Premature senescence and cellular phenotype transformation of mesangial cells induced by TGF-B1.
Ren Fail
; 35(8): 1142-5, 2013 Sep.
Article
em En
| MEDLINE
| ID: mdl-23883105
ABSTRACT
BACKGROUND:
Transforming growth factor-ß1 (TGF-ß1) is a polypeptide member of the transforming growth factor ß superfamily of cytokines and performs many cellular functions. Its overexpression may lead to renal fibrosis.AIM:
This study planed to investigate the effects of TGF-ß1 on the cell cycle and phenotype of mesangial cells.METHODS:
Rat mesangial cells were cultured together with different concentrations (0, 1, 2, 5, and 10 ng/mL) of TGF-ß1 for specified times from 0 min to 72 h. 0 ng/mL TGF-ß1 and 0 min served as controls. Cell cycles were assessed by flow cytometry and α-smooth muscle actin expression (α-SMA) protein expression by western blot analysis. All data were presented as Mean ± SD. Statistical analysis was performed by using one-way analysis of variance and correlation analysis. Results were considered significant at p < 0.05.RESULTS:
After 15 min of co-culture with different concentrations of TGF-ß1, the percentage of mesangial cells in G0/G1 phase was significantly elevated compared to the control (p < 0.05). 12 h co-culture induced cell hyperplasia, 24 h co-culture obvious up-regulation of α-SMA (p < 0.01) and one or two cells' myofibroblast phenotype transition, and 36 h co-culture several cells' phenotype transition. Correlation analysis prompted that the TGF-ß1-induced premature aging was time-dependent (p < 0.01).CONCLUSION:
TGF-ß1 may induce mesangial cells' premature senescence and myofibroblast-like phenotype transformation time-dependently, which may contribute to the development of early stage of glomerulosclerosis.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Ciclo Celular
/
Senescência Celular
/
Células Mesangiais
/
Fator de Crescimento Transformador beta1
Limite:
Animals
Idioma:
En
Revista:
Ren Fail
Assunto da revista:
NEFROLOGIA
Ano de publicação:
2013
Tipo de documento:
Article