ALVAREZ CECILIA INÉS
Congresos y reuniones científicas
Título:
Rab1b modulates the TSH response in thyroid cells in culture
Autor/es:
SAMPIERI, L; MARTINEZ, H; GARCIA IA; ALVAREZ, C
Lugar:
Puerto Natales, CHile
Reunión:
Workshop; EMBO workshop: Current advances in membrane trafficking; 2014
Institución organizadora:
EMBO
Resumen:
Rab1b belongs to the Rab-GTPase family that regulates membrane trafficking and signal
transduction systems able to control diverse cellular activities, including gene expression.
Rab1b is essential for endoplasmic reticulum?Golgi transport. Although it is ubiquitously
expressed, its mRNA levels vary among different tissues, but the importance of this
variability in Rab expression levels remains unclear. In this study we examined different
cellular effects induced by changes in Rab1b levels.
FRTL-5 thyroid cells were chosen as a secretory model. In these cells, secretory activity is
induced by thyroid stimulating hormone (TSH) which stimulates the synthesis of cell
specific proteins that require the secretory pathway to reach their final destination. To
assess the effects of Rab1b on the secretory response in our model, we performed
transient transfections with GFP-Rab1bwt or its dominant-negative mutant. In order to
evaluate the consequences of Rab1b depletion, silencing of Rab1b was carried out in the
same cell line. Analysis were performed comparing cells grown in basal (-TSH) or
stimulated (+TSH) condition.
Our results show that TSH addition increases NIS (Sodium/Iodide Symporter), as well as
Rab1b and GM130. Moreover, an increase in Rab1b enhances NIS expression and NIS
promoter activity, suggesting a role of Rab1b in NIS activation pathway. On the other
hand, we also found that Rab1b inhibition blocked the TSH-stimulated NIS and GM130
increase.
Our data strongly suggests that activation of secretion (or membrane transport) by a
secretory stimulus induces an increase in Rab1b levels. Additionally, changes in Rab1b
expression in FRTL5 cells modify the specific TSH response. Our results show, for the first
time, that changes in Rab1b levels modulate gene promoter activity and strongly suggest
that a Rab1b increase is required to elicit a secretory response.
transduction systems able to control diverse cellular activities, including gene expression.
Rab1b is essential for endoplasmic reticulum?Golgi transport. Although it is ubiquitously
expressed, its mRNA levels vary among different tissues, but the importance of this
variability in Rab expression levels remains unclear. In this study we examined different
cellular effects induced by changes in Rab1b levels.
FRTL-5 thyroid cells were chosen as a secretory model. In these cells, secretory activity is
induced by thyroid stimulating hormone (TSH) which stimulates the synthesis of cell
specific proteins that require the secretory pathway to reach their final destination. To
assess the effects of Rab1b on the secretory response in our model, we performed
transient transfections with GFP-Rab1bwt or its dominant-negative mutant. In order to
evaluate the consequences of Rab1b depletion, silencing of Rab1b was carried out in the
same cell line. Analysis were performed comparing cells grown in basal (-TSH) or
stimulated (+TSH) condition.
Our results show that TSH addition increases NIS (Sodium/Iodide Symporter), as well as
Rab1b and GM130. Moreover, an increase in Rab1b enhances NIS expression and NIS
promoter activity, suggesting a role of Rab1b in NIS activation pathway. On the other
hand, we also found that Rab1b inhibition blocked the TSH-stimulated NIS and GM130
increase.
Our data strongly suggests that activation of secretion (or membrane transport) by a
secretory stimulus induces an increase in Rab1b levels. Additionally, changes in Rab1b
expression in FRTL5 cells modify the specific TSH response. Our results show, for the first
time, that changes in Rab1b levels modulate gene promoter activity and strongly suggest
that a Rab1b increase is required to elicit a secretory response.
