Hz and a stroke of 1.50 mm. The sterility in the cell chamber as well as the functionality of the realised bioreactor stimulation system could be successfully confirmed

Influence of experimental conditions on osteoblast activity in human primary bone cell cultures

1990 ◽  
Vol 5 (4) ◽  
pp. 337-343 ◽  
Author(s):  
Pascale M. Chavassieux ◽  
Chantal Chenu ◽  
Alexandre Valentin-Opran ◽  
Blandine Merle ◽  
Pierre D. Delmas ◽  
...  
Keyword(s):  
Cell Cultures ◽  
Bone Cell ◽  
Experimental Conditions ◽  
Osteoblast Activity ◽  
Primary Bone ◽  
Bone Cell Cultures

PTH induces modification of transductive events in otosclerotic bone cell cultures

1993 ◽  
Vol 11 (4) ◽  
pp. 257-261 ◽  
Author(s):  
G. Fanó ◽  
G. Venti-Donti ◽  
S. Belia ◽  
G. Paludetti ◽  
A. Antonica ◽  
...  
Keyword(s):  
Cell Cultures ◽  
Bone Cell ◽  
Bone Cell Cultures

Response of normal and osteoporotic human bone cells to mechanical stress in vitro

1998 ◽  
Vol 274 (6) ◽  
pp. E1113-E1120 ◽  
Author(s):  
Jozien G. H. Sterck ◽  
Jenneke Klein-Nulend ◽  
Paul Lips ◽  
Elisabeth H. Burger
Keyword(s):  
Nitric Oxide ◽  
Mechanical Stress ◽  
Cell Cultures ◽  
Bone Cells ◽  
Bone Cell ◽  
Human Bone ◽  
Animal Bone ◽  
Bone Cell Cultures

Bone adapts to mechanical stress, and bone cell cultures from animal origin have been shown to be highly sensitive to mechanical stress in vitro. In this study, we tested whether bone cell cultures from human bone biopsies respond to stress in a similar manner as animal bone cells and whether bone cells from osteoporotic patients respond similarly to nonosteoporotic donors. Bone cell cultures were obtained as outgrowth from collagenase-stripped trabecular bone fragments from 17 nonosteoporotic donors between 7 and 77 yr of age and from 6 osteoporotic donors between 42 and 72 yr of age. After passage, the cells were mechanically stressed by treatment with pulsating fluid flow (PFF; 0.7 ± 0.03 Pa at 5 Hz for 1 h) to mimic the stress-driven flow of interstitial fluid through the bone canaliculi, which is likely the stimulus for mechanosensation in bone in vivo. Similar to earlier studies in rodent and chicken bone cells, the bone cells from nonosteoporotic donors responded to PFF with enhanced release of prostaglandin E2(PGE2) and nitric oxide as well as a reduced release of transforming growth factor-β (TGF-β). The upregulation of PGE2 but not the other responses continued for 24 h after 1 h of PFF treatment. The bone cells from osteoporotic donors responded in a similar manner as the nonosteoporotic donors except for the long-term PGE2 release. The PFF-mediated upregulation of PGE2 release during 24 h of postincubation after 1 h of PFF was significantly reduced in osteoporotic patients compared with six age-matched controls as well as with the whole nonosteoporotic group. These results indicate that enhanced release of PGE2 and nitric oxide, as well as reduced release of TGF-β, is a characteristic response of human bone cells to fluid shear stress, similar to animal bone cells. The results also suggest that bone cells from osteoporotic patients may be impaired in their long-term response to mechanical stress.

Determination and expression of platelet-derived growth factor-AA in bone cell cultures.

Endocrinology ◽  
1992 ◽  
Vol 130 (4) ◽  
pp. 1916-1922
Author(s):  
S Rydziel ◽  
C Ladd ◽  
T L McCarthy ◽  
M Centrella ◽  
E Canalis
Keyword(s):  
Growth Factor ◽  
Cell Cultures ◽  
Bone Cell ◽  
Platelet Derived Growth Factor ◽  
Bone Cell Cultures

Recombinant transforming growth factor type beta 3: biological activities and receptor-binding properties in isolated bone cells

1990 ◽  
Vol 10 (9) ◽  
pp. 4473-4479
Author(s):  
P ten Dijke ◽  
K K Iwata ◽  
C Goddard ◽  
C Pieler ◽  
E Canalis ◽  
...  
Keyword(s):  
Growth Factor ◽  
Cell Cultures ◽  
Binding Sites ◽  
Transforming Growth Factor ◽  
Bone Cell ◽  
Scatchard Analysis ◽  
Tgf Beta ◽  
Surface Binding ◽  
Factor Type ◽  
Bone Cell Cultures

We have recently cloned the cDNA for transforming growth factor type beta 3 (TGF-beta 3), a new member of the TGF-beta gene family. We examined the biological effects of recombinant TGF-beta 3 protein in osteoblast-enriched bone cell cultures. In this report we demonstrate that TGF-beta 3 is a potent regulator of functions associated with bone formation, i.e., mitogenesis, collagen synthesis, and alkaline phosphatase activity. In a direct comparison between TGF-beta 3 and TGF-beta 1, TGF-beta 3 appeared to be three- to fivefold more potent than TGF-beta 1. Our cross-linking experiments with iodinated TGF-beta showed that in osteoblast-enriched bone cell cultures, both TGF-beta 3 and TGF-beta 1 associated with the same three cell surface binding sites. Scatchard analysis of receptor competition studies indicated the presence of high-affinity binding sites for TGF-beta 3 in the picomolar range. TGF-beta 3 showed an approximately fourfold-higher apparent affinity than TGF-beta 1 in overall binding.

