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Recombinant Cholinergic Differentiation Factor (Leukemia Inhibitory Factor) Regulates Sympathetic Neuron Phenotype by Alterations in the Size and Amounts of Neuropeptide mRNAs
Author(s) -
Nawa Hiroyuki,
Nakanishi Shigetada,
Patterson Paul H.
Publication year - 1991
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1991.tb03479.x
Subject(s) - choline acetyltransferase , leukemia inhibitory factor , neuropeptide y receptor , vasoactive intestinal peptide , neuropeptide , somatostatin , tyrosine hydroxylase , medicine , cholinergic , endocrinology , cholinergic neuron , biology , recombinant dna , nerve growth factor , chemistry , microbiology and biotechnology , dopamine , biochemistry , receptor , gene , embryonic stem cell
The cholinergic differentiation factor (CDF) in heart cells is identical to leukemia inhibitory factor (LIF). Recombinant CDF/LIF was shown to alter dramatically neurotransmitter production as well as the levels of several neuropeptides in cultured rat sympathetic neurons. Here it is shown that these changes are likely to be caused by alterations in the mRNA for these proteins and peptides. Growth in 1 n M recombinant CDF/LIF induces mRNA for acetyl CoA: choline‐ O ‐acetyltransferase [EC 2.3.1.6; choline acetyltransferase (ChAT)], somatostatin (SOM), substance P, and vasoactive intestinal polypeptide while lowering mRNA levels of tyrosine hydroxylase (EC 1.14.16.2) and neuropeptide Y (NPY). In addition, the sizes of the mRNAs for ChAT, SOM, and NPY are larger after recombinant CDF/LIF treatment.