Downregulation of transketolase activity is related to inhibition of hippocampal progenitor cell proliferation induced by thiamine deficiency.

Abstract

In animal experiments, hippocampal neurogenesis and the activity of thiamine-dependent transketolase decrease markedly under conditions of thiamine deficiency. To further investigate the effect of thiamine deficiency on the proliferation of hippocampal progenitor cells (HPCs) and the potential mechanisms involved in this effect, we cultured HPCs in vitro in the absence of thiamine and found that proliferation and transketolase activity were both significantly repressed. Furthermore, specific inhibition of transketolase activity by oxythiamine strongly inhibited HPC proliferation in a dose-dependent manner. However, thiamine deficiency itself inhibited the proliferation to a greater degree than did oxythiamine. Taken together, our results suggest that modulation of transketolase activity might be one of the mechanisms by which thiamine regulates the proliferation of hippocampal progenitor cells.

• Authors: Yanling Zhao, Yiying Wu, Haolu Hu, Jinghui Cai, Min Ning, Xiushi Ni, Chunjiu Zhong
• Journal: BioMed research international (Biomed Res Int) Vol. 2014 Pg. 572915 ( 2014) ISSN: 2314-6141 [Electronic] United States
• PMID: 25028661 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Antimetabolites
• Oxythiamine
• Transketolase

Topics

• Animals
• Antimetabolites (pharmacology)
• Cell Proliferation
• Cells, Cultured
• Dose-Response Relationship, Drug
• Down-Regulation
• Gene Expression Regulation, Enzymologic
• Hippocampus (enzymology, pathology)
• Neural Stem Cells (enzymology, pathology)
• Oxythiamine (pharmacology)
• Rats
• Rats, Sprague-Dawley
• Thiamine Deficiency (enzymology, pathology)
• Transketolase (biosynthesis)