IP3R and RyR channels are involved in traffic-related PM2.5-induced disorders of calcium homeostasis

  • Huichao Zhao (Contributor)
  • Guoqiang Tong (Contributor)
  • Jiejing Liu (Contributor)
  • Jing Wang (Creator)
  • Hongmei Zhang (Contributor)
  • Jianying Bai (Contributor)
  • Lifang Hou (Contributor)
  • Zhihong Zhang (Contributor)
  • Bai Jianying (Contributor)



Traffic-related PM2.5 can result in immune system damage and diseases; however, the possible mechanism of its effect remains unclear. Calcium (Ca2+) is a critical signaling molecule in a variety of cells. Indeed, Ca2+ is involved in numerous basic functions, including cell growth and death. In this study, Jurkat T cells were used to explore the possible mechanisms of PM2.5-elicited intracellular Ca2+signal responses. The results indicate that PM2.5 could raise the level of intracellular Ca2+ concentration ([Ca2+]i). The [Ca2+]i in Jurkat T cells significantly decreased after treatment with heparin as an inhibitor of inositol trisphosphate receptors (IP3 R), or procaine as an inhibitor of ryanodine receptors (RyR). The expression of calmodulin (CAM) protein decreased in a time-dependent manner after exposure to PM2.5, whereas the activity of Ca2+-Mg2+-ATPase seemed to show a slight drop trend after exposure to PM2.5. Our findings demonstrate that PM2.5 stimulation to Jurkat T cells would result in an increase in [Ca2+]i, which is modulated by IP3 R and RyR, as well as CAM.
Date made available2019

Cite this