Kupffer cells and endothelial cells

Tri-iodothyronine differentially induces Kupffer cell ED1/ED2 subpopulations

“…Kupffer cell activation results in mononuclear cell recruitment from circulation, receptor expression, and the secretion of several molecules, such as enzymes, eicosanoids, PAF, cytokines, complement proteins, oxygen and nitrogen reactive species, and apolipoprotein E (Winwood and Arthur, 1998;Armbrust and Ramadori, 1996). Sinusoidal endothelium and Ito cells respond to factors released by activated Kupffer cells, thus amplifying the spectrum of released substances during inflammation.…”

Kupffer cell stimulation in the isolated perfused rat liver triggers nuclear factor-κB DNA binding activity

“…10 Activation of NF-kB in Kupffer cells is central in the homeostatic response to liver injury, 8 although enhanced and/or sustained DNA binding activity of the transcription factor may result in acute and chronic liver damage. 8,11,12 Direct evidence that the cellular level of ROS regulates NF-kB activity is provided by exposure of cells to hydrogen peroxide (H 2 O 2 ). 5,13 However, the response is highly cell-type dependent 6 and is questioned by the rather large range of H 2 O 2 concentrations required, which can alter cell viability.…”

Interaction networks: coordinating responses to xenobiotic exposure

“…Kupffer cells are the most abundant non-parenchymal cells in the liver, and act as liver-specific macrophages (Winwood and Arthur, 1998). As Kupffer cells do not appear to express the PPAR␣ (Peters et al, 2000), this suggests that PPAR-independent function of peroxisome proliferators may exist: one of these suggested functions is the hyperplasic response of the liver to peroxisome proliferators.…”