Down-Regulation of the M6P/IGF-II Receptor Increases Cell Proliferation and Reduces Apoptosis in Neonatal Rat Cardiac Myocytes

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Down-Regulation of the M6P/IGF-II Receptor Increases Cell Proliferation and Reduces Apoptosis in Neonatal Rat Cardiac Myocytes

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Title: Down-Regulation of the M6P/IGF-II Receptor Increases Cell Proliferation and Reduces Apoptosis in Neonatal Rat Cardiac Myocytes
Author: Chen, Zhihong; Ge, Yinlin; Kang, Jing Xuan

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Citation: Chen, Zhihong, Yinlin Ge, and Jing X. Kang. 2004. Down-regulation of the M6P/IGF-II receptor increases cell proliferation and reduces apoptosis in neonatal rat cardiac myocytes. BMC Cell Biology 5:15.
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Abstract: Background: The mannose 6-phosphate/insulin-like growth factor-II receptor (M6P/IGF2R) is a multi-functional protein that has been implicated in regulation of cell growth and apoptosis. Cardiac myocytes express relatively high levels of M6P/IGF2R, and cardiomyocyte apoptosis has been identified in a variety of cardiovascular disorders, such as myocardial infarction and heart failure. However, involvement of M6P/IGF2R in the pathogenesis of these conditions has not been determined. Thus, the objective of this study was to determine the role of M6P/IGF2R in regulation of cardiac myocyte growth and apoptosis. Results: We down-regulated the expression of M6P/IGF2R in neonatal rat cardiac myocytes and examined the effect on cell proliferation and apoptosis. Infection of neonatal cardiomyocytes with an adenovirus expressing a ribozyme targeted against the M6P/IGF2R significantly reduced the level of M6P/IGF2R mRNA, as determined by RT-PCR and Ribonuclease Protection Assay (RPA). M6P-containing protein binding and endocytosis as well as the M6P/IGF2R-mediated internalization of 125I-IGF-II were lower in the ribozyme-treated cells than the control myocytes, indicating that the number of functional M6P/IGF2R in the ribozyme treated cells was reduced. Accordingly, a marked increase in cell proliferation and a reduced cell susceptibility to hypoxia- and TNF-induced apoptosis were observed in the ribozyme-treated cells. Conclusions: These findings suggest that M6P/IGF2R may play a role in regulation of cardiac myocyte growth and apoptosis. Down regulation of this gene in cardiac tissues might be a new approach to prevention of cell death or promotion of mitogenesis for certain heart diseases.
Published Version: doi://10.1186/1471-2121-5-15
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC411032/pdf/
http://www.biomedcentral.com/1471-2121/5/15
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:10139273
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