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BioMed Research International
Volume 2017, Article ID 9716087, 11 pages
Research Article

Downregulation of Profilin-1 Expression Attenuates Cardiomyocytes Hypertrophy and Apoptosis Induced by Advanced Glycation End Products in H9c2 Cells

1Department of Cardiology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China
2Department of Cardiology, Third Xiangya Hospital, Central South University, Changsha, Hunan 410006, China
3Department of Endocrinology, The First Affiliated Hospital of Nanchang University, Jiangxi 330006, China
4Department of Geriatric Medicine, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China

Correspondence should be addressed to Tianlun Yang; moc.361@ynulnait and Meifang Chen; moc.uhos@121gnafiem

Received 15 June 2017; Revised 8 September 2017; Accepted 4 October 2017; Published 7 November 2017

Academic Editor: Shoichiro Ono

Copyright © 2017 Dafeng Yang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Cardiomyocytes hypertrophy and apoptosis induced by advanced glycation end products (AGEs) is the crucial pathological foundation contributing to the onset and development of diabetic cardiomyopathy (DCM). However, the mechanism remains poorly understood. Here, we report that profilin-1 (PFN-1), a well-known actin-binding protein, serves as a potent regulator in AGEs-induced cardiomyocytes hypertrophy and apoptosis. PFN-1 was upregulated in AGEs-treated H9c2 cells, which was associated with increased cardiomyocytes hypertrophy and apoptosis. Silencing PFN-1 expression remarkably attenuated AGEs-induced H9c2 cell hypertrophy and apoptosis. Mechanistically, AGEs increased PFN-1 expression through elevating ROS production and RhoA and ROCK2 expression. Consequently, elevated PFN-1 promoted actin cytoskeleton disorganization. When either ROS production/ROCK activation was blocked or cells were treated with Cytochalasin D (actin depolymerizer), H9c2 cells were protected against AGEs-induced cardiac myocyte abnormalities, concomitantly with downregulated expression of PFN-1 and improved actin cytoskeleton alteration. Collectively, these data suggest that PFN-1 may play an important role in AGEs-induced hypertrophy and apoptosis in H9c2 cells.