Increased Expression of Acetylcholinesterase T and R Transcripts During Hematopoietic Differentiation is Accompanied by Parallel Elevations in the Levels of Their Respective Molecular Forms

Abstract

Acetylcholinesterase (AChE) is an essential component of cholinergic synapses in both central and peripheral nervous systems where it is responsible for the rapid hydrolysis of acetylcholine released from presynaptic nerve terminals. However, recent evidence suggests that AChE may also play a role in the regulation of hematopoietic cell development. For example, exogenous application of AChE significantly inhibits the growth of murine erythroleukemia (MEL) cells (1). Moreover, exposure to AChE-inhibitory insecticides increases the risk of developing leukemias (2). Further evidence also links genetic abnormalities in the AChE gene such as incomplete somatic amplification (3) and mutations/deletions (4), to proliferative disorders including myelodysplastic syndromes and acute myeloid leukemias. Together, these observations are coherent with the notion that in hematopoietic cells, AChE acts as a tumor suppressor by regulating the proliferation and differentiation of progenitor cells (2,4,5).