Organic cation transporter-mediated ergothioneine uptake in mouse neural progenitor cells suppresses proliferation and promotes differentiation into neurons

PLoS One. 2014 Feb 25;9(2):e89434. doi: 10.1371/journal.pone.0089434. eCollection 2014.

Abstract

The aim of the present study is to clarify the functional expression and physiological role in neural progenitor cells (NPCs) of carnitine/organic cation transporter OCTN1/SLC22A4, which accepts the naturally occurring food-derived antioxidant ergothioneine (ERGO) as a substrate in vivo. Real-time PCR analysis revealed that mRNA expression of OCTN1 was much higher than that of other organic cation transporters in mouse cultured cortical NPCs. Immunocytochemical analysis showed colocalization of OCTN1 with the NPC marker nestin in cultured NPCs and mouse embryonic carcinoma P19 cells differentiated into neural progenitor-like cells (P19-NPCs). These cells exhibited time-dependent [(3)H]ERGO uptake. These results demonstrate that OCTN1 is functionally expressed in murine NPCs. Cultured NPCs and P19-NPCs formed neurospheres from clusters of proliferating cells in a culture time-dependent manner. Exposure of cultured NPCs to ERGO or other antioxidants (edaravone and ascorbic acid) led to a significant decrease in the area of neurospheres with concomitant elimination of intracellular reactive oxygen species. Transfection of P19-NPCs with small interfering RNA for OCTN1 markedly promoted formation of neurospheres with a concomitant decrease of [(3)H]ERGO uptake. On the other hand, exposure of cultured NPCs to ERGO markedly increased the number of cells immunoreactive for the neuronal marker βIII-tubulin, but decreased the number immunoreactive for the astroglial marker glial fibrillary acidic protein (GFAP), with concomitant up-regulation of neuronal differentiation activator gene Math1. Interestingly, edaravone and ascorbic acid did not affect such differentiation of NPCs, in contrast to the case of proliferation. Knockdown of OCTN1 increased the number of cells immunoreactive for GFAP, but decreased the number immunoreactive for βIII-tubulin, with concomitant down-regulation of Math1 in P19-NPCs. Thus, OCTN1-mediated uptake of ERGO in NPCs inhibits cellular proliferation via regulation of oxidative stress, and also promotes cellular differentiation by modulating the expression of basic helix-loop-helix transcription factors via an unidentified mechanism different from antioxidant action.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antioxidants / metabolism
  • Basic Helix-Loop-Helix Transcription Factors / genetics
  • Basic Helix-Loop-Helix Transcription Factors / metabolism
  • Carnitine / genetics
  • Carnitine / metabolism
  • Carrier Proteins / genetics
  • Carrier Proteins / metabolism
  • Cell Differentiation / genetics
  • Cell Differentiation / physiology*
  • Cell Line, Tumor
  • Cell Proliferation / genetics
  • Cell Proliferation / physiology*
  • Cells, Cultured
  • Down-Regulation / genetics
  • Down-Regulation / physiology
  • Ergothioneine / genetics
  • Ergothioneine / metabolism*
  • Glial Fibrillary Acidic Protein / genetics
  • Glial Fibrillary Acidic Protein / metabolism
  • Membrane Proteins / genetics
  • Membrane Proteins / metabolism
  • Mice
  • Mice, Inbred C57BL
  • Neural Stem Cells / metabolism
  • Neural Stem Cells / physiology
  • Neurons / metabolism
  • Neurons / physiology*
  • Organic Cation Transport Proteins / genetics
  • Organic Cation Transport Proteins / metabolism*
  • RNA, Messenger / genetics
  • Reactive Oxygen Species / metabolism
  • Stem Cells / metabolism
  • Stem Cells / physiology*
  • Symporters
  • Up-Regulation / genetics
  • Up-Regulation / physiology

Substances

  • Antioxidants
  • Basic Helix-Loop-Helix Transcription Factors
  • Carrier Proteins
  • Glial Fibrillary Acidic Protein
  • Membrane Proteins
  • Organic Cation Transport Proteins
  • RNA, Messenger
  • Reactive Oxygen Species
  • Slc22a4 protein, mouse
  • Symporters
  • Ergothioneine
  • Carnitine

Grants and funding

This study was supported in part by a Grant-in-Aid for Scientific Research provided by the Ministry of Education, Science and Culture of Japan, the Advanced Research for Medical Products Mining Programme of the National Institute of Biomedical Innovation and a grant from the Mochida Memorial Foundation for Medical and Pharmaceutical Research. The funders had no role in study design, data collection or analysis, decision to publish, or preparation of the manuscript.