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Transcriptome analysis revealed that PME-1 suppresses inflammatory signaling, activates PI3K/Akt signaling, and

Shunta Ikeda1, Koichi Sato1, Takashi Ohama1

  • 1Laboratory of Veterinary Pharmacology, Joint Faculty of Veterinary Medicine, Yamaguchi University, 1677-1 Yoshida, Yamaguchi 753-8515, Japan.

Biochemical and Biophysical Research Communications
|December 3, 2023
PubMed

Insights

Protein phosphatase methyl-esterase-1 (PME-1) regulates cellular signaling. PME-1 knockout impacts inflammatory and PI3K/Akt pathways, and epithelial-mesenchymal transition in mouse cells.

Area of Science:

  • Molecular Biology
  • Cellular Signaling
  • Gene Expression

Background:

  • Protein phosphatase 2A (PP2A) is a crucial serine/threonine phosphatase involved in various cellular processes.
  • PP2A holoenzyme composition is regulated by methylation, a process reversed by protein phosphatase methyl-esterase-1 (PME-1).
  • The physiological and pathophysiological roles of PME-1 are significant, yet its impact on the transcriptome remains largely unexplored.

Purpose of the Study:

  • To investigate the effects of PME-1 knockout on the transcriptome of mouse embryonic fibroblasts.
  • To comprehensively understand the impact of PME-1 on intracellular signaling pathways.
  • To elucidate the role of PME-1 in regulating inflammatory responses, PI3K/Akt signaling, and epithelial-mesenchymal transition.

Main Methods:

  • Transcriptome analysis of PME-1 knockout mouse embryonic fibroblasts.
  • Comparative analysis of gene expression profiles between wild-type and PME-1 knockout cells.
  • Bioinformatic analysis to identify affected signaling pathways.

Main Results:

  • PME-1 knockout significantly altered the transcriptome of mouse embryonic fibroblasts.
  • PME-1 was found to suppress inflammatory signaling pathways.
  • PME-1 activation of PI3K/Akt signaling and promotion of epithelial-mesenchymal transition were observed.

Conclusions:

  • PME-1 plays a critical role in regulating cellular signaling pathways.
  • The absence of PME-1 leads to suppressed inflammation and altered PI3K/Akt signaling.
  • PME-1 influences epithelial-mesenchymal transition, suggesting its involvement in cellular differentiation and migration.
Keywords:
AktEMTInflammationPME-1PP2ARNA-seq

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