کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2485351 | 1114352 | 2008 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Cellular Activation by Plasmid DNA in Various Macrophages in Primary Culture
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کلمات کلیدی
موضوعات مرتبط
علوم پزشکی و سلامت
داروسازی، سم شناسی و علوم دارویی
اکتشاف دارویی
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چکیده انگلیسی
Macrophages are an important group of cells responsible for the inflammatory response to unmethylated CpG dinucleotide (CpG motif) in plasmid DNA (pDNA) via Toll-like receptor 9 (TLR9). This finding is primarily based on in vitro studies. Previous in vivo studies also have suggested that tissue macrophages are involved in inflammatory cytokine release in the circulation following intravenous administration of pDNA to mice. However, the relationship between the in vitro and in vivo studies has not been sufficiently clarified. To gain insight into which types of cells are responsible for the production of cytokines upon interaction with pDNA, peritoneal macrophages, splenic macrophages, hepatic nonparenchymal cells (NPCs) including Kupffer cells and mesangial cells were isolated from mice. All types of primary cultured cells, except for mesangial cells, express TLR9 at varying levels. Splenic macrophages and hepatic NPCs were activated to produce tumor necrosis factor-α (TNF-α) by naked pDNA, whereas peritoneal macrophages and mesangial cells were not. pDNA complexed with N-[1-(2,3-dioleyloxy)propyl]-N,N,N-trimethyl-ammonium chloride/cholesterol liposome induced TNF-α in the splenic macrophages but not in the other cell types. These results indicate that splenic macrophages and hepatic NPCs are closely involved in TNF-α production in response to pDNA.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Pharmaceutical Sciences - Volume 97, Issue 10, October 2008, Pages 4575-4585
Journal: Journal of Pharmaceutical Sciences - Volume 97, Issue 10, October 2008, Pages 4575-4585
نویسندگان
Hiroyuki Yoshida, Makiya Nishikawa, Sachiyo Yasuda, Yumiko Mizuno, Yoshinobu Takakura,