ArticleProceedings of the National Academy of Sciences of the United States of America1994
Antisense oligonucleotide inhibition of acetylcholinesterase gene expression induces progenitor cell expansion and suppresses hematopoietic apoptosis ex vivo.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 111 citations in OpenAlex.
- Preliminary exploration of the expression of acetylcholinesterase in normal human T lymphocytes and leukemic Jurkat T cells.Biomedical reports · 2024Article
- Validation of Acetylcholinesterase Inhibition Machine Learning Models for Multiple Species.Chemical research in toxicology · 2023Article
- Acetylcholinesterase and human cancers.Advances in cancer research · 2021Review
- In Vitro Innervation as an Experimental Model to Study the Expression and Functions of Acetylcholinesterase and Agrin in Human Skeletal Muscle.Molecules (Basel, Switzerland) · 2017Review
- Linking Pesticide Exposure with Pediatric Leukemia: Potential Underlying Mechanisms.International journal of molecular sciences · 2016Review
- Non-synaptic roles of acetylcholinesterase and agrin.Journal of molecular neuroscience : MN · 2014Article
- New pharmacological approaches to the cholinergic system: an overview on muscarinic receptor ligands and cholinesterase inhibitors.Recent patents on CNS drug discovery · 2013Review
- Acetylcholinesterase (AChE) is an important link in the apoptotic pathway induced by hyperglycemia in Y79 retinoblastoma cell line.Frontiers in molecular neuroscience · 2012Article
- Role for parasite genetic diversity in differential host responses to Trypanosoma brucei infection.Infection and immunity · 2010Article
- Acetylcholinesterase supports anchorage independence in colon cancer.Clinical & experimental metastasis · 2008Article
- Acetylcholinesterase readthrough peptide shares sequence similarity to the 28-53 peptide sequence of the acetylcholinesterase adhesion-mediating site and competes for ligand binding in vitro.Journal of molecular neuroscience : MN · 2007Article
- Differential localization of acetylcholinesterase in neuronal and non-neuronal cells.Journal of cellular biochemistry · 2005Article
- Acetylcholinesterase in Hirschsprung's disease.Pediatric surgery international · 2005Review
- The vagal nerve stimulates activation of the hepatic progenitor cell compartment via muscarinic acetylcholine receptor type 3.The American journal of pathology · 2002Article
- Morphogenetic roles of acetylcholine.Environmental health perspectives · 1999Review
- Cholinesterases in neural development: new findings and toxicologic implications.Environmental health perspectives · 1999Review
- Human osteogenesis involves differentiation-dependent increases in the morphogenically active 3' alternative splicing variant of acetylcholinesterase.Molecular and cellular biology · 1999Article
- Antisense inhibition of butyrylcholinesterase gene expression predicts adverse hematopoietic consequences to cholinesterase inhibitors.Cellular and molecular neurobiology · 1994Article
- Inhibition of gene expression with ribozymes.Cellular and molecular neurobiology · 1994Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To examine the role of acetylcholinesterase (EC 3.1.1.7) in hematopoietic cell proliferation and differentiation, we administered a 15-mer phosphorothioate oligonucleotide, antisense to the corresponding ACHE gene (AS-ACHE), to primary mouse bone marrow cultures. Within 2 hr of AS-ACHE addition to the culture, ACHE mRNA levels dropped by approximately 90%, as compared with those in cells treated with the "sense" oligomer, S-ACHE. Four days after AS-ACHE treatment, ACHE mRNA increased to levels 10-fold higher than in S-ACHE cultures or in fresh bone marrow. At this later time point, differential PCR display revealed significant differences between cellular mRNA transcripts in bone marrow and those in AS-ACHE- or S-ACHE-treated cultures. These oligonucleotide-triggered effects underlay considerable alterations at the cellular level: AS-ACHE but not S-ACHE increased cell counts, reflecting enhanced proliferation. In the presence of erythropoietin it also enhanced colony counts, reflecting expansion of progenitors. AS-ACHE further suppressed apoptosis-related fragmentation of cellular DNA in the progeny cells, and it diverted hematopoiesis toward production of primitive blasts and macrophages in a dose-dependent manner promoted by erythropoietin. These findings suggest that the hematopoietic role of acetylcholinesterase, anticipated to be inverse to the observed antisense effects, is to reduce proliferation of the multipotent stem cells committed to erythropoiesis and megakaryocytopoiesis and macrophage production and to promote apoptosis in their progeny. Moreover, these findings may explain the tumorigenic association of perturbations in ACHE gene expression with leukemia.
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