|  Help  |  About  |  Contact Us

Publication : Islet-1 gene delivery improves myocardial performance after experimental infarction.

First Author  Barzelay A Year  2012
Journal  Atherosclerosis Volume  223
Issue  2 Pages  284-90
PubMed ID  22727192 Mgi Jnum  J:187645
Mgi Id  MGI:5437583 Doi  10.1016/j.atherosclerosis.2012.05.025
Citation  Barzelay A, et al. (2012) Islet-1 gene delivery improves myocardial performance after experimental infarction. Atherosclerosis 223(2):284-90
abstractText  OBJECTIVE: The LIM-homeobox transcription factor Isl1 plays a crucial role during heart embryogenesis and later on gives rise to adult resident cardiac stem cells. In this study, we aimed to discover new extra cardiac populations of Isl1 stem cells. We then investigated endogenous Isl1 kinetics after myocardial infarction (MI), and the effect of intra-myocardial gene transfer of naked DNA encoding Isl1 on functional recovery after MI. METHODS: We used the transgenic mice Isl1/cre/Z/EG for lineage tracing of extra cardiac Isl1 stem cells. Non transgenic mice were used to study Isl1 kinetics post-MI by RT-PCR and FACS analysis. MI was induced in non transgenic mice by permanent ligation of the left anterior descending coronary artery (LAD). Naked DNA encoding Isl1 was injected to the peri-infarct region. Evaluation of cardiac performance was conducted by echocardiogram. Analysis of myocardial fibrosis and number of vessels was performed on histological cryosections. RESULTS AND CONCLUSIONS: Isl1 gives rise to subpopulations of progenitors in both the bone marrow and spleen, and is re-expressed in the spleen and left ventricle following MI. Intramyocardial gene transfer of Isl1 to the border zone of the infarcted hearts resulted in partial salvage of left ventricular function, enhanced vascularization, and reduced myocardial fibrosis. The Isl1 gene appears to be an attractive reparative target for future management of myocardial dysfunction.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

1 Bio Entities

0 Expression