The different expression patterns of hsp22, a late embryogenesis abundant-like protein, in hypertrophic h9c2 cells induced by nacl and angiotensin II

Jae Hwi Sung, Ahran Song, Taegun Park, Eunyoung Kim, Seung Kwan Lee

Research output: Contribution to journalArticle

Abstract

Background: 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 Ca 2+ homeostasis between a high-NaCl and angiotensin II-induced hypertrophic cellular H9C2 model. Methods: Real-time PCR was performed to compare the mRNA expression. Flow cytometry and confocal microscopy were used to analyze the cells. Results: 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 Ca 2+ decreased in the angiotensin II model and further decreased in the in vitro hypernatremic model. Impaired intracellular Ca 2+ homeostasis was more evident in the in vitro hypernatremic model. Conclusion: The results showed that NaCl significantly decreased HSP22. Decreased HSP22, due to the hypernatremic condition, affected the Ca 2+ homeostasis in the H9C2 cells. Therefore, hypernatremia induces cellular hypertrophy via impaired Ca 2+ homeostasis. The additional mechanisms of HSP22 need to be explored further.

Original languageEnglish
Pages (from-to)1-10
Number of pages10
JournalElectrolyte and Blood Pressure
Volume16
Issue number1
DOIs
Publication statusPublished - 2018 Jun 1

Fingerprint

Angiotensin II
Embryonic Development
Cardiomegaly
Homeostasis
Hypernatremia
Proteins
Artemia
Consensus Sequence
Confocal Microscopy
Hypertrophy
Real-Time Polymerase Chain Reaction
Flow Cytometry
In Vitro Techniques
Diet
Messenger RNA

Keywords

  • Cardiac hypertrophy
  • Homeostasis
  • HSP22 protein
  • Late embryogenesis abundant protein

ASJC Scopus subject areas

  • Internal Medicine
  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

The different expression patterns of hsp22, a late embryogenesis abundant-like protein, in hypertrophic h9c2 cells induced by nacl and angiotensin II. / Sung, Jae Hwi; Song, Ahran; Park, Taegun; Kim, Eunyoung; Lee, Seung Kwan.

In: Electrolyte and Blood Pressure, Vol. 16, No. 1, 01.06.2018, p. 1-10.

Research output: Contribution to journalArticle

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abstract = "Background: 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 Ca 2+ homeostasis between a high-NaCl and angiotensin II-induced hypertrophic cellular H9C2 model. Methods: Real-time PCR was performed to compare the mRNA expression. Flow cytometry and confocal microscopy were used to analyze the cells. Results: 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 Ca 2+ decreased in the angiotensin II model and further decreased in the in vitro hypernatremic model. Impaired intracellular Ca 2+ homeostasis was more evident in the in vitro hypernatremic model. Conclusion: The results showed that NaCl significantly decreased HSP22. Decreased HSP22, due to the hypernatremic condition, affected the Ca 2+ homeostasis in the H9C2 cells. Therefore, hypernatremia induces cellular hypertrophy via impaired Ca 2+ homeostasis. The additional mechanisms of HSP22 need to be explored further.",
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AB - Background: 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 Ca 2+ homeostasis between a high-NaCl and angiotensin II-induced hypertrophic cellular H9C2 model. Methods: Real-time PCR was performed to compare the mRNA expression. Flow cytometry and confocal microscopy were used to analyze the cells. Results: 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 Ca 2+ decreased in the angiotensin II model and further decreased in the in vitro hypernatremic model. Impaired intracellular Ca 2+ homeostasis was more evident in the in vitro hypernatremic model. Conclusion: The results showed that NaCl significantly decreased HSP22. Decreased HSP22, due to the hypernatremic condition, affected the Ca 2+ homeostasis in the H9C2 cells. Therefore, hypernatremia induces cellular hypertrophy via impaired Ca 2+ homeostasis. The additional mechanisms of HSP22 need to be explored further.

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