Disease relevance of Ccl3

• MIP-1 alpha and IL-8, but not the other chemokines, also stimulated osteoclastic motility and increased the osteoclast spread area in a dose-dependent manner, over the same concentration range as that which inhibited bone resorption [1].
• We conclude that MCP-1 and MIP-1 alpha mRNAs and proteins are induced after cerebral ischemia in the rat [2].
• Crucial role of CCL3/MIP-1alpha in the recurrence of autoimmune anterior uveitis induced with myelin basic protein in Lewis rats [3].
• Role of macrophage inflammatory protein-1 alpha (MIP-1 alpha) in acute lung injury in rats [4].
• Identification of cell types producing RANTES, MIP-1 alpha and MIP-1 beta in rat experimental autoimmune encephalomyelitis by in situ hybridization [5].

High impact information on Ccl3

• Repeated administration of the constructs encoding MCP-1, MIP-1 alpha, or RANTES inhibited the development and progression of AA, even when each vaccine was administered only after the onset of disease [6].
• Both H2O2 and MQ-induced up-regulation of MIP-1 alpha mRNA was suppressed by co-treatment with N-acetylcysteine, a synthetic antioxidant [7].
• In addition, MIP-1 alpha induced osteoclast orientation in a gradient of the chemokine, and stimulated osteoclast migration [1].
• We found that macrophage inflammatory protein-1 alpha (MIP-1 alpha) and IL-8 inhibited bone resorption by rat osteoclasts, primarily through reduction in the proportion of osteoclasts resorbing bone, a pattern of inhibition previously observed in response to macrophage CSF (M-CSF) [1].
• Recombinant rat MIP-1 alpha exhibited dose-dependent chemotactic activity for both rat and human monocytes and neutrophils, which could be blocked by anti-murine MIP-1 alpha Ab [4].

Biological context of Ccl3

• Kinetics of the neutrophil (MIP-2) and macrophage (MIP-1 alpha) chemokines revealed an early onset (12-24 h), a plateau from 1 to 4 days, and expression abruptly declining by Day 6 [8].
• To further investigate transcriptional regulation of the MIP-1 alpha gene expression, RAM cells were exposed to nicotine [9].
• In addition, the increase in MIP-1 alpha mRNA level involves, both transcriptional activation and post-transcriptional stabilization [9].
• Our studies further imply that in a developing system, stimulation with a MIP-1 alpha like substance is necessary for neuronal survival and interference with this action results in neuronal cell death [10].
• Macrophage inflammatory protein-1 alpha (MIP-1 alpha), a member of CC chemokines, has been shown to contribute to monocyte/macrophage and neutrophil chemotaxis and activation [9].

Anatomical context of Ccl3

• Macrophage inflammatory protein-1 alpha and IL-8 stimulate the motility but suppress the resorption of isolated rat osteoclasts [1].
• The distribution and morphology of MIP-1 alpha immunoreactive cells were identical with activated astrocytes [2].
• Incubation of rat basophil leukemia 2H3 cells with CCL2 or CCL3 decreased surface c-Kit expression, an effect blocked by protease inhibitors [11].
• Increased expression of CC chemokine ligand (CCL) 2 and CCL3 by RMCP I-positive cells identified mast cells as epithelial and mesenchymal sources of chemoattractant chemokines in allograft airways [11].
• We have successfully cloned nine NKR-P1+ TCR alpha beta + cells from PVG rat spleens, utilizing murine macrophage inflammatory protein-1 alpha (MIP-1 alpha) and IL-2 [12].

Associations of Ccl3 with chemical compounds

• The induction of MIP-1 alpha mRNA by LPS was partially the result of mRNA stabilization, as half life increased to over 6 hours [13].
• CCL3 induced an intracellular rise in Ca(2+), a typical signalling event of G protein-coupled receptors [14].
• These observations indicate that nicotine can induce MIP-1 alpha mRNA expression and protein synthesis in RAM cells, mediating, at least in part, via the generation of ROS [9].
• The induction of MIP-1 alpha mRNA expression by LPS in NR8383 cells was attenuated by cotreatment with the antioxidants N-acetylcysteine and dimethylsulfoxide, suggesting that the induction of MIP-1 alpha mRNA by LPS is mediated via the generation of reactive oxygen species [15].
• Treatment of RAM cells with the transcriptional inhibitor actinomycin D following exposure to nicotine revealed that the half-life of MIP-1 alpha mRNA was markedly increased by nicotine treatment, supporting a role of post-transcriptional stabilization in MIP-1 alpha gene expression [9].

Other interactions of Ccl3

• RESULTS: Excess amounts of the Abs significantly neutralized CINC-1 and almost completely neutralized CINC-2, CINC-3 and MIP-1 alpha in the pouch fluid, and a significant suppression (about 60% inhibition) of neutrophil infiltration by the Abs was found [16].
• MIP-1 alpha and MIP-1 beta mRNA-positive cells appeared around day 10, increased further on days 12-13 and then gradually decreased [5].
• To investigate the factors which regulate lymphocyte traffic in experimental autoimmune encephalomyelitis (EAE), we studied, by in situ hybridization analysis, the kinetics of mRNA expression and the potent cellular sources of RANTES, MIP-1 alpha and MIP-1 beta in the central nervous system (CNS) during the course of EAE [5].
• Since the chemokine CCL3 (macrophage inflammatory protein-1alpha) is expressed in various CNS diseases, we have used the oligodendrocyte precursor cell lines CG4 and OLN-93 to study the expression of receptors for CCL3 and the influence of CCL3 on oligodendrocyte precursor behaviour [14].
• The mRNA levels of TNF alpha, IL-1 beta, and MIP-1 alpha in rat lung were assessed by slot blot analysis [17].

Analytical, diagnostic and therapeutic context of Ccl3

• The mRNA transcripts of MCP-1 and MIP-1 alpha were detected by Northern hybridization and reverse transcriptase polymerase chain reaction (RT/PCR), respectively, and the anatomic distribution of specific proteins was analyzed by immunohistochemistry [2].
• In the LPS model, MIP-1 alpha protein could also be detected in bronchoalveolar lavage (BAL) fluids by Western blot analysis [4].
• Molecular cloning and posttranscriptional regulation of macrophage inflammatory protein-1 alpha in alveolar macrophages [13].
• Western blot analysis demonstrated a single band with an estimated molecular weight of 10 kD for MIP-1 alpha which was induced after nicotine treatment, suggesting that expression of MIP-1 alpha mRNA could reflect in protein synthesis [9].
• Northern blot analysis showed that the induction of MIP-1 alpha mRNA expression was dose-dependent [9].

References