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RNA-seq analysis of IL-10 treatment of wildtype and Ptpn1-/- knockout peritoneal macrophages

ABSTRACT: We report here the deep sequencing of the mRNA from peritoneal exudate cells (macrophages) purified from wildtype or Ptpn1 (PTP1B) knockout mice, either treated or untreated with IL-10. In periotenal macrophages IL-10 activates the transcription factor STAT3 to execute and anti-inflammatory gene expression programme. The tyrosine phosphatase PTPN1 targets STAT3 for dephosphorylation and leads to the deactivation of STAT3. In this study we examined the role of PTP1B in controlling the normal homeostatic level phosphorylation of STAT3 by comparing the IL-10/STAT3-mediated anti-inflammatory gene expression programme. We find that loss of PTP1B leads to an up-regulation of the activity of STAT3, both at the level of phosphorylation and also in enhanced expression of anti-inflammatory gene products. RNA-seq of wildtype and Ptpn1 (PTP1B) knockout mouse peritoneal macrophages, treated or untreated with IL-10

ORGANISM(S): Mus musculus

SUBMITTER: Andrew Hutchins 

PROVIDER: E-GEOD-49449 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Protein tyrosine phosphatase 1B is a regulator of the interleukin-10-induced transcriptional program in macrophages.

Pike Kelly A KA   Hutchins Andrew P AP   Vinette Valerie V   Théberge Jean-François JF   Sabbagh Laurent L   Tremblay Michel L ML   Miranda-Saavedra Diego D  

Science signaling 20140506 324

Both pro- and anti-inflammatory cytokines activate the Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway; however, they elicit distinct transcriptional programs. Posttranslational modifications of STAT proteins, such as tyrosine phosphorylation, are critical to ensure the differential expression of STAT target genes. Although JAK-STAT signaling is dependent on reversible tyrosine phosphorylation, whether phosphatases contribute to the specificity of STAT-dependen  ...[more]

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