Fetal Mammalian Heart Generates a Robust Compensatory Response to Cell Loss.

نویسندگان

  • Anthony C Sturzu
  • Kuppusamy Rajarajan
  • Derek Passer
  • Karolina Plonowska
  • Alyssa Riley
  • Timothy C Tan
  • Arun Sharma
  • Adele F Xu
  • Marc C Engels
  • Rebecca Feistritzer
  • Guang Li
  • Martin K Selig
  • Richard Geissler
  • Keston D Robertson
  • Marielle Scherrer-Crosbie
  • Ibrahim J Domian
  • Sean M Wu
چکیده

BACKGROUND Heart development is tightly regulated by signaling events acting on a defined number of progenitor and differentiated cardiac cells. Although loss of function of these signaling pathways leads to congenital malformation, the consequences of cardiac progenitor cell or embryonic cardiomyocyte loss are less clear. In this study, we tested the hypothesis that embryonic mouse hearts exhibit a robust mechanism for regeneration after extensive cell loss. METHODS AND RESULTS By combining a conditional cell ablation approach with a novel blastocyst complementation strategy, we generated murine embryos that exhibit a full spectrum of cardiac progenitor cell or cardiomyocyte ablation. Remarkably, ablation of up to 60% of cardiac progenitor cells at embryonic day 7.5 was well tolerated and permitted embryo survival. Ablation of embryonic cardiomyocytes to a similar degree (50% to 60%) at embryonic day 9.0 could be fully rescued by residual myocytes with no obvious adult cardiac functional deficit. In both ablation models, an increase in cardiomyocyte proliferation rate was detected and accounted for at least some of the rapid recovery of myocardial cellularity and heart size. CONCLUSION Our study defines the threshold for cell loss in the embryonic mammalian heart and reveals a robust cardiomyocyte compensatory response that sustains normal fetal development.

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

Harnessing fetal and adult genetic reprograming for therapy of heart disease.

Heart is the first organ formed during organogenesis. The fetal heart undergoes several structural and functional modifications to form the four-chambered mammalian heart. The adult heart shows different adaptations during compensatory and decompensatory heart failure. However, one common adaptation in the pathological heart is fetal reprogramming, where the adult heart expresses several genes ...

متن کامل

The Influence of Signal Loss Episodes on Fetal Heart Rate Variability Measures

The most important features indicating appropriate fetal development are the measures of instantaneous variability of a fetal heart rate (FHR), describing fluctuations of the beat-to-beat heart intervals. The most popular method for the FHR acquisition is the Doppler ultrasound technique. However, it is very sensitive to various motion artifacts distorting the signal being acquired. The aim of ...

متن کامل

A novel isolated dual perfusion/superfusion heart model for physiological and pharmacological evaluation of mammalian heart preparations

Abstract Introduction: Isolated perfused heart models such as perfusion and superfusion are commonly used for mammalian heart research. However, there are several fundamental limitations in the current techniques. In perfusion model, a suitable cannula is connected to the aorta and the perfusion is retrogradely performed. But, electrode displacement is a potential unwanted event resulted fr...

متن کامل

Identification of a Specific Pseudo attP Site for Phage PhiC31 Integrase in Bovine Genome

Background: PhiC31 integrase system provides a new platform in various felid of research, mainly in gene therapy and creation of transgenic animals. This system enables integration of exogenous DNA into preferred locations in mammalian genomes, which results in robust, long-term expression of the integrated transgene. Objectives: Identification of a novel pseudo attP site. Materials and Methods...

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:
  • Circulation

دوره 132 2  شماره 

صفحات  -

تاریخ انتشار 2015