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Electrolyte Blood Press. 2018 Jun;16(1):1-10. English. Original Article.
Sung JH , Song A , Park T , Kim E , Lee S .
Integrated Biomedical and Life Science, College of Health Science, Korea University, Seoul, Korea.


High-NaCl diet is a contributing factor for cardiac hypertrophy. The role of HSP22 as a protective protein during cardiac hypertrophy due to hypernatremia is unclear. Accordingly, this study aimed to establish a cellular hypernatremic H9C2 model and to compare the expression of HSP22 in Ca²⁺ homeostasis between a high-NaCl and angiotensin II-induced hypertrophic cellular H9C2 model.


Real-time PCR was performed to compare the mRNA expression. Flow cytometry and confocal microscopy were used to analyze the cells.


The addition of 30 mM NaCl for 48 h was the most effective condition for the induction of hypertrophic H9C2 cells (termed the in vitro hypernatremic model). Cardiac cellular hypertrophy was induced with 30 mM NaCl and 1 µM angiotensin II for 48 h, without causing abnormal morphological changes or cytotoxicity of the culture conditions. HSP22 contains a similar domain to that found in the consensus sequences of the late embryogenesis abundant protein group 3 from Artemia. The expression of HSP22 gradually decreased in the in vitro hypernatremic model. In contrast to the in vitro hypernatremic model, HSP22 increased after exposure to angiotensin II for 48 h. Intracellular Ca²⁺ decreased in the angiotensin II model and further decreased in the in vitro hypernatremic model. Impaired intracellular Ca²⁺ homeostasis was more evident in the in vitro hypernatremic model.


The results showed that NaCl significantly decreased HSP22. Decreased HSP22, due to the hypernatremic condition, affected the Ca²⁺ homeostasis in the H9C2 cells. Therefore, hypernatremia induces cellular hypertrophy via impaired Ca²⁺ homeostasis. The additional mechanisms of HSP22 need to be explored further.

Copyright © 2019. Korean Association of Medical Journal Editors.