Document Detail

Transplantation of induced pluripotent stem cells ameliorates neural remodeling and reduces ventricular arrhythmias in a post-infarcted swine model.
MedLine Citation:
PMID:  24122925     Owner:  NLM     Status:  Publisher    
Neural remodeling after myocardial infarction (MI) may cause malignant ventricular arrhythmia, which is the main cause of sudden cardiac death following MI. Herein, we aimed to examine whether iPSc transplantation can ameliorate neural remodeling and reduce ventricular arrhythmias (VA) in a post-infarcted swine model. Left anterior descending coronary arteries were balloon-occluded to generate MI. Animals were then divided into Sham, PBS control, and iPS groups. Dynamic electrocardiography programmed electric stimulation were performed to evaluate ventricular arrhythmia. The spatial distribution of vascularization, Cx43 and autonomic nerve regeneration were evaluated by immunofluorescence staining. Associated protein expression was detected by Western blotting. Likewise, we measured the enzymatic activities of superoxide dismutase and content of malondialdehyde. Six weeks later, the number of blood vessels increased significantly in the iPSc group. The expression of vascular endothelial growth factor and connexin 43 in the iPS group was significantly higher than the PBS group; however, the levels of nerve growth factor and tyrosine hydroxylase were lower. The oxidative stress was ameliorated by iPSc transplantation. Moreover, the number of sympathetic nerves in the iPSc group was reduced, while the parasympathetic nerve fibers had no obvious change. The transplantation of iPSc also significantly decreased the low-/high-frequency ratio and arrhythmia score of programmed electric stimulation-induced VA. In conclusion, iPSc intramyocardial transplantation reduces vulnerability to VAs, and the mechanism was related to the remodeling amelioration of autonomic nerves and gap junctions. Moreover, possible mechanisms of iPSc transplantation in improving neural remodeling may be related to attenuated oxidative stress and inflammatory response. J. Cell. Biochem. © 2013 Wiley Periodicals, Inc.
Fengxiang Zhang; Guixian Song; Xiaorong Li; Weijuan Gu; Yahui Shen; Minglong Chen; Bing Yang; Lingmei Qian; Kejiang Cao
Related Documents :
9439545 - Myocardial infarction in a 35-year-old man with homocysteinemia, high plasminogen activ...
17380165 - Drug insight: statins for nonischemic heart failure--evidence and potential mechanisms.
2142355 - Morphological detection and quantification of lipoprotein(a) deposition in atheromatous...
19627175 - Simvastatin alleviates myocardial contractile dysfunction and lethal ischemic injury in...
17577375 - Unexpected sensitization routes and general frequency of contact allergies in an elderl...
22079205 - Puerarin prevents isoprenaline-induced myocardial fibrosis in mice by reduction of myoc...
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2013-10-5
Journal Detail:
Title:  Journal of cellular biochemistry     Volume:  -     ISSN:  1097-4644     ISO Abbreviation:  J. Cell. Biochem.     Publication Date:  2013 Oct 
Date Detail:
Created Date:  2013-10-14     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8205768     Medline TA:  J Cell Biochem     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
© 2013 Wiley Periodicals, Inc.
Department of Cardiology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, People's Republic of China.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Release of growth factors from a reinforced collagen GAG matrix supplemented with platelet rich plas...
Next Document:  Regression analysis of multivariate current status data with dependent censoring: application to ank...