کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9913301 | 1550308 | 2005 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
LPS regulates a set of genes in primary murine macrophages by antagonising CSF-1 action
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کلمات کلیدی
TLR9Receptor activity-modifying protein 2CT DNACSF-1HprtTACETLRBMMRPMERK1/2 - ERK1 / 2MAPK - MAPKMicro-array - آرایه میکروinflammation - التهاب( توروم) Gene regulation - تنظیم ژنToll-like receptor - تیالآرlipopolysaccharide - لیپوپلی ساکاریدbone marrow-derived macrophage - ماکروفاژ حاصل از مغز استخوانMonocytes/macrophages - مونوسیت ها / ماکروفاژهاhypoxanthine-guanine phosphoribosyl transferase - هیپوکسانتین-گوانین فسفریبوسیل ترانسفرازmitogen-activated protein kinase - پروتئین کیناز فعال با mitogenextracellular signal-regulated kinase 1/2 - کیناز 1/2 تنظیم سیگنال خارج سلولی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
We previously reported that bacterial products such as LPS and CpG DNA down-modulated cell surface levels of the Colony Stimulating Factor (CSF)-1 receptor (CSF-1R) on primary murine macrophages in an all-or-nothing manner. Here we show that the ability of bacterial products to down-modulate the CSF-1R rendered bone marrow-derived macrophages (BMM) unresponsive to CSF-1 as assessed by Akt and ERK1/2 phosphorylation. Using toll-like receptor (tlr)9 as a model CSF-1-repressed gene, we show that LPS induced tlr9 expression in BMM only when CSF-1 was present, suggesting that LPS relieves CSF-1-mediated inhibition to induce gene expression. Using cDNA micro-arrays, we identified a cluster of similarly CSF-1 repressed genes in BMM. By real time PCR we confirmed that the expression of a selection of these genes, including integral membrane protein 2B (itm2b), receptor activity-modifying protein 2 (ramp2) and macrophage-specific gene 1 (mpg-1), were repressed by CSF-1 and were induced by LPS only in the presence of CSF-1. This pattern of gene regulation was also apparent in thioglycollate-elicited peritoneal macrophages (TEPM). LPS also counteracted CSF-1 action to induce mRNA expression of a number of transcription factors including interferon consensus sequence binding protein 1 (Icsbp1), suggesting that this mechanism leads to transcriptional reprogramming in macrophages. Since the majority of in vitro studies on macrophage biology do not include CSF-1, these genes represent a set of previously uncharacterised LPS-inducible genes. This study identifies a new mechanism of macrophage activation, in which LPS (and other toll-like receptor agonists) regulate gene expression by switching off the CSF-1R signal. This finding also provides a biological relevance to the well-documented ability of macrophage activators to down-modulate surface expression of the CSF-1R.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Immunobiology - Volume 210, Issues 2â4, 19 August 2005, Pages 97-107
Journal: Immunobiology - Volume 210, Issues 2â4, 19 August 2005, Pages 97-107
نویسندگان
David P. Sester, Angela Trieu, Kristian Brion, Kate Schroder, Timothy Ravasi, Jodie A. Robinson, Rebecca C. McDonald, Vera Ripoll, Christine A. Wells, Harukazu Suzuki, Yoshihide Hayashizaki, Katryn J. Stacey, David A. Hume, Matthew J. Sweet,