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Biomedical subjects

M E Peele

Publications and source records attributed to M E Peele.

3 recordsLinked to original sources
PubMed1993

TSH beta subunit gene expression in human lymphocytes.

Production of neuroendocrine peptides by human lymphocytes is thought to facilitate control of the immune response. The presence of neuroendocrine peptide gene expression, specifically the TSH beta subunit gene, was studied in human lymphocytes using Northern blot analysis and polymerase chain reaction (PCR) techniques. Northern blot analysis of human lymphocyte RNA probed with a TSH beta cDNA probe failed to demonstrate TSH beta subunit steady state message levels. PCR amplification of lymphocyte-derived cDNA using TSH beta subunit complementary primers resulted in amplification of a .38 Kb DNA fragment, confirming expression and initial exonic splicing of TSH beta subunit gene exons 2 and 3 in human lymphocytes. Sequence analysis of this .38 Kb DNA fragment demonstrated conservation of exon borders after splicing (exons 2 and 3) and predicted an amino acid translation product similar, if not identical, to human TSH beta peptide sequence. Hybridization with a TSH beta subunit cDNA probe of PCR-amplified reverse-transcribed lymphocyte RNA suggested that: (1) the abundance of TSH beta subunit gene transcripts in human lymphocytes is less than the relative abundance in T3-treated pituitary; and (2) this messenger RNA may be modulated by the presence of certain thyromimetic compounds (T2, T3, TRIAC).

Amino Acid Sequence↗
PubMed1984

Beta-adrenergic antagonist inhibition of hepatic 3,5,3'-triiodothyronine production.

beta-Adrenergic antagonists provide moderate symptomatic relief for most hyperthyroid patients, although these agents have no direct antithyroid effects. Propranolol administration results in modest declines in serum T3 concentrations in both hyperthyroid and normal subjects and also inhibits T4 to T3 conversion in various tissue preparations in vitro. Other beta-adrenergic antagonists have not been shown to consistently alter serum T3 concentrations in vivo or T3 production in vitro. To evaluate the ability of beta-adrenergic antagonists to inhibit T4-5'-deiodination, we measured T3 production from T4 in rat liver homogenates (10,000 X g supernatant) using 1 microM T4 in the presence of varying concentrations of the beta-adrenergic antagonists available in the United States. Each drug inhibited T3 production, and the dose-dependent responses were linear and parallel when plotted as percent inhibition vs. log dose concentration. The calculated drug concentrations required to produce 50% inhibition were: propranolol, 1.7 mM; pindolol, 6.7 mM; timolol, 11.5 mM; atenolol, 23.2 mM; metoprolol, 30.5 mM, and nadolol, 106.1 mM. The IC50 values were similar in the presence of 4 mM dithiothreitol. In separate studies, the ability of D- and L-propranolol to inhibit T3 production was compared with that of D,L-propranolol, the common form. Both D- and L-propranolol were as effective as the racemic mixture. The propranolol metabolites 4-hydroxypropranolol, 4-methylpropranolol, propranolol glycol, and N-desisopropyl propranolol were also effective inhibitors. Thus, beta-adrenergic antagonists inhibit T3 production in vitro. This inhibition is not related to beta-adrenergic antagonism per se, but is correlated with the lipid solubility of the drugs, which may explain the effects of propranolol on serum T3 in vivo.

Adrenergic beta-Agonists↗