Abstract
The effect of uni-axial cyclic mechanical stretch on the expression of cyclooxygenases (COX) was investigated in a human lung fibroblast cell line (TIG-1). In response to uni-axial cyclic stretch, the level of COX2 mRNA significantly increased and peaked at 3 h (9.09 ± 3.82-fold, mean ± standard error, n = 6, compared with that at 1 h). The level of the expression of COX2 protein peaked at 6 h, whereas the level of COX1 protein was not significantly changed. The involvement of stretch-activated (SA) channel was investigated in the stretch-induced COX2 production. The application of Gd3+, a blocker for SA channel, or the removal of extracellular Ca2+ inhibited the production of COX2 mRNA without any effect on the production of COX1 or GAPDH mRNA. These data strongly suggest that COX2 expression is up-regulated by uni-axial cyclic stretch via the activation of SA channel in human lung fibroblasts.
| Original language | English |
|---|---|
| Pages (from-to) | 615-619 |
| Number of pages | 5 |
| Journal | Biochemical and Biophysical Research Communications |
| Volume | 244 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - Mar 27 1998 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Biochemistry
- Biophysics
- Molecular Biology
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Up-regulation of COX2 expression by uni-axial cyclic stretch in human lung fibroblast cells. / Kato, Takefumi; Ishiguro, Naoki; Iwata, Hisashi; Kojima, Toshihisa; Ito, Takayasu; Naruse, Keiji.
In: Biochemical and Biophysical Research Communications, Vol. 244, No. 3, 27.03.1998, p. 615-619.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Up-regulation of COX2 expression by uni-axial cyclic stretch in human lung fibroblast cells
AU - Kato, Takefumi
AU - Ishiguro, Naoki
AU - Iwata, Hisashi
AU - Kojima, Toshihisa
AU - Ito, Takayasu
AU - Naruse, Keiji
PY - 1998/3/27
Y1 - 1998/3/27
N2 - The effect of uni-axial cyclic mechanical stretch on the expression of cyclooxygenases (COX) was investigated in a human lung fibroblast cell line (TIG-1). In response to uni-axial cyclic stretch, the level of COX2 mRNA significantly increased and peaked at 3 h (9.09 ± 3.82-fold, mean ± standard error, n = 6, compared with that at 1 h). The level of the expression of COX2 protein peaked at 6 h, whereas the level of COX1 protein was not significantly changed. The involvement of stretch-activated (SA) channel was investigated in the stretch-induced COX2 production. The application of Gd3+, a blocker for SA channel, or the removal of extracellular Ca2+ inhibited the production of COX2 mRNA without any effect on the production of COX1 or GAPDH mRNA. These data strongly suggest that COX2 expression is up-regulated by uni-axial cyclic stretch via the activation of SA channel in human lung fibroblasts.
AB - The effect of uni-axial cyclic mechanical stretch on the expression of cyclooxygenases (COX) was investigated in a human lung fibroblast cell line (TIG-1). In response to uni-axial cyclic stretch, the level of COX2 mRNA significantly increased and peaked at 3 h (9.09 ± 3.82-fold, mean ± standard error, n = 6, compared with that at 1 h). The level of the expression of COX2 protein peaked at 6 h, whereas the level of COX1 protein was not significantly changed. The involvement of stretch-activated (SA) channel was investigated in the stretch-induced COX2 production. The application of Gd3+, a blocker for SA channel, or the removal of extracellular Ca2+ inhibited the production of COX2 mRNA without any effect on the production of COX1 or GAPDH mRNA. These data strongly suggest that COX2 expression is up-regulated by uni-axial cyclic stretch via the activation of SA channel in human lung fibroblasts.
UR - http://www.scopus.com/inward/record.url?scp=0032571133&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0032571133&partnerID=8YFLogxK
U2 - 10.1006/bbrc.1998.8335
DO - 10.1006/bbrc.1998.8335
M3 - Article
C2 - 9535714
AN - SCOPUS:0032571133
VL - 244
SP - 615
EP - 619
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
SN - 0006-291X
IS - 3
ER -