Recombinant high‑mobility group box 1 induces cardiomyocyte hypertrophy by regulating the 14‑3‑3η, PI3K and nuclear factor of activated T cells signaling pathways
- Feifei Su
- Miaoqian Shi
- Jian Zhang
- Yan Li
- Jianwei Tian
Affiliations: Department of Cardiology, Air Force Medical Center, People's Liberation Army, Beijing 100142, P.R. China, Department of Cardiology, The Seventh Medical Centre of The People's Liberation Army General Hospital, Beijing 100700, P.R. China, Department of Cardiology, Beijing Chest Hospital Heart Center, Capital Medical University, Beijing 101149, P.R. China, Department of Cardiology, Tangdu Hospital Affiliated to The Fourth Military Medical University, Xi'an, Shaanxi 710038, P.R. China
- Published online on: January 20, 2021 https://doi.org/10.3892/mmr.2021.11853
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High‑mobility group box 1 (HMGB1) is released by necrotic cells and serves an important role in cardiovascular pathology. However, the effects of HMGB1 in cardiomyocyte hypertrophy remain unclear. Therefore, the aim of the present study was to investigate the potential role of HMGB1 in cardiomyocyte hypertrophy and the underlying mechanisms of its action. Neonatal mouse cardiomyocytes (NMCs) were co‑cultured with recombinant HMGB1 (rHMGB1). Wortmannin was used to inhibit PI3K activity in cardiomyocytes. Subsequently, atrial natriuretic peptide (ANP), 14‑3‑3 and phosphorylated‑Akt (p‑Akt) protein levels were detected using western blot analysis. In addition, nuclear factor of activated T cells 3 (NFAT3) protein levels were measured by western blot analysis and observed in NMCs under a confocal microscope. The results revealed that rHMGB1 increased ANP and p‑Akt, and decreased 14‑3‑3η protein levels. Furthermore, wortmannin abrogated the effects of rHMGB1 on ANP, 14‑3‑3η and p‑Akt protein levels. In addition, rHMGB1 induced nuclear translocation of NFAT3, which was also inhibited by wortmannin pretreatment. The results of this study suggest that rHMGB1 induces cardiac hypertrophy by regulating the 14‑3‑3η/PI3K/Akt/NFAT3 signaling pathway.