Store-Operated Ca2+Entry is involved in Transforming Growth Factor-β1 Facilitated Proliferation of Rat Airway Smooth Muscle Cells

2013 ◽  
Vol 50 (5) ◽  
pp. 439-448 ◽  
Author(s):  
Ya-dong Gao ◽  
Jun-wen Zheng ◽  
Ping Li ◽  
Ming Cheng ◽  
Jiong Yang
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Smooth Muscle Cells ◽  
Airway Smooth Muscle ◽  
Transforming Growth Factor ◽  
Muscle Cells ◽  
Transforming Growth Factor Β1 ◽  
Airway Smooth Muscle Cells

Hyperin Ameliorates Proliferation, Migration, and Extracellular Matrix Formation in Airway Smooth Muscle Cells by Inhibiting Transforming Growth Factor-β1-Induced Nuclear Factor-κB Activation

2020 ◽  
Vol 19 (2) ◽  
pp. 222-227
Author(s):  
Nan Zhang ◽  
Tingting Zhao ◽  
Meirong Bi ◽  
Xuejia He ◽  
Yamin Zhang ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Smooth Muscle Cells ◽  
Airway Smooth Muscle ◽  
Nuclear Factor Kappa B ◽  
Transforming Growth Factor ◽  
Muscle Cells ◽  
Transforming Growth Factor Β1 ◽  
Airway Smooth Muscle Cells ◽  
Nuclear Factor

We have explored the role of hyperin remodeling of airway smooth muscle cells during asthma. To this end, airway smooth muscle cells were isolated from tracheae and bronchi of mice, treated with transforming growth factor-β1 and increasing concentrations of hyperin followed by analysis of cell viability, proliferation, and migration. The levels of extracellular matrix formation were evaluated by analysis of fibronectin and type I collagen. Western blot analysis was used to assess the function of the downstream pathway of nuclear factor-kappa B. Transforming growth factor-β1 treatment led to a dose-dependent increase in type I collagen and fibronectin that was reversed by hyperin. Transforming growth factor-β1 promoted activation of nuclear factor-kappa B pathway with reduced IκBα and enhanced phospho (p)-p65 and p-IκBα. However, hyperin treatment upregulated IκBα and downregulated p-p65/p-IκBα to inactivate NF-κB pathway. In conclusion, hyperin ameliorates proliferation, migration, and extracellular matrix formation in airway smooth muscle cells by inhibiting transforming growth factor-β1-induced nuclear factor-kappa B activation suggesting potential prevention of airway remodeling during asthma.

Response of airway smooth muscle cells to TGF-beta 1: effects on growth and synthesis of glycosaminoglycans

1996 ◽  
Vol 271 (6) ◽  
pp. L910-L917 ◽  
Author(s):  
P. N. Black ◽  
P. G. Young ◽  
S. J. Skinner
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Smooth Muscle Cells ◽  
Cell Size ◽  
Airway Smooth Muscle ◽  
Thymidine Incorporation ◽  
Muscle Cells ◽  
Cell Number ◽  
Airway Smooth Muscle Cells ◽  
Tgf Beta

Transforming growth factor-beta (TGF-beta) is formed in the airways and may have a role in airway remodeling in asthma. We have studied the effects of TGF-beta on bovine airway smooth muscle cells (BASMC) in vitro. Thymidine incorporation by BASMC was inhibited after a 24-h incubation with TGF-beta 1. In contrast, thymidine incorporation by BASMC was stimulated (35.1 +/- 11.2%) after a 48-h incubation with 1 ng/ml TGF-beta 1. Cell number was also increased (25.9 +/- 7.6%) after a 72-h incubation with 3 ng/ml TGF-beta 1. TGF-beta 1 also increased cell size at 72 h, with a 24.3 +/- 6.2% increase in cell, diameter. Increases in BASMC size were accompanied by increased [3H]proline incorporation into cell protein. In cells from any individual animal, there was a strong inverse correlation (r = -0.97) between changes in cell number and cell size. In cells from some animals, the main effect of TGF-beta 1 was to promote an increase in cell number, whereas in others the predominant effect was cell hypertrophy. In contrast epidermal growth factor (EGF) led to an increase in thymidine incorporation and cell number in all preparations but did not increase cell size. TGF-beta 1 also promoted secretion of glycosaminoglycans into culture medium by BASMC with a preferential increase in hyaluronan secretion (4.5-fold) after 24 h. Latent TGF-beta (0.89 +/- 0.06 ng/ml) was also detected in conditioned medium from cultured BASMC, and TGF-beta 1 expression was demonstrated with RNA extracts from BASMC. Varying degrees of both smooth muscle cell hypertrophy and hyperplasia occur in asthma. These results obtained with airway smooth muscle cells indicate that TGF-beta could play a role in the structural changes seen in asthma.

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