West China Journal of Stomatology ›› 2018, Vol. 36 ›› Issue (2): 133-139.doi: 10.7518/hxkq.2018.02.004

• Orginal Article • Previous Articles     Next Articles

Effects of protein kinase C and motigen-activated protein kinase kinase/extracellular regulated protein kinases signaling pathway on mRNA level of inducible nitric oxide synthase in Tca8113 cells

Xuefeng Gao(), Haibin Jiao, Changcheng Ye, Yingqun. Liu   

  1. The Affiliated Stomatological Hospital of Harbin Medical University, Harbin 150001, China
  • Received:2017-06-27 Revised:2018-01-30 Online:2018-04-10 Published:2018-04-10

Abstract:

Objective To explore the regulatory mechanism of inducible nitric oxide synthase (NOS-2) expression related to proliferation of Tca8113 cells. Methods RNAi mediated by short hairpin RNAs was utilized to knock down NOS-2, protein kinase C (PKC)-α, PKC-β and PKC-δ. Griess Reagent played a significant role on the detection of NO product after NOS-2 silence. The cell proliferation was determined by CCK8 method. Quantitative real-time polymerase chain reaction (q-PCR) was recruited to check the mRNA level of NOS-2, PKC-α, PKC-β and PKC-δ after treated by a variety of ways. Eventually, the measure of phosphorylation of extracellular regulated protein kinases (ERK)1/2 was performed by Western blotting in PMA-treated Tca8113 cells. Results The cell viability of Tca8113 decreased obviously after transfected with NOS-2 siRNA (P<0.01). PKC reduced the expression level of NOS-2 mRNA (P<0.05). PKC-α, PKC-β and PKC-δ worked together to regulate the level of NOS-2 mRNA (P<0.01). Motigen-activated protein kinase kinase (MEK)/ERK signaling pathway regulated the level of NOS-2 mRNA negatively (P<0.05). PKC down regulated the level of NOS-2 mRNA through MEK/ERK signaling pathway (P<0.05). Conclusion PKC regulates the mRNA level of NOS-2 related to proliferation through MEK/ERK signaling pathway in Tca8113 cells..

Key words: inducible nitric oxide synthase, protein kinase C, motigen-activated protein kinase kinase/extracellular regulated protein kinases signaling pathway, cell proliferation

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