Transgenic expression of COL1A1-chloramphenicol acetyltransferase fusion genes in bone: differential utilization of promoter elements in vivo and in cultured cells

1993 ◽  
Vol 13 (9) ◽  
pp. 5168-5174
Author(s):  
P H Krebsbach ◽  
J R Harrison ◽  
A C Lichtler ◽  
C O Woody ◽  
D W Rowe ◽  
...  
Keyword(s):  
Cell Cultures ◽  
Collagen Synthesis ◽  
Cultured Cells ◽  
Bone Cells ◽  
Chloramphenicol Acetyltransferase ◽  
Bone Cell ◽  
Mrna Levels ◽  
Fusion Genes ◽  
Primary Bone ◽  
Bone Cell Cultures

To directly compare the patterns of collagen promoter expression in cells and tissues, the activity of COL1A1 fusion genes in calvariae of neonatal transgenic mice and in primary bone cell cultures derived by sequential digestion of transgenic calvariae was measured. ColCAT3.6 contains 3.6 kb (positions -3521 to +115) of the rat COL1A1 gene ligated to the chloramphenicol acetyltransferase (CAT) reporter gene. ColCAT2.3 and ColCAT1.7 are 5' deletion mutants which contain 2,296 and 1,672 bp, respectively, of COL1A1 DNA upstream from the transcription start site. ColCAT3.6 activity was 4- to 6-fold lower in primary bone cell cultures than in intact calvariae, while ColCAT2.3 activity was at least 100-fold lower in primary bone cells than in calvariae. These changes were accompanied by a threefold decrease in collagen synthesis and COL1A1 mRNA levels in primary bone cells compared with collagen synthesis and COL1A1 mRNA levels in freshly isolated calvariae. ColCAT3.6 and ColCAT2.3 activity was maintained in calvariae cultured in the presence or absence of serum for 4 to 7 days. Thus, when bone cells are removed from their normal microenvironment, there is parallel downregulation of collagen synthesis, collagen mRNA levels, and ColCAT3.6 activity, with a much greater decrease in ColCAT2.3. These data suggest that a 624-bp region of the COL1A1 promoter between positions -2296 and -1672 is active in intact and cultured bone but inactive in cultured cells derived from the bone. We suggest that the downregulation of COL1A1 activity in primary bone cells may be due to the loss of cell shape or to alterations in cell-cell and/or cell-matrix interactions that normally occur in intact bone.

Effect of Exogenous Lipid on Lipid Synthesis by Bone and Bone Cell Cultures

1975 ◽  
Vol 54 (1) ◽  
pp. 131-139 ◽  
Author(s):  
George S. Schuster ◽  
Thomas R. Dirksen ◽  
William S. Harms
Keyword(s):  
Cell Cultures ◽  
Lipid Synthesis ◽  
Bone Cell ◽  
Exogenous Lipid ◽  
Bone Cell Cultures

scholarly journals Transgenic expression of COL1A1-chloramphenicol acetyltransferase fusion genes in bone: differential utilization of promoter elements in vivo and in cultured cells.

1993 ◽  
Vol 13 (9) ◽  
pp. 5168-5174 ◽  
Author(s):  
P H Krebsbach ◽  
J R Harrison ◽  
A C Lichtler ◽  
C O Woody ◽  
D W Rowe ◽  
...  
Keyword(s):  
Cell Cultures ◽  
Collagen Synthesis ◽  
Cultured Cells ◽  
Bone Cells ◽  
Chloramphenicol Acetyltransferase ◽  
Bone Cell ◽  
Mrna Levels ◽  
Fusion Genes ◽  
Primary Bone ◽  
Bone Cell Cultures

To directly compare the patterns of collagen promoter expression in cells and tissues, the activity of COL1A1 fusion genes in calvariae of neonatal transgenic mice and in primary bone cell cultures derived by sequential digestion of transgenic calvariae was measured. ColCAT3.6 contains 3.6 kb (positions -3521 to +115) of the rat COL1A1 gene ligated to the chloramphenicol acetyltransferase (CAT) reporter gene. ColCAT2.3 and ColCAT1.7 are 5' deletion mutants which contain 2,296 and 1,672 bp, respectively, of COL1A1 DNA upstream from the transcription start site. ColCAT3.6 activity was 4- to 6-fold lower in primary bone cell cultures than in intact calvariae, while ColCAT2.3 activity was at least 100-fold lower in primary bone cells than in calvariae. These changes were accompanied by a threefold decrease in collagen synthesis and COL1A1 mRNA levels in primary bone cells compared with collagen synthesis and COL1A1 mRNA levels in freshly isolated calvariae. ColCAT3.6 and ColCAT2.3 activity was maintained in calvariae cultured in the presence or absence of serum for 4 to 7 days. Thus, when bone cells are removed from their normal microenvironment, there is parallel downregulation of collagen synthesis, collagen mRNA levels, and ColCAT3.6 activity, with a much greater decrease in ColCAT2.3. These data suggest that a 624-bp region of the COL1A1 promoter between positions -2296 and -1672 is active in intact and cultured bone but inactive in cultured cells derived from the bone. We suggest that the downregulation of COL1A1 activity in primary bone cells may be due to the loss of cell shape or to alterations in cell-cell and/or cell-matrix interactions that normally occur in intact bone.

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