RGD Reference Report - Allograft inflammatory factor-1 (AIF-1) is crucial for the survival and pro-inflammatory activity of macrophages. - Rat Genome Database

RGD Reference Report - Allograft inflammatory factor-1 (AIF-1) is crucial for the survival and pro-inflammatory activity of macrophages. - Rat Genome Database

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Allograft inflammatory factor-1 (AIF-1) is crucial for the survival and pro-inflammatory activity of macrophages.
Authors:	Yang, ZF Ho, DW Lau, CK Lam, CT Lum, CT Poon, RT Fan, ST
Citation:	Yang ZF, etal., Int Immunol. 2005 Nov;17(11):1391-7. Epub 2005 Sep 12.
RGD ID:	2313017
Pubmed:	PMID:16157606 (View Abstract at PubMed)
DOI:	DOI:10.1093/intimm/dxh316 (Journal Full-text)
Our previous studies revealed that macrophages played an important role in linking injury, inflammatory and immune response in small-for-size liver transplantation. However, the molecular basis that promoted macrophage activation was not clear. In the present study, we explored the potential role of allograft inflammatory factor-1 (AIF-1) in mediating the survival and pro-inflammatory activity of macrophages in a macrophage cell line. First, the expression of AIF-1 was investigated with the stimulation of pro-inflammatory cytokines and anti-inflammatory treatment. Second, the level of inducible nitric oxide synthase (iNOS) and the survival and migration activity of macrophages were determined with the alterations of AIF-1 expression. Finally, a potential molecule that regulated AIF-1 expression was identified by the proteomic approach. The macrophage cell line expressed a certain level of endogenous AIF-1, which could be enhanced by pro-inflammatory cytokines IL-1beta or tumor necrosis factor-alpha and suppressed by anti-inflammatory drug sodium salicylate. AIF-1 augmentation induced by AIF-1/PCDNA3.1(+) transfection enhanced the levels of iNOS and monocyte chemoattractant protein-1, and promoted the cell migration. On the other hand, suppression of AIF-1 expression by AIF-1/short interference RNA (siRNA) inhibited iNOS production, induced macrophage cell apoptosis and blocked the cell migration. Using two-dimensional electrophoresis, a disintegrin and metalloproteinase domain 3 (ADAM3) was identified after AIF-1/siRNA transfection. Transfection of ADAM3/PCDNA3.1(+) up-regulated the expression of AIF-1 and iNOS, whereas suppression of ADAM3 expression down-regulated AIF-1 and iNOS expression. In conclusion, AIF-1 played an important role in the survival and pro-inflammatory activity of macrophages, and ADAM3 might be an upstream molecule that regulated AIF-1 expression.

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Biological Process

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Object Symbol	Species	Term	Qualifier	Evidence	With	Notes	Source	Original Reference(s)
Aif1	Rat	negative regulation of apoptotic process		IDA		macrophages	RGD
Aif1	Rat	negative regulation of apoptotic process		IMP		macrophages	RGD
Aif1	Rat	negative regulation of gene expression		IMP		10 proteins and including ADAM3	RGD
Aif1	Rat	positive regulation of cell migration		IDA		macrophages	RGD
Aif1	Rat	positive regulation of cell migration		IMP		macrophages	RGD
Aif1	Rat	positive regulation of nitric oxide biosynthetic process		IDA			RGD
Aif1	Rat	positive regulation of nitric oxide biosynthetic process		IMP			RGD

Objects Annotated

Genes (Rattus norvegicus)

Aif1 (allograft inflammatory factor 1)

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