Disease relevance of Aif1

• However, neither LPS nor Escherichia coli (E. coli) administration had an affect on AIF-1 expression [1].
• We induced 1 h of focal cerebral ischemia or 10 min of global cerebral ischemia in the rat, and investigated the expression of MRF-1 immunoreactivity following ischemia [2].
• Expression of allograft inflammatory factor-1 and haeme oxygenase-1 in brains of rats infected with the neurotropic Borna disease virus [3].
• Effects of autoantigen and dexamethasone treatment on expression of endothelial-monocyte activating polypeptide II and allograft-inflammatory factor-1 by activated macrophages and microglial cells in lesions of experimental autoimmune encephalomyelitis, neuritis and uveitis [4].
• After 1.5 hours of transient ischemia, Iba1 expression was examined by immunohistochemical and immunoblot analyses [5].

High impact information on Aif1

• Activated microglia and macrophages were identified morphologically and by expression of ED1 and allograft inhibitory factor-1 (AIF-1), and differentiated by their morphological phenotype [6].
• MRF-1 levels in microglia purified from cerebral cortex also upregulated in the presence of 5 DIV granule cells [7].
• One of the genes isolated was microglial response factor-1 (mrf-1), which encoded a sequence of 177 amino acids with a single EF-hand calcium-binding motif [7].
• In the developing cerebellum in vivo, levels of mrf-1 mRNA transiently increased in the early postnatal stages, reaching a peak at P7 when cerebellar neurons and astrocytes undergo extensive apoptosis [7].
• Upregulation of a new microglial gene, mrf-1, in response to programmed neuronal cell death and degeneration [7].

Biological context of Aif1

• Therefore, mrf-1 appears to be one of the microglial genes that respond to neuronal cell death and degeneration [7].
• A novel gene iba1 in the major histocompatibility complex class III region encoding an EF hand protein expressed in a monocytic lineage [8].
• The physiological function of AIF-1 in injured skeletal muscle was analyzed using a rat in-vitro model of satellite cell proliferation and differentiation [9].
• TG/N2-treated microglia showed a marked reduction in the activity of phagocytosis and showed down-regulated expression of MRF-1 or F4/80, which are markers for activated microglia [10].
• Using two-dimensional electrophoresis, a disintegrin and metalloproteinase domain 3 (ADAM3) was identified after AIF-1/siRNA transfection [11].

Anatomical context of Aif1

• The iba1 gene was shown to be highly expressed in testis and spleen, but weakly expressed in brain, lung, and kidney [8].
• A screening of hemopoietic cell lines showed that the Iba1 protein was clearly expressed in monoblastic cell lines but only very weakly expressed in myeloid cell lines [8].
• Isolation and characterization of BART-1: A novel balloon angioplasty responsive transcript in rat carotid arteries [12].
• AIF-1 expression in peripheral blood leukocytes was also significantly greater in the rejection model than in the acceptance model [1].
• Flow cytometric analysis of peripheral blood leukocytes demonstrated that AIF-1 was expressed in ED2-positive cells, a marker for Kupffer cells [1].

Associations of Aif1 with chemical compounds

• MRF-1 release was enhanced by Ca(2+)-ionophore A23187 (sixfold), thapsigargin (threefold); however, it was not enhanced by glutamate or lipopolysaccharide [13].
• Moreover, the ATP-stimulated MRF-1 release was inhibited by a P2X(7) selective antagonist, oxidized ATP (oATP), and also under a Ca(2+)-free condition [13].
• 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 [11].
• These results indicate that ATP selectively suppresses MRF-1 synthesis at the transcription level via Ca(2+) influx through P2X(7) receptors [14].
• Dexamethasone prevented or abolished local expression of EMAP II and AIF-1 at days 10-16 [4].

Other interactions of Aif1

• The majority of PCNA immunopositive cells were Mrf-1 positive with a smaller number Neu-N positive [15].
• Image analysis of glial fibrillary acidic protein- and ionized calcium binding adapter molecule 1-immunostained sections revealed astrocytic activation in the ipsilateral thalamus and microglial activation in both ipsilateral thalamus and hippocampus of traumatized animals, but no significant differences between the trauma groups [16].

Analytical, diagnostic and therapeutic context of Aif1

• By immunocytochemistry, MRF-1 was detected at 5 DIV in OX-42-positive cells (microglia), and it exhibited an increase in response to granule cell death [7].
• In adult brain sections, MRF-1 was detected in the perikarya and processes of ramified/resting microglia, and peripheral motor nerve dissection prominently increased the expression in activated microglia surrounding injured central motoneurons [7].
• Over-expression of AIF-1 in liver allografts and peripheral blood correlates with acute rejection after transplantation in rats [1].
• We hypothesized that expression of allograft inflammatory factor (AIF)-1 would be associated with liver allograft rejection as previous studies have shown that a relationship exists between kidney and heart transplantation [1].
• In vitro studies showed that AIF-1 expression in Kupffer cells was up-regulated by coculture with Th1 cytokines [1].

References