R. Matsuno, Y. Aramaki, H. Arima, Y. Adachi, N. Ohno, T. Yadomae and S. Tsuchiya, “Contribution of CR3 to Nitric Oxide Production from Macrophages Stimulated with High-Dose of LPS,” Biochemical Biophysical Research Communications, Vol. 244, No. 1, 1998, pp. 115119. doi:10.1006/bbrc.1998.8231

has been cited by the following article:

• TITLE: Down Regulation of MyD88 in Macrophages Treated with Liposomes Composed of Phosphatidylserine

  AUTHORS: Yuka Takasugi, Futoshi Kurai, Issei Kazume, Masaki Otsuka, Yoichi Negishi, Rui Tada, Yukihiko Aramaki

  KEYWORDS: Phosphatidylserine; Liposome; MyD88; TGF-β; Macrophage

  JOURNAL NAME: Pharmacology & Pharmacy, Vol.4 No.2, April 28, 2013

  ABSTRACT: We have recently demonstrated that liposomes composed of phosphatidylserine (PS-liposomes) suppressed nitric oxide and inflammatory cytokine productions following LPS stimulation in macrophages. In this study, we examined the effect of PS-liposomes on expressions of TLR-4 and MyD88, which are essential for the signal transduction in LPS stimulation. Expression of MyD88 was suppressed when macrophages were treated with PS-liposomes, but not with liposomes of phosphatidylcholine. No change in TLR-4 expression was observed. MyD88 suppression was restored to the control levels when cells were pre-treated with anti-TGF-β antibody, suggesting that TGF-β plays an important role in down-regulation of MyD88 following PS-liposome treatment.