Distinct functions of junD in cardiac hypertrophy and heart failure.

نویسندگان

  • Romeo Ricci
  • Urs Eriksson
  • Gavin Y Oudit
  • Robert Eferl
  • Alexander Akhmedov
  • Izabela Sumara
  • Grzegorz Sumara
  • Zamaneh Kassiri
  • Jean-Pierre David
  • Latifa Bakiri
  • Bernd Sasse
  • Maria-Helena Idarraga
  • Martina Rath
  • David Kurz
  • Hans-Christian Theussl
  • Jean-Claude Perriard
  • Peter Backx
  • Josef M Penninger
  • Erwin F Wagner
چکیده

Cardiac hypertrophic stimuli induce both adaptive and maladaptive growth response pathways in heart. Here we show that mice lacking junD develop less adaptive hypertrophy in heart after mechanical pressure overload, while cardiomyocyte-specific expression of junD in mice results in spontaneous ventricular dilation and decreased contractility. In contrast, fra-1 conditional knock-out mice have a normal hypertrophic response, whereas hearts from fra-1 transgenic mice decompensate prematurely. Moreover, fra-1 transgenic mice simultaneously lacking junD reveal a spontaneous dilated cardiomyopathy associated with increased cardiomyocyte apoptosis and a primary mitochondrial defect. These data suggest that junD promotes both adaptive-protective and maladaptive hypertrophy in heart, depending on its expression levels.

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Lactobacillus Paracasei Has Anti-Inflammatory Effect on the Heart Failure Induced by Isoproterenol in Rats

Background: Heart failure (HF) has become one of the most prevalent cardiovascular problems worldwide. Considering the beneficial effects of probiotics on human health, we aimed to investigate the anti-inflammatory effect of oral administration of Lactobacillus paracasei in HF induced by isoproterenol. Methods: Forty Wistar male rats weighing 80g on average were randomly assigned to five grou...

متن کامل

Lack of JunD promotes pressure overload-induced apoptosis, hypertrophic growth, and angiogenesis in the heart.

BACKGROUND The Jun family of activator protein 1 (AP-1) transcription factors (c-Jun, JunB, and JunD) is involved in fundamental biological processes such as proliferation, apoptosis, tumor angiogenesis, and hypertrophy. The role of individual AP-1 transcription factors in the stressed heart is not clear. In the present study we analyzed the role of JunD in survival, hypertrophy, and angiogenes...

متن کامل

تأثیر هشت هفته تمرین تناوبی خیلی شدید بر بیان ژن خانواده miR-29 و هایپرتروفی عضله‌ی قلبی رت‌های نر سالم

Background and Objective: In this study the effect of high intensity interval training on miR-29 expression that is expressed in the heart and in the regulation of physiological processes, including extracellular matrix and cardiac hypertrophy of healthy male rats were examined. Materials and Methods: 16 Wistar rats were divided into training (n=8) and control (n=8) groups. After one week of fa...

متن کامل

Detection of Cardiac Hypertrophy by RVM and SVM Algorithms

The meaning of the hypertropy word is the increasing size.Heart hypertropy is symptoms of increase the thickness of the heart muscle that the left ventricular hypertrophy of them is the most common.The causes of hypertrophy heart disease are high blood pressure , aortic valve stenosis and sport activities respectively. Assessment of that by using ECG signal analysis is essential Because the ris...

متن کامل

Carvacrol Ameliorates Pathological Cardiac Hypertrophy in Both In-vivo and In-vitro Models

Hypertension-induced left ventricular hypertrophy is the most important risk factor for heart failure. This study aimed at investigating the effects of monoterpenoid phenol, carvacrol, on myocardial hypertrophy using both in-vivo and in-vitro models. Male Wistar rats were divided into the control (Ctl), un-treated hypertrophy (H), and carvacrol-treated hypertrophy gro...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:
  • Genes & development

دوره 19 2  شماره 

صفحات  -

تاریخ انتشار 2005