Selected article for: "cell cycle arrest and expression level"

Author: Kang, Hee; Park, Sung-Hyun; Yun, Jeong-Moon; Nam, Tae-Gyu; Kim, Young-Eun; Kim, Dae-Ok; Kim, Youn Jung
Title: Effect of cinnamon water extract on monocyte-to-macrophage differentiation and scavenger receptor activity
  • Document date: 2014_3_7
  • ID: 0bqhbm9p_40
    Snippet: PMA, an analogue of diacylglycerol, activates protein kinase C (PKC), which is a key enzyme of cell differentiation. PMA treatment causes cell cycle arrest in THP-1 cells through the upregulation of p21, a negative regulator of cyclin dependent kinases [32] ; the increased expression of p21 is due to the generation of ROS and PKC-mediated ERK1/2 activation. ROS inhibitors are reported to inhibit the level of SRA gene expression and acetyl LDL upt.....
    Document: PMA, an analogue of diacylglycerol, activates protein kinase C (PKC), which is a key enzyme of cell differentiation. PMA treatment causes cell cycle arrest in THP-1 cells through the upregulation of p21, a negative regulator of cyclin dependent kinases [32] ; the increased expression of p21 is due to the generation of ROS and PKC-mediated ERK1/2 activation. ROS inhibitors are reported to inhibit the level of SRA gene expression and acetyl LDL uptake in PMA-stimulated THP-1 cells [17] . This may explain why some antioxidants reduce atherosclerosis [33] . Cinnamon has antioxidant hydrophilic polyphenols such as catechin, epicatechin, and tannins [6, 34] . Our previous study showed that the high molecular fraction of CWE (over 10 kDa) occupied most of its phenolics and was responsible for its inhibitory effect on LPS-induced ERK1/2 and other inflammatory signaling molecules [1] . The same components in CWE may exert a similar effect on PMAmediated ERK1/2 activity. However, the inhibition of SRA and other surface molecules by CWE cannot be fully accounted for by its effect on ERK1/2 because effective inhibitory concentration ranges are different.

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