scholarly journals Suppression of Urokinase Receptor Expression by Thalidomide Is Associated with Inhibition of Nuclear Factor κB Activation and Subsequently Suppressed Ovarian Cancer Dissemination

2005 ◽  
Vol 65 (22) ◽  
pp. 10464-10471 ◽  
Author(s):  
Hiroshi Kobayashi ◽  
Tatsuo Yagyu ◽  
Toshiharu Kondo ◽  
Noriyuki Kurita ◽  
Kiyokazu Inagaki ◽  
...  
1999 ◽  
Vol 337 (2) ◽  
pp. 269-274 ◽  
Author(s):  
Sylvie CASPAR-BAUGUIL ◽  
Jean TKACZUK ◽  
Marie-José HAURE ◽  
Martine DURAND ◽  
Julie ALCOUFFE ◽  
...  

Activated T-lymphocytes are found early in atherosclerosis lesions, but little is known about their role. Oxidized low-density lipoproteins (oxLDLs) are considered to be involved in the pathogenesis of the lesions, and we have previously demonstrated that oxLDLs inhibit not only interleukin (IL)-2-receptor expression on the surface of in vitro-activated T-lymphocytes but also their proliferation. We have now investigated the effect of oxLDLs on blast differentiation, on IL-2 synthesis and on the activation of the nuclear factor κB (NF-κB) system in activated lymphocytes. Mildly oxLDLs (50 and 100 µg/ml) decreased the number of lymphoblasts and the level of IL-2 concentration in the culture supernatants after activation of lymphocytes by phytohaemagglutinin and PMA+ionomycin. The inhibition of IL-2 production was observed in the CD3+ T-lymphocyte cytoplasm as early as 4 h after activation by PMA+ionomycin. The study of NF-κB showed that oxLDLs led to a decrease of activation-induced p65/p50 NF-κB heterodimer binding to DNA, whereas the presence of the constitutive nuclear form of p50 dimer was unchanged. This was correlated with an unchanged level of the active form of the cytosolic inhibitor protein IκB-α. Taken together, these observations suggest that the immunosuppressive effect of oxLDLs might operate via a dysregulation of the T-lymphocyte activation mechanisms.


Cancer ◽  
2010 ◽  
Vol 116 (13) ◽  
pp. 3276-3284 ◽  
Author(s):  
Christina M. Annunziata ◽  
Helene Tuft Stavnes ◽  
Lilach Kleinberg ◽  
Aasmund Berner ◽  
Lidia F. Hernandez ◽  
...  

2004 ◽  
Vol 10 (22) ◽  
pp. 7645-7654 ◽  
Author(s):  
Seiji Mabuchi ◽  
Masahide Ohmichi ◽  
Yukihiro Nishio ◽  
Tadashi Hayasaka ◽  
Akiko Kimura ◽  
...  

2014 ◽  
Vol 21 (12) ◽  
pp. 907-915 ◽  
Author(s):  
Li-ling Hu ◽  
Dong-sheng Chen ◽  
Yan-yan Wang ◽  
You Qin ◽  
Pu Huang ◽  
...  

1998 ◽  
Vol 53 (4) ◽  
pp. 663-669 ◽  
Author(s):  
Zhongzhen Nie ◽  
Yun Mei ◽  
Mary Ford ◽  
Leonard Rybak ◽  
Adrianna Marcuzzi ◽  
...  

2002 ◽  
Vol 16 (2) ◽  
pp. 353-366 ◽  
Author(s):  
Chiara Fiorentini ◽  
Nicoletta Guerra ◽  
Marco Facchetti ◽  
Alessandra Finardi ◽  
Laura Tiberio ◽  
...  

Endocrinology ◽  
2007 ◽  
Vol 150 (8) ◽  
pp. 3457-3464 ◽  
Author(s):  
Mohan R. Dasu ◽  
Samuel Park ◽  
Sridevi Devaraj ◽  
Ishwarlal Jialal

Toll-like receptors (TLRs) are key innate immune sensors of endogenous damage signals and play an important role in inflammatory diseases like diabetes and atherosclerosis. Pioglitazone (PIO), a peroxisome proliferator-activated receptor (PPAR)-γ agonist, has been reported to be an antiinflammatory agent. Thus, in the present study, we examined the antiinflammatory effects of PIO on TLR2 and TLR4 expression in human monocytes exposed to Pam3CSK4 (Pam; TLR2 ligand) and purified lipopolysaccharide (LPS; TLR4 ligand) using flow cytometry and real-time RT-PCR. Monocytes were isolated from healthy human volunteers and pretreated with PIO (1 μm) followed by Pam (170 ng/ml) and LPS (160 ng/ml) challenge. PIO significantly decreased Pam- and LPS-induced TLR2 (−56%) and TLR4 (−78%) expression (P < 0.05). In addition, PIO decreased TLR ligand-induced nuclear factor-κB activity (−63%), IL-1β (−50%), IL-6 (−52%), monocyte chemoattractant protein-1(−83%), and TNF-α (−87%) compared with control. Next, PIO-treated db/db mice (n = 6/group) showed decreased TLR2 (−60%) and TLR4 (−45%) expression in peritoneal macrophages compared with vehicle control mice (P < 0.001) with associated decrease in MyD88-dependent signaling and nuclear factor-κB activation. Data suggest that Pam- and LPS-induced TLR2 and TLR4 expression are inhibited by PIO in human monocytes and db/db mice. Thus, we define a novel pathway by which PIO could induce antiinflammatory effects.


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