Abstract
PTPRJ/CD148 is a tyrosine phosphatase that has tumour suppressor-like activity. Quantitative PCR of various cells and tissues revealed that it is preferentially expressed in macrophage-enriched tissues. Within lymphoid tissues immunohistochemistry revealed that PTPRJ/CD148 co-localised with F4/80, indicating that macrophages most strongly express the protein. Macrophages express the highest basal level of ptprj, and this is elevated further by treatment with LPS and other Toll-like receptor ligands. In contrast, CSF-1 treatment reduced basal and stimulated Ptprj expression in human and mouse cells, and interferon also repressed Ptprj expression. We identified a 1006 nucleotide long noncoding RNA species, Ptprj-as1 that is transcribed antisense to Ptprj. Ptprj-as1 was highly expressed in macrophage-enriched tissue and was transiently induced by Toll-like receptor ligands with a similar time course to Ptprj. Finally, putative transcription factor binding sites in the promoter region of Ptprj were identified.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Animals
-
Base Sequence
-
Cell Line
-
HEK293 Cells
-
Humans
-
Inflammation / genetics*
-
Inflammation / metabolism
-
Macrophage Colony-Stimulating Factor / genetics
-
Macrophage Colony-Stimulating Factor / metabolism
-
Macrophages / metabolism*
-
Male
-
Mice
-
Mice, Inbred C57BL
-
Molecular Sequence Data
-
NIH 3T3 Cells
-
Phagocytes / metabolism
-
RNA, Messenger / genetics
-
RNA, Messenger / metabolism
-
RNA, Untranslated / genetics*
-
RNA, Untranslated / metabolism
-
Receptor-Like Protein Tyrosine Phosphatases, Class 3 / genetics*
-
Receptor-Like Protein Tyrosine Phosphatases, Class 3 / metabolism*
-
Toll-Like Receptors / genetics
-
Toll-Like Receptors / metabolism
Substances
-
RNA, Messenger
-
RNA, Untranslated
-
Toll-Like Receptors
-
Macrophage Colony-Stimulating Factor
-
Receptor-Like Protein Tyrosine Phosphatases, Class 3
Grants and funding
Part of this work was funded by the CRC for Chronic Inflammatory Diseases. RKD was in receipt of an NHMRC Dora Lush scholarship. MED is in receipt of an NHMRC Career Development Award. The authors wish to acknowledge the ARC Special Research Centre for Functional and Applied Genomics. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.