Submit Data |  Help |  Video Tutorials |  News |  Publications |  FTP Download |  REST API |  Citing RGD |  Contact   

Interferons induce the expression of IFITM1 and IFITM3 and suppress the proliferation of rat neonatal cardiomyocytes.

Authors: Lau, SL  Yuen, ML  Kou, CY  Au, KW  Zhou, J  Tsui, SK 
Citation: Lau SL, etal., J Cell Biochem. 2012 Mar;113(3):841-7. doi: 10.1002/jcb.23412.
Pubmed: (View Article at PubMed) PMID:22021094
DOI: Full-text: DOI:10.1002/jcb.23412

Cardiovascular diseases have been one of the leading killers among the human population worldwide. During the heart development, cardiomyocytes undergo a transition from hyperplastic to hypertrophic growth with an unclear underlying mechanism. In this study, we aim to investigate how interferons differentially stimulate the interferon-inducible transmembrane (IFITM) family proteins and further be involved in the process of heart development. The expression levels of three IFITM family members, IFITM1, IFITM2, and IFITM3 were investigated during Sprague-Dawley rat myocardial development and differentiation of H9C2 cardiomyocytes. The effects of interferon-alpha, -beta, and -gamma on DNA synthesis in H9C2 cells were also characterized. Up-regulation of IFITM1 and IFITM3 were observed during the heart development of Sprague-Dawley rat and the differentiation of H9C2 cells. Moreover, interferon-alpha and -beta induce the expression of IFITM3 while interferon-gamma up-regulates IFITM1. Finally, interferon-alpha and -beta were demonstrated to inhibit DNA synthesis during H9C2 cell differentiation. Our results indicated interferons are potentially involved in the differentiation and cell proliferation during heart development.

Annotation

Gene Ontology Annotations
Objects Annotated

Additional Information

 
CRRD Object Information
CRRD ID: 7495752
Created: 2013-12-11
Species: All species
Last Modified: 2013-12-11
Status: ACTIVE



NHLBI Logo

RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.