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

Yanling Zhao,Xiushi Ni,Yiying Wu,Jinghui Cai,Haolu Hu,Min Ning,Chunjiu Zhong

doi:10.1155/2014/572915

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.

Highlights

In recent years, an increasing number of studies support the view that neurogenesis in the mammalian central nervous system is an important component of learning and memory
We found that hippocampal neurogenesis is significantly decreased in a Thiamine deficiency (TD) mouse model established by feeding mice with a thiamine-depleted diet
In contrast with the continuous increase in the optical density (OD) value observed in the control group, no significant change was seen in the TD group, demonstrating that the proliferation of the hippocampal progenitor cells (HPCs) had been totally inhibited

Summary

Introduction

An increasing number of studies support the view that neurogenesis in the mammalian central nervous system is an important component of learning and memory. In the hippocampus, which has long been considered the most important structure associated with cognition, it has been proven that neural progenitor cells located in the SGZ can persistently proliferate and mature into new adult neurons that integrate into neural circuits, where they participate in learning and memory. This is considered the cellular basis of cognition [3].

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