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Cyclic stretching establishes cardiac model expressing ANF and β‐MHC that responds to anti‐oxidizing drug
Author(s) -
Wong TzyyYue,
Tseng YuKai,
Jhong RongChang,
Lee WenHsien,
Cheng PeiWen
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.662.34
Subject(s) - in vivo , stimulation , chemistry , medicine , microbiology and biotechnology , pharmacology , cardiology , biology , genetics
The road to drug discovery for heart‐related diseases is challenged by advancement in whole‐heart and reliable animal heart models. In vitro model is a solution to replacing the unpredictable in vivo heart models. However, the techniques are time‐ and cost‐consuming. Cardiomyocyte cell line that expands in culture can be trained by mechanical stimulation to express cardiac biomarkers. The use of mechanical stimulation such as cyclic stretching can be more predictable, reliable in terms of cardiac marker expressions. The heart is an organ that is in constant dynamic which requires regulation for reactive oxygen species (ROS) to prevent pathological process. Here, we used cyclic stretching to stimulate cardiomyocytes with mild (5%), and aggressive (25%) strains at 1Hz. The stimulated cardiomyocytes expressed the cardiac characteristic markers Atrial natriuretic factor (ANF), and β‐myosin heavy chain (β‐MHC) after 24h of stretching. The 3H‐1,2‐dithiole‐3‐thione (D3T) has been reported to be a potent inducer of antioxidant genes through activation of the transcription factor Nrf2, and Nrf2 has been reported to play a role in cardiac remodeling. In this study, we investigated the effect of the D3T on the cardiomyocytes stimulated at mild, or aggressive strain. Results show that the aggressive strain reduced the β‐MHC expression, and the D3T enhanced the β‐MHC expression in cardiomyocytes that were stimulated with aggressive strain. Support or Funding Information This research is supported by VGHKS107‐076, VGHKS107‐168, VGHKS107‐175, MOST104‐2320‐B‐0751B‐003‐MY3, and MOST106‐2320‐B‐075B‐001. This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .