Poster Presentation: Cardiovascular
Dr. Szakadáti, Gyöngyi
Department of Physiology, Faculty of Medicine, Semmelweis University, Budapest
06-1 459 1500/60444
szakadati.gyongyi@med.semmelweis-univ.hu
Determination of type 1 angiotensin II receptor activation induced gene expression changes in rat vascular smooth muscle cells
Gyöngyi Szakadáti1, András Balla1,2, László Hunyady1,2
1 Department of Physiology, Faculty of Medicine, Semmelweis University, Budapest
2 MTA-SE Laboratory of Molecular Physiology, Budapest
Poster Presentation: Cardiovascular
Doctoral School: Molecular Medicine
Program: 01. Cellular and Molecular Physiology
Supervisors: László Hunyady, András Balla
E-mail address: szakadati.gyongyi@med.semmelweis-univ.hu
Angiotensin II (AngII) is a peptide hormone that mainly acts through type 1 angiotensin II receptor (AT1R) to promote a broad variety of biological effects. Hypertrophy, proliferation and cell migration are responses that involve changes in gene expression. We examined several genes (i.e. HB-EGF, DUSP5 etc.) that are upregulated by AngII stimulation in primary rat aortic smooth muscle cells.
Our aim was to investigate their roles in AngII signaling and to identify which arm of the AT1R signaling pathway is responsible for these effects.
In our investigation we used vascular smooth muscle cells isolated from the thoracic aorta of Wistar rats. To verify the presence and function of the AT1R in the isolated cells we used Western blot technique. We applied 100 nM AngII to stimulate the vascular smooth muscle cells for various period of time and mRNA was prepared from the stimulated cells followed by cDNA production using reverse transcriptase. We applied real-time PCR (RT-PCR) technique to evaluate gene expressions. We examined the role of the transactivation of the epidermal growth factor receptor (EGFR) in regulating the expression of the investigated genes. The role of the extracellular regulated kinase (ERK) in the regulation the gene expression was also investigated.
The results of the quantitative PCR measurements confirmed the AngII induced the upregulation of the investigated genes. The maximal induction of the most genes appeared two hours after the AngII stimulation. Inhibition of either the transactivation of EGFR or ERK phosphorylation lowered AngII induced upregulation of the examined genes significantly.
Firstly, the maximal gene expression occurring in one hour and two hours after stimulation suppose different signaling mechanisms. Transactivation of EGFR and ERK activation was found to have an important role in the upregulation of several genes which has not been described yet. Supported by ÚNKP-16-3-III.
P64
Szabad
nem rendelkezett róla
1007
Gyöngyi Szakadáti1, András Balla1,2, László Hunyady1,2
1 Department of Physiology, Faculty of Medicine, Semmelweis University, Budapest
2 MTA-SE Laboratory of Molecular Physiology, Budapest