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Research Paper|Volume 12, Issue 16|pp 16035—16045

Systems biology approach to exploring the effect of cyclic stretching on cardiac cell physiology

Chien-Cheng Chen1, Tzyy-Yue Wong2, Tzu-Yun Chin3, Wen-Hsien Lee4,5,6, Chan-Yen Kuo7, Yi-Chiung Hsu3
  • 1Department of Cardiology, Show Chwan Memorial Hospital, Changhua, Taiwan
  • 2International Center for Wound Repair and Regeneration National Cheng Kung University, Tainan, Taiwan
  • 3Department of Biomedical Sciences and Engineering, National Central University, Taoyuan, Taiwan
  • 4Graduate Institute of Clinical Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan
  • 5Department of Internal Medicine, Kaohsiung Municipal Hsiao-Kang Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan
  • 6Department of Internal Medicine, School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan
  • 7Department of Research, Taipei Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, New Taipei, Taiwan
* Equal contribution
Received: March 11, 2020Accepted: May 27, 2020Published: August 5, 2020

Copyright © 2020 Chen et al. This is an open-access article distributed under the terms of the Creative Commons Attribution (CC BY) 3.0 License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Although mechanical forces are involved in pressure-overloaded cardiomyopathy, their effects on gene transcription profiles are not fully understood. Here, we used next-generation sequencing (NGS) to investigate changes in genomic profiles after cyclic mechanical stretching of human cardiomyocytes. We found that 85, 87, 32, 29, and 28 genes were differentially expressed after 1, 4, 12, 24, and 48 hours of stretching. Furthermore, 10 of the 29 genes that were up-regulated and 11 of the 28 that were down-regulated after 24 h showed the same changes after 48 h. We then examined expression of the genes that encode serpin family E member 1 (SERPINE1), DNA-binding protein inhibitor 1 (ID1), DNA-binding protein inhibitor 3 (ID3), and CCL2, a cytokine that acts as chemotactic factor in monocytes, in an RT-PCR experiment. The same changes were observed for all four genes after all cyclic stretching durations, confirming the NGS results. Taken together, these findings suggest that cyclical stretching can alter cardiac cell physiology by activating cardiac cell metabolism and impacting cholesterol biosynthesis signaling.