INFORMATION

Date: 27-29 November 2008

Fax: +36-1-4586842
Email: symposium@kardio.sote.hu
Visit the homepage of the Heart Center.
CONFERENCE NEWS
Symposium lectures on-line
20 February, 2009
Most of the lectures of the Symposium were published on-line. You can find the video presentations at the top of each lecture abstract. We hope to complete the whole on-line program in the near feature.
Pictures of Semmelweis Symposium 2008
1 January, 2009
You can find the pictures of all the three days of Semmelweis Symposium 2008 here.
Lecture of Prof. Sándor Kovács
31 December, 2008
You can find the whole video-presentation of Prof. Sándor Kovács at "Lectures" on the following page.
Summary
30 November, 2008
More than 500 participants from 20 countries attended Semmelweis Symposium 2008. You can find a detailed summary of the event here. A summary of press echo in the Hungarian media you can find here.
Poster abstracts
27 November, 2008
You can find the poster abstracts of Semmelweis Symposium 2008 here.
Scientific Program - printable version
23 November, 2008
You can download the printable version of the Scientific Program here.
Cardiovascular pharmacogenomics course
22 November, 2008
According to the program of Semmelweis Symposium, Peter Pokreisz (Katholieke Universiteit Leuven, Belgium) will give a lecture (in Hungarian) on cGMP regulatory mechanisms in cardiology at 18:00 Wednesday, 26 November.
Abstract submission period extended
14 November 2008
The deadline for abstract submission was extended until 18 November 2008. More detailes on the Abstract submission form.
On-line registration
4 November. 2008
Participation in the program of Semmelweis Symposium 2008 is free.
However, completion the on-line registration form is required to attend the Symposium.
Abstract submission for poster presentation
3 November, 2008
Abstracts for poster presentation are welcome to the Semmelweis Symposium. Deadline for abstract submission  is 15 November. More detailes on the Abstract Submission Form.
PhD course registration
2 November, 2008
Semmelweis Symposium 2008 was accredited by the School of Doctoral Studies of Semmelweis University. Students attending all the three days of the Symposium will get 2 PhD credits.
OFTEX registration
2 November, 2008
Semmelweis Symposium 2008 was registred to the OFTEX system. Colleagues attending all the three days of the Symposium will get 20 OFTEX credits. For detailed information look for SE-TK/2008-07/00383 at www.oftex.hu .
Final program
30 October, 2008
The final program of the Symposium has been completed. For detailes visit to the Scientific Program pages.
Current trends in Cardiology
18 August. 2008
This year cardiology is in the focus of Semmelweis Symposium. The members of the Heart Center take the opportunity to kindly invite you to this event.
Scientific Program | Pictures | Lectures | Posters | Location

Role of Signal Transducer and Activator of Transcription 3 in Angiotensin II-Induced Left Ventricular Hypertrophy In Vivo

  • Réka, Skoumal; Gábor, Füredi; Ábel, Perjés; Jaana, Rysa; Béla, Merkely; Miklós, Tóth; Heikki, Ruskoaho; István, Szokodi
  • RS, JR, HR - Department of Pharmacology and Toxicology, University of Oulu
    GF, ÁP, IS - Heart Institute, University of Pécs
    BM - Heart Center, Semmelweis University
    MT - Department of Health Sciences and Sport Medicine, Faculty of Physical Education and Sport Sciences, Semmelweis University
The transcription factor Signal Transducer and Activator of Transcription 3 (STAT3) has been implicated in the hypertrophic response of cultured cardiomyocytes; however, its precise function in the hypertrophic process in vivo is unknown. In this study we characterized the role of STAT3 in pressure overload-induced left ventricular (LV) hypertrophy. Male Sprague-Dawley rats were infused with vehicle or angiotensin II (Ang II) at a pressor dose (33 μg/kg/h) via subcutaneously implantated osmotic minipumps for 1 week in the presence and absence of parthenolide (0.5 mg/kg/day, i.p.), an inhibitor of STAT3. Western blot analysis revealed that Ang II infusion for 1 week increased the phosphorylation of Janus kinase 2 (JAK2) on Tyr1007/1008 (1.5-fold, P<0.01), the upstream activator of STAT proteins, and STAT3 on Tyr705 (1.6-fold, P<0.05) and Ser727 (1.7-fold, P<0.01). Administration of parthenolide abolished tyrosine and serine phosphorylation of STAT3 (P<0.05), while JAK2 phosphorylation was not altered (P=NS). Infusion of Ang II for 1 week increased LV weight/body weight ratio by 34±6% (P<0.001), which was significantly attenuated by parthenolide (13±3% increase, P<0.05). Echocardiography demonstrated that LV systolic function was preserved in Ang II + parthenolide treated animals despite the reduction in LV mass. Northern blot analysis showed that parthenolide significantly decreased the Ang II-induced increases in the mRNA levels of collagen I (5.2-fold vs. 1.6-fold; P<0.01) and fibronectin (5.3-fold vs. 2.3-fold; P<0.05). Moreover the reduction in fibrosis was also confirmed by histology. In summary, our work presents an in vivo evidence for a critical role of STAT3 signaling in the hypertrophic process. Our results demonstrate that selective inhibition of STAT3 activation prevents LV hypertrophy without compromising cardiac function. Thus, the suppression of STAT3 signaling appears to be a potential therapeutic strategy targeting the maladaptive features of cardiac hypertrophy.
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