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CSF1 — IL1A

Text-mined interactions from Literome

Green et al., J Hematother Stem Cell Res 2000 (Hemangioendothelioma) : As a step toward identifying a representative endothelial-like cell line, serum dependent and IL-1 dependent changes in M-CSF gene expression in two endothelial-like cell lines were compared to that detected in primary EC cultures ... In both types of cell cultures, IL-1alpha stimulation increased M-CSF mRNA levels 2-7-fold, whereas serum stimulation elicited a more modest effect ( 2-3-fold increase ) ... The IL-1alpha induced change in M-CSF gene expression is mediated at the transcriptional level, and M-CSF promoter activity is, in part, dependent on the activity of the NF-kappaB inducing kinase
Kamthong et al., Biochem J 2000 : Expression of M-CSF was inducible by interleukin-1alpha (IL-1alpha) , lipopolysaccharide (LPS) and PMA as demonstrated by a biological activity assay, Northern-blot analysis and reverse transcriptase ( RT ) PCR ... Treatment of the cells with forskolin or dibutyryl-cAMP attenuated the expression of M-CSF induced by IL-1alpha or LPS, but not by PMA ... Relative RT-PCR demonstrated that the expression of a 1.6-kb M-CSF mRNA transcript was more effectively induced by IL-1alpha than a 4.0-kb transcript ... M-CSF promoter-driven luciferase reporter-gene assays revealed that cAMP elevation attenuated the IL-1 induced transcription activation of the M-CSF promoter, but it had no effect on PMA induced transcription
Yang et al., Arthritis Rheum 2001 (Arthritis...) : Since in vitro studies have found that IL-1 can enhance GM-CSF and M-CSF production, we reasoned that they might be playing a part in IL-1 mediated arthritis
Kamthong et al., Biochem J 2001 : Wholly, these studies indicate that elevated cAMP antagonizes IL-1 induced M-CSF transcription by up-regulating IkappaBalpha gene induction and its consequent attenuation of NF-kappaB activation
Ku et al., Arch Biochem Biophys 1992 (Pancreatic Neoplasms) : IL-1 induced CSF-1 production was markedly suppressed ( 70 % ) by pertussis toxin ... Similarly, IL-1 induced CSF-1 production was inhibited by cholera toxin and this inhibition was reversed by an arginine analog, p-methoxy-benzylaminodecamethylene guanidine sulfate ... Dibutyryl-cAMP as well as other cAMP elevating agents such as theophylline and forskolin also suppressed IL-1 induced CSF-1 production, suggesting that cAMP concentrations inversely regulate the biosynthesis of CSF-1 ... IL-1 induced CSF-1 production was not suppressed by the protein kinase C ( PKC ) inhibitor, H7, under conditions in which 12-O-tetradecanoylphorbol-13-acetate induced CSF-1 production was completely abolished ... These data suggest that IL-1 induced CSF-1 production is not mediated via the activation of PKC
Kawano et al., Am J Reprod Immunol 2004 : Our data indicated that M-CSF and MCP-1 were regulated by IL-1alpha and TNF-alpha
Kawano et al., Fertil Steril 2004 : The effects of IL-1alpha , IL-1 receptor antagonist (IL-1RA), C2-ceramide, and C6-ceramide on the production of IL-6, IL-8, and M-CSF by ESC ... Production of IL-6, IL-8, and M-CSF was not statistically significantly increased by IL-1alpha plus C2-ceramide as compared with IL-1alpha alone ... Production of both IL-8 and M-CSF was statistically significantly increased by IL-1alpha plus C6-ceramide as compared with IL-1alpha alone ; however, IL-6 production was not increased ... The results suggest that IL-1alpha stimulates the production of IL-8 and M-CSF by a mechanism that involves the sphingomyelin-ceramide system
Tanabe et al., Life Sci 2005 : We examined the effect of the inflammatory mediator IL-1alpha on the expression of macrophage colony stimulating factor ( M-CSF ), osteoprotegerin (OPG), and prostaglandin E2 ( PGE2 ) in rat osteoblasts, and the indirect effect of IL-1alpha on the formation of osteoclast-like cells
Falkenburg et al., Blood 1991 : Interleukin-1 (IL-1) combined with fetal bovine serum ( FBS ) strongly induces the expression of macrophage-CSF (M-CSF) , granulocyte-CSF (G-CSF), and granulocyte-macrophage-CSF (GM-CSF) in fibroblasts ... Our results indicate that M-CSF expression induced by FBS or IL-1 in these fibroblasts is primarily regulated at the transcriptional level
