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Expression of the cAMP Phosphodiesterase 7A1 Gene by Endoplasmic Reticulum Stress

소포체스트레스에 의한 cAMP phosphodiesterase 7A1 유전자의 발현

  • Kwon, Ki-Sang (Department of Anatomy, School of Medicine, Chungnam National University) ;
  • Kwon, Young-Sook (Department of Nursing, Joongbu University) ;
  • Kwon, O-Yu (Department of Anatomy, School of Medicine, Chungnam National University)
  • 권기상 (충남대학교 의학전문대학원 해부학교실) ;
  • 권영숙 (중부대학교 간호학과) ;
  • 권오유 (충남대학교 의학전문대학원 해부학교실)
  • Received : 2011.12.21
  • Accepted : 2012.02.08
  • Published : 2012.02.28

Abstract

This study demonstrated that upregulation of gene expression of endoplasmic reticulum (ER) stress chaperones (Bip, ERp29, calnexin, and PDI), ER stress sensors (PERK, ATF6, and Ire1), and cAMP phosphodiesterase 7A1 (cAMP PDE7A1) was induced by ER stresses in FRTL5 cells. While removing A23187 from the culture medium restored upregulation of cAMP PDE7A1 gene expression, removal of thapsigargin did not recover its expression. In addition, cAMP PDE7A1 gene expression was strongly inhibited by treatment with A23187 combined with thyroid stimulating hormone (TSH). The results are the first to show that ER stress induces cAMP PDE7A1 gene expression.

갑상선 배양세포(FRTL5)에서 ER stress에 의해서 ER chaperone (Bip, ERp29, Calnexin and PDI), ER stress sensor (PERK, ATF6 and Ire1)와 cAMP phosphodiesterase 7A1 (cAMP PDE7A1) 유전자발현이 증가하는 것을 알았다. 세포배양배지에서 A23187을 제거하면 cAMP PDE7A1 유전자발현이 회복되지만, thapsigagin의 경우는 회복되지 않았다. 그리고 A23187과 TSH를 함께 처리한 경우는 아주 강하게 cAMP PDE7A1 유전자의 발현이 억제되었다. 이 같은 결과는 ER stress에 의해서 cAMP PDE7A1 유전자발현이 상승 발현된다는 첫 보고이다.

Keywords

References

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