Clinton et al., Am J Pathol 1992 (Arteriosclerosis) : Bacterial lipopolysaccharide (LPS), recombinant human interleukin-1 alpha (IL-1 alpha) or tumor necrosis factor alpha (TNF alpha) induced MCSF mRNA accumulation in a concentration dependent manner in both EC and SMC
Strassmann et al., J Immunol 1991 : Furthermore, Northern blot analysis of macrophage RNA revealed a strong induction of IL-1 alpha and IL-6 mRNA by LPS but not by M-CSF
Eda et al., Rheumatol Int 2011 (MAP Kinase Signaling System) : On the other hand, M-CSF mRNA expression level was significantly induced by both IL-1ß and TNF-a by up to 7- and 11-fold, respectively
Falkenburg et al., J Immunol 1990 : IL-1 increased M-CSF expression both in quiescent and proliferating fibroblasts, and induced the expression and release of granulocyte-, and granulocyte/macrophage-CSF
Evans et al., J Leukoc Biol 1989 (Sarcoma, Experimental) : In this paper, the hypothesis was tested that macrophage IL-1 alpha and beta gene expression was regulated by the specific macrophage growth factor, CSF-1 , produced by tumor cells
Candler et al., J Interferon Res 1985 : The results indicate that preincubation with IFN alpha + beta enhances IL-1 production in response to CSF-1 as well as to LPS
Hestdal et al., Blood 1994 : Therefore, the synergistic effects of IL-1 alpha on IL-3-, CSF-1- , and granulocyte macrophage (GM)-CSF induced progenitor growth, both in CFU-c and single-cell assays, were determined in the presence of monoclonal antibodies ( MoAbs ) 35F5 and 4E2 that block the binding of IL-1 alpha to type I and type II IL-1R, respectively ... In contrast, the MoAb antitype II IL-1R ( MoAb 4E2 ) could not inhibit the direct synergistic effects of IL-1 alpha on CSF-1- or GM-CSF induced progenitor growth
Gruber et al., J Immunol 1994 : Moreover, soluble IL-1 receptors inhibited the effect of IL-1 beta on M-CSF production thus confirming that these effects were IL-1 receptor mediated
Shafit-Zagardo et al., Int J Dev Neurosci 1993 : In the presence of IL-1 an increase in biologically active CSF-1 was detected in the astrocyte conditioned medium at 6 hr
Campbell et al., Biochim Biophys Acta 1993 : A specific radioimmunoassay was employed to demonstrate that human articular cartilage and chondrocyte monolayers in organ and cell culture, respectively, produce macrophage colony stimulating factor ( M-CSF ) in response to stimulation with interleukin-1 alpha (IL-1 alpha) , IL-1 beta, tumor necrosis factor alpha (TNF alpha) and TNF beta ... Low levels of M-CSF were observed in the supernatants of nonstimulated cultures while increased levels of M-CSF in response to IL-1 alpha and TNF alpha were detected following 2 h exposure to the cytokines ... We propose that chondrocyte M-CSF production in response to IL-1 and TNF alpha, and the concurrent destruction of cartilage by these cytokines, could provide a mechanism for the chronic nature of rheumatoid disease
Haynesworth et al., J Cell Physiol 1996 : In contrast, IL-1 alpha increased the expression of G-CSF, M-CSF , LIF, IL-6 and IL-11 and induced the expression of GM-CSF
Lajeunesse et al., J Clin Invest 1996 (Osteopetrosis) : Osteopetrotic Ob-like cells obtained pre-BMT showed normal and abnormal 1,25 ( OH ) 2D3 induced alkaline phosphatase ( ALPase ) and osteocalcin production, respectively, and failed to produce macrophage colony stimulating factor ( M-CSF ) in response to IL-1a and TNF-alpha
Wise et al., Arch Oral Biol 1998 : In vivo effect of interleukin-1 alpha on colony stimulating factor-1 gene expression in the dental follicle of the rat molar ... Because the dental follicle is required for tooth eruption and because CSF-1 appears to be a key molecule in initiating eruption, it was the aim of this study to determine if IL-1 alpha could enhance the expression of the CSF-1 gene in the dental follicle in vivo ... Reverse transcription-polymerase chain reaction showed that IL-1 alpha enhanced the expression of CSF-1 in the follicle
Song et al., Int J Hematol 1998 (Second Messenger Systems) : IL-1 alpha- or serum-stimulation of growth arrested fibroblasts had no effect on PLA2 enzyme activity and inhibitors of cytosolic or Ca ( 2+ ) -independent PLA2 activity had no effect on IL-1 alpha- or serum mediated increases in CSF-1 mRNA levels